Chronic Wasting Disease Still Confounds Researchers. But Some Important New Clues Have Emerged

by Vern Evans

In the lineup of wildlife diseases across the country, few are more studied and yet still more mysterious than chronic wasting disease.

The prion disease, first identified in a Colorado research facility in the 1970s, has been making headlines for decades. Every year brings developments and setbacks, studies showing promise and others pointing to disaster, leaving wildlife managers trying (or trying not) to implement the latest method of control. 

“One constant with CWD is that the news always seems to get worse,” says Krysten Schuler, a wildlife disease ecologist and director of the Cornell Wildlife Health Lab.

Depending on which researcher you ask (and there are many), chronic wasting disease could be solvable or it could be a scourge on our landscape and in our wildlife herds until the end of time. 

It’s easy to get lost in the technicalities of every new paper or theory. And equally hard to parse out exactly what the new ideas or developments mean for those of us who hunt deer and elk in one of the 35 states and five Canadian provinces currently infected with CWD. 

So Outdoor Life asked experts to break down the most recent newsworthy breakthroughs and ideas related to the disease.

CWD Testing Could Get Quicker

One major hunter concern has been the lag between pulling the trigger and checking an online portal to find out if a deer had CWD. The Wyoming Game and Fish Department, for example, tells hunters it could take up to two weeks to receive their results, and the Minnesota Department of Natural Resources says results can take 10 to 14 days. Those wait times are longer than most hunters can usually hang an elk or deer in their garage in mild weather.

A recent paper out of coordinating state labs in New York, Michigan, Minnesota, Missouri, Pennsylvania, and Wisconsin analyzed results from a new relatively technique called RT-QuIC to test for the disease. This one is a PCR-like test, which might sound familiar from when we all lived in the throes of Covid-19 testing. A PCR is done quickly in a lab and causes whatever it’s looking for to multiply. 

“That means if CWD is at very low concentrations, you can still find the disease,” Schuler says. “This is the method that’s been used to identify prions in urine or blood or skeletal muscle before.”

As a result, the new test may also open the door to detecting CWD in bodily tissues other than just the lymph nodes, which aren’t always easy for the average hunter to find and remove. This doesn’t, however, solve the issue of a field test done by hunters, which is what everyone really wants. 

“There aren’t many tests you can do well in the field, and this is too important to get wrong,” Schuler says. “There are at-home pregnancy tests, but billions of people have taken them. You need a long time and a lot of accuracy out there for a hunter to be able to know, yes, it’s positive or no, it’s not.”

The U.S. Department of Agriculture, which doesn’t have jurisdiction over wildlife but does approve CWD tests, hasn’t given the recent RT-QuIC test its stamp, which means state wildlife agencies aren’t largely using it yet. But Schuler feels hopeful the recent paper will help push it in the right direction. USDA approval could then mean states begin using the test and hunters may get their results back more quickly. It could also mean fewer false negatives because the test new picks up the disease earlier than the current one. All of these benefits could make hunters more willing to submit their deer and elk for CWD testing. 

We Shouldn’t Freak Out Over Diseased Soils

In the nearly 15 years I’ve spent reporting on CWD throughout the West, few topics seem to deflate researchers and the public more than the prion’s ability to remain infectious in soil. Most of us can wrap our heads around the concept of a virus or bacteria, understanding that it spreads in the air when someone sneezes, or can live for a short time on surfaces. But CWD prions seem to defy all our normal rules about staying germ-free: They cling to knives and butchering surfaces, can only be destroyed by concoctions of lye or high concentrations of bleach, stay viable in soil, and, some studies show, can even be drawn into blades of wheat grass.

The fear of environmental transmission has led to regulations in states across the country preventing people from dumping carcasses along roadsides or transporting them across state lines, which most researchers will argue is a good thing. 

Yet as more researchers and management agencies accept environmental transmission as gospel, Bryan Richards, Emerging Disease Coordinator at the USGS National Wildlife Health Center in Wisconsin, is raising his hand with a counter perspective. 

Saying animals that live in an area where CWD was once detected are at as high a risk of contracting the disease as ones that gather in big groups in captive facilities or at artificial feed grounds can quickly lead to a collective feeling of overwhelm and even resignation. 

“From the agency, landowner, and hunter standpoint, it likely contributes to the attitude, ‘if it’s been there for more than the briefest of periods, we’re likely screwed. Even if we could make the deer go away for a while, that residual contamination would keep the epidemic going once new deer were in that space,’” Richards says. “The data and science do not confirm that.”

The data and science also don’t disprove it, he says “but it has become somewhat of a mantra.”

While Richards can point to examples of indoor and outdoor facilities that were depopulated, left fallow, then repopulated only for the new animals to contract the disease, he wants to see a deeper look into where we’re putting our focus and concern. The scientific and wildlife community do know, through repeated studies, that culling herds reduces transmission — while also lowering environmental load. Targeting older adult males can also cut down on spread. But focusing exclusively on environmental transmission like prions in soils or grass risks taking the focus off more proven methods of control.

Relying on Genetic Resistance Will Be Risky

Researchers, politicians, wildlife managers, and hunters all seek solutions to wildlife diseases through genetics. Even diseases as deadly as the plague don’t kill every prairie dog in a colony. CWD, on the other hand, is always fatal to deer it infects, but some cervids seem to live longer than others. 

A 2017 paper authored largely by National Park Service biologists in Fort Collins, Colorado, showed some elk with a “naturally occurring but underrepresented prion protein variant” lived longer and reproduced for more years than their counterparts. The paper went on to say that elk in herds infected with CWD for between 30 and 50 years had twice has high of a chance to have that genetic variation than elk in herds where the disease is more recent. The natural conclusion? Give a herd long enough, and the resistant genetics could rise to the top. 

Unfortunately, the paper also says, “it remains unknown if this will allow elk to mitigate the negative population impacts of CWD.”

Similar work has been done in captive deer facilities across the Southeast, with researchers in Texas finding in 2020 a genetic variation in deer that could help them survive longer with the disease. The billion-dollar captive deer industry is more than a little interested. 

Fast forward to earlier this year, and Oklahoma lawmakers passed a bill not only requiring the state pursue research into a genetic rescue, but also allowing private landowners to release deer with the genetic variation onto their land in hopes of eventually changing the genetics of wild, free-ranging herds.

Schuler has some very real concerns, and so does the National Deer Association.

“The work that’s been done is all in captive deer, saying that there are certain genotypes that live longer,” Schuler says. “But they haven’t tested it where they actually give the animal the disease and see if they survive longer, or survive, period.

“I think that’s a critical first step before we jump ahead and say, ‘Let’s just go and release these animals out on the landscape.’”

Because while deer with these unique genetics may potentially live longer, they aren’t more resistant to getting the disease. And that distinction matters, says Schuler. If these animals live longer with the disease, they could be spending a lot longer shedding their prions into the environment and passing the disease along to other animals. 

The National Deer Association also worries that without a “foolproof live deer test for CWD,” states could also be releasing CWD-positive deer out onto a landscape that doesn’t yet have the disease.

“To fight the ongoing spread of CWD, we need to stop the movement of live deer and elk,” the NDA states. “Period.”

No Human Has Been Infected with CWD

Little rocked the CWD world more than a 2017 presentation by Canadian researchers that showed after being fed infected with CWD brain tissue, some captive macaque monkeys contracted the disease. 

While that study has since raised questions from researchers around the U.S. and Canada, that fear of CWD crossing the species barrier to humans remains strong. An abstract published in the journal Neurology earlier this year added even more fuel to the fire when it reported that two hunters who died from Creutzfeldt-Jakob disease, the human version of CWD, had been at the same hunting camp. Wildlife experts across the country refuted the claim, but headlines proclaiming that “zombie deer” gave CWD to humans persisted.

The risk of human infection does exist, experts say, or at least can’t be ruled out. That’s why the Centers for Disease Control and Prevention and the World Health Organization advise hunters not to eat meat from an animal that tests positive for the disease. But a June 2024 paper out of the high-powered Rocky Mountain Laboratories in Hamilton, Montana, provides some important new insight.

Researchers at the lab tried infecting two types of “human cerebral organoids” — tissue that closely resembles and acts as human brain—with CWD. They exposed the tissue to “high concentrations” of CWD from three sources for seven days, then tested for infection for about six months. 

The result? No infection. 

Their conclusion was “the unsuccessful propagation of CWD in cerebral organoids supports a strong species barrier to transmission of CWD prions in humans.”

Read Next: Does Chronic Wasting Disease Infect Humans? Despite Shocking Headlines, Recent Research Suggests It Does Not

Does this mean we’re all clear to eat a CWD positive animal? No, researchers say. Even the paper qualifies its results by saying human organoid tissue is not exactly the same as real human brain tissue, and that it’s possible another strain of CWD could be more virulent. 

But, it’s important to remember that there is no documented evidence of a human ever becoming infected with chronic wasting disease. 

A Prion Map Could Lead to a Vaccine

The ability to see, and thus map, a gene or protein has been the first step toward researchers figuring out a potential solution to the problem caused by that gene or protein. But as much as CWD has been studied, researchers haven’t been able to visualize certain parts of its structure. Until now. 

The same Montana lab that tried infecting imitation human brain tissue with CWD published a paper that maps the bottom of the CWD prion. The prion has a 180-degree twist in it, which might not mean much to almost any of us, but could lead to a possible vaccine, the paper’s authors say.

It also introduces another bit of data in the debate over human transmission. That twist at the bottom may be why humans haven’t — at least so far — seemed to be infected by CWD. 

“It’s very informative,” Richards says, “But it doesn’t finish the book.”

 

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