Chronic wasting disease is contagious and relentless. There is no cure, no way to test living animals, and once infections are introduced into wild populations, there is no realistic way to stop them from spreading.
An infected deer typically will survive for 18 months to two years. There’s a long incubation period in which they don’t usually show symptoms, but as the disease progresses, the animals will begin to appear listless and lose weight.
In the final six weeks or so they can seem aimless and oblivious to danger, become emaciated and drool. They often stand with their legs spread like sawhorses, as if trying not to topple over.
These so-called “zombie deer” often get media attention, but as the disease progresses in the wild, deer become more susceptible to other diseases, less able to protect themselves, more prone to predation and more apt to be hit by cars. They rarely live long enough to become zombies.
How long have scientists known about CWD?
Chronic wasting disease was first detected in the mid-1960s when penned deer in Colorado began to exhibit symptoms generally described as “wasting away.” Researchers attributed it to stress until the late 1970s, when wildlife veterinarian Beth Williams performed necropsies on deer that had died of a similar syndrome. She found brain lesions consistent with transmissible spongiform encephalopathies – diseases of the nervous system that afflict both animals and humans.
A year later, neurologist Dr. Stanley Prusiner was studying TSE diseases and discovered that a very small protein could become misshapen and resistant to the body’s ability to take it apart. It entered cells, tricking them into replicating it, then moved into the lymph and nervous systems. Eventually it moved to the brain, where small clumps aggregated and caused TSE. Prusiner called that nonliving, infectious protein a “prion.”
For example, while no one knows how or where CWD originated, some scholars think a mutated prion jumped the species barrier to deer from sheep infected with another animal prion disease called scrapie. https://www.youtube.com/embed/N0Y5IHRbtqU?wmode=transparent&start=0 Animals with chronic wasting disease don’t typically show symptoms in the early stages of infection.
Why are prion diseases so hard to combat?
Because of their structure and the fact that they don’t contain genetic material, prions like the one that causes CWD are nearly indestructible. Breaking a prion apart, or denaturing it, would require a very high concentration of chlorine solution or heat exceeding 1,800 degrees F (980 C).
Once they are deposited on the landscape in urine or feces, CWD prions can persist for decades. Years after deer infected with chronic wasting disease were removed from pens, other deer placed on the contaminated soil in those same pens also became infected.
In wild herds the prion is spread as deer, which are highly social animals, groom and lick one another. During the fall mating season, bucks search for mates, fight and breed. They also visit spots known as scrapes, where they lick the soil and overhead branches where other deer have left their own calling cards. Thanks to these behaviors, bucks usually have CWD at double the rate of does.
Because the disease does not kill quickly, infected animals are able to breed for a season or two, so there is no strong genetic selection pressure favoring the development of herdwide immunity. And recent research suggests infected does can occasionally transmit the prion to their fawns before birth.
In some places where CWD occurs, the infection rate may only be 1% to 5%, and the disease’s herdwide impact may not be apparent, even to hunters. Elsewhere, the infection rate can reach 50% and maybe even 100%. In those cases, population impacts will inevitably lead to a smaller and younger herd.
What do hunters need to know?
No one wants a disease named after them. With infected deer often appearing healthy, even at close range post-harvest, the only way to be sure an animal is disease-free is to have it tested, usually using lymph nodes.
As CWD spreads and more people are having deer tested, it can take weeks to receive the results. That makes meat processing a much more onerous affair.
It is critical to recognize that once a single deer is infected it acts like tinder to ignite a conflagration. Moving deer around, either alive or dead, can introduce and spread the disease.
CWD was detected in northern Mississippi and western Tennessee, where I work, in 2019. Based on what was then a relatively high infection rate, it had likely been on the landscape for a number of years and was spreading rapidly. Currently, about 40% of the Ames research station’s herd is infected.
Research on CWD has been ongoing for decades around the country. But it is in the South now. At Ames, in cooperation with other scientists from around the country, we are analyzing soil and twig samples for prion concentrations and quantifying deer visits at scrape sites and salt stations. We are also investigating ways to destroy salt stations to avoid continued exposure.
Other studies include training dogs to detect metabolites associated with the disease, and developing an early warning system before the prion can metastasize across a landscape.
We are studying how hunters react when CWD is detected locally, and comparing hunting success before and after a herd has become infected. The perspectives of hunters are important because they love the outdoors and are the first stopgap in CWD’s spread. Hunting is the primary tool for deer management, especially control of overabundant deer populations where CWD can run rampant.
Our deer hunters participate in the research at every step and often collect samples from deer they harvest. As one hunter said, “We’ve brought in everything except the tracks.”
We hope we can scale up our efforts along with other scientists as we analyze an ailing herd to provide insights into chronic wasting disease for the benefit of animals and humans alike.
ABOUT THE AUTHOR
Allan Houston, Professor of Forest and Wildlife Ecology, University of Tennessee. I am located in the Department of Forestry, Wildlife and Fisheries in Knoxville, but live and work on the 18,400-acre Research and Education Center in western Tennessee. There, I manage the forests and wildlife, including timber sales and hunting clubs for deer and turkey and ducks. I conduct research, or have been involved, in all manner of natural resource questions in forestry and wildlife, ranging from quail, beavers, deer, coyotes, hawks, ticks and tick-borne disease, small mammals, mesopredators … to short rotation woody crops for carbon sequestration, domestication of hardwoods with development of pedigreed orchard stock and artificial regeneration (primarily oak) leading to enrichment of developing natural stands, and crop tree release in mid-rotational stands. I teach a UT senior-level silviculture course for forestry students at Ames. I am author and co-author of well over 100 scientific articles and have given hundreds of professional and public presentations.