Deer get chronic wasting disease (CWD) by encountering misfolded proteins called prions, which are shed by infected animals through saliva, urine, feces, and blood. These prions spread both through direct contact between deer and through contaminated environments where they can persist for years. CWD has now been detected in 36 U.S. states and five Canadian provinces, and understanding how it spreads is central to slowing its advance.
Direct Contact Between Deer
The most straightforward route of infection is nose-to-nose contact and shared saliva. Deer are social animals that groom each other, touch muzzles, and share feeding areas. An infected deer sheds prions in its saliva, urine, feces, and blood long before it shows any visible signs of illness. The average incubation period for CWD is 18 to 24 months, meaning a deer can appear perfectly healthy while spreading prions to every animal it contacts.
This long silent period is what makes CWD so difficult to control. A single infected deer interacting normally with its family group can expose dozens of other animals before anyone, human or otherwise, notices anything wrong.
How Prions Enter the Body
Most deer are infected orally, by eating or drinking something contaminated with prions. Once swallowed, prions cross the intestinal lining through specialized immune cells in patches of tissue that line the gut. These cells, which normally sample bacteria and other foreign particles to help the immune system, inadvertently transport prions into the lymphatic system.
From there, prions replicate in lymph nodes and eventually spread to the brain and spinal cord, where they cause the progressive neurological damage that defines the disease. The process is slow and irreversible. There is no immune response that clears the infection, because prions are not viruses or bacteria. They are simply proteins folded into the wrong shape, and they convert normal proteins into copies of themselves.
Contaminated Soil and Landscapes
Prions don’t break down like typical biological contaminants. They bind tightly to certain clay minerals in soil, particularly a type called smectite, which is common across much of North America. Research on a related prion disease in sheep found that the infectious agent persisted in the environment for at least 16 years. In experiments with mule deer, animals became infected from environmental contamination alone in less than one year, without ever contacting a sick deer directly.
This environmental persistence means that a single contaminated site, whether it’s a patch of ground where an infected deer urinated repeatedly or a spot where a carcass decomposed, can remain a source of infection long after the original animal is gone. The type of soil matters: clay-rich soils hold onto prions more effectively and keep them in a form that animals can still absorb. Sandy or organic soils may bind prions less tightly, but the risk is never zero.
Plants Can Carry Prions
Lab research has shown that plants growing in prion-contaminated soil can absorb those prions into their roots, stems, and leaves. Alfalfa, barley, and wheat grass have all been shown to accumulate enough prions in their above-ground tissues to infect mice that ate the plants. Prions diluted in brain material, urine, or feces bound to wheat-grass roots and leaves in one study, and hamsters that ate the contaminated grass developed prion disease.
Plants can’t replicate prions the way animal tissue does, so they function as carriers rather than hosts. But the practical implication is significant: if a farmer grows alfalfa on contaminated land and stores the hay for a season or two, those prions remain infectious when the hay is eventually fed to animals. While deer have not yet been experimentally infected through this specific route, the mechanism is biologically plausible and adds another layer to how landscapes stay contaminated.
Baiting and Feeding Sites Accelerate Spread
Artificial feeding stations, bait piles, and salt licks dramatically increase transmission risk. Deer visit these sites more intensively than natural food sources, spending more time in close contact with one another and with contaminated ground. Research has found that baiting concentrates deer and increases face-to-face contacts, which raises both direct and indirect exposure.
Perhaps more importantly, bait piles break down the natural spatial separation between maternal family groups. Under normal conditions, unrelated deer don’t spend much time together. Baiting forces them into the same small area, mixing animals that would otherwise never share saliva or step in each other’s urine. The consequences of this are measurable. In Saskatchewan, where baiting and feeding were widespread and unregulated, infection rates in mule deer rose from roughly 3% to 70% over just 15 years in core areas.
Scavengers Spread Prions to New Areas
When crows and other scavengers feed on infected carcasses, prions survive passage through their digestive systems and are excreted in their feces. Research on American crows confirmed that prions remained infectious after moving through the birds’ guts, meaning a crow that feeds on a CWD-positive carcass in one county can deposit infectious material miles away. Studies on coyotes are ongoing, but the principle is the same: any scavenger that doesn’t destroy prions during digestion could be moving the disease to previously clean areas.
This is one reason CWD keeps appearing in locations far from known infection zones. It’s not always a matter of an infected deer walking into new territory. Birds, predators, and scavengers may be carrying prions across boundaries that wildlife managers can’t easily monitor.
Why Some Deer Are More Vulnerable
Not all deer are equally susceptible. The gene that produces the normal prion protein (which the misfolded version corrupts) comes in several variants. White-tailed deer with the most common version of this gene, called the 96GG genotype, progress through the disease more rapidly once infected. Deer carrying rarer genetic variants, such as 95H, 116G, or 226K, show significantly slower disease progression.
This doesn’t mean those deer are immune. They still get infected. But they may live longer before developing symptoms, which has complex implications: slower-progressing deer survive longer but also shed prions for a longer period before dying. Wildlife managers are watching whether natural selection will gradually shift deer populations toward more resistant genotypes over time, though CWD’s spread is currently outpacing any such genetic shift.
Deer Scrapes as Transmission Hotspots
Bucks create scrapes during the breeding season by pawing at the ground and urinating on the exposed soil, often licking overhead branches in the process. These scrapes function as communication hubs: other deer visit them, sniff them, and add their own scent. A single scrape visited by an infected buck becomes a concentrated deposit of prions in saliva and urine, sitting in freshly exposed soil where clay minerals can bind and preserve them. Every deer that investigates that scrape risks oral exposure. Because scrapes are reused year after year, often in the same locations, they can become persistent sources of environmental contamination even if the original infected buck has long since died.