Editor's note: Robert Zink is a professor in the School of Biological Sciences at the University of Nebraska-Lincoln. Zink was the Breckenridge Chair of Ornithology at the University of Minnesota’s Bell Museum from 1993 to 2015.
The frequency of chronic wasting disease (CWD), the brain ailment that is fatal to deer, increased from near zero in 2002 to 56 % in 2018 in adult male whitetail deer in southwest Sauk County, in Wisconsin. Females and young deer showed less dramatic increases, according to Wisconsin Department of Natural Resources reporting.
The figure raises an obvious question: What will happen when all the deer in that area have CWD?
The cause of the infectious disease is a prion — a protein that otherwise serves a normal function, that for some reason becomes misshapen. Misshapen proteins beget more of their kind. An infected deer will experience an ever-expanding pool of prions in its body followed by inevitable death, depending on their genetic composition at the “prion gene.” Once infected, a deer’s CWD will progress to the clinical stage in from one to three years.
The clinical stage is the one we hear about — whitetails that are emaciated, staggering around, with a loss of fear. Why aren’t the woods littered with dead deer? Most CWD deer in the wild don’t live long enough to reach the clinical stage. Preclinical but infected deer are killed by predators and cars more often than those without CWD. If a deer dies from CWD, scavengers quickly disperse the carcass. If you’re a deer with CWD, you’re among the walking dead.
How could all deer acquire CWD? Fawns can get the disease before and after birth from their mothers. Infectious prions occur in the semen of whitetail deer. They also could be obtained by ingesting saliva from infected (late-stage) deer, perhaps on contaminated food sources. When crows and coyotes scavenge the carcass of a deer that died from CWD, their droppings contain infectious prions. Prions from decomposed deer, saliva, urine or feces can become incorporated into plants, and subsequently be eaten by deer. Prions remain infectious in the soil for years. As the environmental reservoir of toxic prions continues to grow, deer can be infected irrespective of whether there are many or few deer in the immediate area. That is why culling works only in the very early stages of a CWD outbreak — you need to get ahead of the environmental accumulation.
If every deer is infected, what might happen to the population? The answer depends partly on the proportion of deer with the form of the prion gene that can delay onset of clinical symptoms.
To simplify: Deer with Gene A live for two years after infection; Gene B two to three years: Gene C up to four years. In a small sample from the Minnesota metro zone, my laboratory found that 70% of deer possess Gene A and 30 % Gene B. CWD acts later in life, like Alzheimer’s disease in humans, and death might not occur until after at least one breeding attempt. That suggests that more numerous 1½-year-olds might be the main contributors to the gene pool, with a smaller contribution from 2½-year-olds. Thus, the population will probably consist of mostly young deer. If deer with gene B leave more offspring, the frequency of B should increase and result in a greater contribution from 2½- to 3½-year- olds. Gene C is in low frequency in most places (e.g., 2-3 % in Nebraska).
In species like bighorned sheep and elephants, breeding shifts to younger males when the old (trophy) males are culled. In some elephant populations under heavy poaching pressure, bulls don’t grow tusks.
Very few trophies
Our trophy rooms might become museums of buck heads past. With shortened life spans and breeding shifted earlier in life, very few trophy class animals will exist. If you see a really large-antlered buck, you might let him walk because he might have a rare genotype (Gene C) that warded off CWD for a relatively long time. Some deer naturally have relatively small antlers, like the Coues deer of the Southwest, so maybe it won’t be that bad.
The elephant in the room is whether we will continue to eat venison if almost all healthy-appearing deer are CWD-positive. I suspect many preclinical deer infected with CWD have been eaten by hunters because the deer appeared normal.
An unintended experiment is underway involving 81 people who unknowingly consumed venison from such a CWD-positive whitetail deer in 2005 in New York. The first follow-up tests in a study at Binghamton University (N.Y.) found no evidence of prion disease. Currently there is no evidence of CWD passing from deer to humans, either in life or in lab experiments with tissue cultures.
Because Mad Cow Disease can take decades to appear in humans, vigilance over CWD is warranted. If nearly all deer become CWD-positive, more research will be directed at risks to humans.