Population-Level Effects of Chronic Wasting Disease

Chronic wasting disease (CWD) is a malady of the deer family.  This disease is caused by a natural protein in the deer’s body called a prion.  Prion proteins can misfold, giving the protein a different conformation that makes it resistant to being broken down by the body’s natural processes.  Because these abnormal proteins are not metabolized, they accumulate.  Furthermore, the misfolded proteins can cause normal versions of the protein to misfold, setting off a chain reaction.  Problems develop in the deer’s brain because the abnormal proteins accumulate to the point they disrupt nervous-system function.  Deer so afflicted lose coordination, become listless, lose body weight, and eventually die.

That CWD is always fatal to deer is well established.  What is not clear is what the disease means for deer populations.  Chronic wasting disease has the potential to cause problems at the population level for 2 reasons.  First, a misfolded prion protein is infectious, meaning it can be passed from one animal to another through feces, urine, and other bodily fluids causing other animals to develop CWD.  Second, the configuration of the misfolded protein makes it resistant to environmental degradation, so that a prion can remain infectious in the environment for years, maybe decades.

Although CWD was first reported in the 1960s and first identified as a prion disease in the 1970s, determining if the disease could cause a decline in deer populations has been difficult for several reasons.  First, survey techniques for deer populations are not precise, so many years of surveys often are necessary to detect changes.  Second, deer populations are influenced by many natural and human-caused factors other than CWD, making it difficult to understand the primary cause of a population decline.  Finally, CWD is a disease that takes years to develop in a deer and decades to have a significant effect on deer populations.

Three studies have been published recently from central Colorado and southeast Wyoming, the area where CWD was first documented in wild deer (Miller et al. 2008, DeVivo 2015, Edmunds et al. 2016).  All three studies measured survival and reproduction of deer with CWD and deer without detectable CWD.  Survival of CWD-positive deer was 20–40% lower than CWD-negative deer.  Curiously, no difference was noted in reproductive rates as a result of CWD status.  Two of the studies had good population monitoring programs that showed declines in population size of 40–50% in the past 10–20 years.  Finally, authors in all 3 studies used reproductive rates and mortality rates to calculate annual changes in population size as a result of CWD.  Populations with CWD declined 3–20% per year but would have been stable or increasing without CWD.

A fourth study from north central Colorado paints a different picture (Geremia et al. 2015).  Whereas CWD prevalence varied between 20 and 42% in the first 3 studies, CWD prevalence was < 10% and appeared to have declined since the late 1990s.  While CWD was contributing to declines in deer populations in portions of this study site, the overall picture was of a population that had stabilized.  The bad news was that hunter harvest had to be curtailed to enable the population to stabilize.

What do these studies mean for CWD management?  First, CWD can cause declines in deer populations, but the effects may take 25 or more years to be apparent.  Second, the population-level effects of the disease may vary geographically, so monitoring and research will be important to understand the effects of CWD on deer populations.  Third, CWD will result in lower deer harvest over the long term because of lower survival imposed by CWD.  Yet high harvests may be necessary in the short term to prevent the disease from spreading by reducing deer density. We are on a long, uncertain journey regarding CWD.  Learning from areas where CWD has been present for a long time will be essential to protecting the wildlife resources we all treasure.

To learn more about these studies, see the original publications:

DeVivo MT.  2015.  Chronic Wasting Disease Ecology and Epidemiology of Mule Deer in Wyoming.  Dissertation.  University of Wyoming, Laramie.

 Edmunds DR, Kauffman MJ, Schumaker BA, Lindzey FG, Cook WE, Kreeger TJ, et al.  2016. Chronic Wasting Disease Drives Population Decline of White-Tailed Deer. PLoS ONE 11(8):e0161127.  doi:10.1371/journal.pone.0161127

Geremia C, Miller MW, Hoeting JA, Antolin MF, Hobbs NT.  2015.  Bayesian Modeling of Prion Disease Dynamics in Mule Deer Using Population Monitoring and Capture-Recapture Data. PLoS ONE 10(10): e0140687. doi:10.1371/journal.pone.0140687

Miller MW, Swanson HM, Wolfe LL, Quartarone FG, Huwer SL, et al. 2008. Lions and Prions and Deer Demise. PLoS ONE 3(12): e4019. doi:10.1371/ journal.pone.0004019

Trophy Points: Big Game Research On Line is complied and edited by David G. Hewitt, a Professional Member of the Boone and Crockett Club and the Stuart W. Stedman Chair for White-tailed Deer Research at the Caesar Kleberg Wildlife Research Institute.