Abstract
The contagious prion disease “chronic wasting disease” (CWD) infects mule deer (Odocoileus hemionus) and related species. Unchecked epidemics raise ecological, socioeconomic, and public health concerns. Prion infection shortens a deer’s lifespan, and when prevalence (proportion of adults infected) becomes sufficiently high CWD can affect herd dynamics. Understanding population responses over time is key to forecasting long-term impacts. Here we describe unexpected stability in prevalence and abundance in a mule deer herd where CWD has been left unmanaged. High apparent prevalence (~30%) since at least 2005 likely drove observed changes in the proportion and age distribution of wild-type native prion protein (PRNP) gene homozygotes among deer sampled. Predation by mountain lions (Puma concolor) may be helping keep CWD in check. Despite stable appearances, prion disease nonetheless impairs adult survival and likely resilience in this deer herd, limiting its potential for growth despite refuge from hunter harvest and favorable habitat and winter conditions.
Highlights
The contagious prion disease “chronic wasting disease” (CWD) infects mule deer (Odocoileus hemionus) and related species
The chronic wasting disease is the only prion disease known to occur in free-living species and one of only two prion diseases shown far to be contagious
Some combination of predation by mountain lions and perhaps subtle genetic shifting in the mule deer host or unidentified environmental factors may have contributed to the net absence of measurable change, at least on the surface
Summary
The contagious prion disease “chronic wasting disease” (CWD) infects mule deer (Odocoileus hemionus) and related species. Agent, and environmental factors seem to drive efficient transmission[2,3,13], leading to epidemics where one in every three or four adult animals become infected annually[5,8,14] At such levels, CWD can affect host population growth and stability[5,6,7,8]. The insidious dynamics, combined with relatively recent emergence or detection and lack of sustained interest and resources, have limited the opportunities to observe long term trends To this end, we revisited the Table Mesa mule deer herd in southwest Boulder, Colorado USA, where we had last studied CWD in 2005–20095. Our analyses revealed unexpected stability in CWD prevalence and deer abundance despite changes in the proportion and age distribution of wild-type PRNP gene homozygotes likely driven by disease, as well as evidence that predation by mountain lions (Puma concolor) may be helping keep CWD in check at
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