Infectious diseases may be key drivers in the extinction vortices of small, isolated wildlife populations due to the loss of immunogenetic heterozygosity. In 2013, an epizootic of Mycoplasma ovipneumoniae (M. ovi.) caused high mortality in desert bighorn sheep (DBH) at Old Dad Peak in the Mojave National Preserve, California and spread to neighboring subpopulations. Genetic diversity varies widely among subpopulations in this system, but the consequences of that diversity during an epizootic were unclear. We expected that less connected subpopulations would have a weaker immune response and have a higher prevalence of M. ovi. infection. The opposing view was that higher connectivity would facilitate infectious disease spread among the metapopulation. We used blood samples (n=72 in 2013, n=44 in 2014) from DBH captured in 13 populations to measure immunity using a variety of immunoassays (hematology, bacterial killing, and lymphocyte proliferation). We evaluated whether those immune function measures were correlated with disease status or subpopulation connectivity.
Results/Conclusions
Our results showed significant differences in pair-wise immune response measures between subpopulations (p<0.05). Connectivity was negatively correlated with disease prevalence at the time of capture (p<0.001), and the bacterial killing ability of blood was positively correlated with an active M. ovi. infection (p<0.01). Therefore, DBH subpopulations demonstrated inherent immune response differences, and more connected subpopulations were able to resist M. ovi. invasion. DBH that were actively infected with M. ovi. had an upregulated innate immune response which aided in infection survival. These findings support management decisions that increase connectivity within a metapopulation, because increasing connectivity could reduce inbreeding and drift and increase disease resistance.