Despite overall downward population trends in most bat species affected by white-nose syndrome (WNS), there exists variation in the magnitude of decline. Developing predictive models based on observed survival patterns can generate testable hypotheses about mechanisms driving population dynamics and contribute to the development of targeted approaches to disease management. We conducted a mark-recapture study of federally endangered Indiana bats (Myotis sodalis) at an infected site in New Jersey during 2011-2016. Based on our survival estimation, we modeled two explanatory mechanisms potentially driving the observed patterns. Combining epidemiological methods with matrix population modeling approaches, we predicted the dynamics of Indiana bat populations experiencing: 1) a phased exposure to an infective dose of Pseudogymnoascus destructans, the causative agent of WNS, through the spatial spread of the pathogen through the hibernaculum; and 2) a cumulative mortality risk from iterative WNS infection.
Survival decreased from 0.78 (95% CI: 0.59, 0.89) and 0.79 (95% CI: 0.70, 0.86) for females and males, respectively, in 2011 to 0.74 (95% CI: 0.33, 0.94) and 0.75 (95% CI: 0.53, 0.89) for females and males, respectively, in 2015. Under a scenario in which bats are experiencing a phased exposure to WNS, models suggest that infected individuals have an average survival probability of 0.64, and prevalence of WNS infection is predicted to reach 100% within 11 years of disease emergence. Under the cumulative mortality risk hypothesis, survival probability of individuals decreases by with each infection cycle. In either case, infected populations are predicted to stabilize at a growth rate of l = 0.99. The results of this work suggest that Indiana bats tolerate a pathogen load prior to onset of infection, leading to a less pronounced population decline than for other susceptible species. However, the long-term risk of WNS to Indiana bats may be more severe than current populations trends suggest because the selective forces acting on infective populations may be too weak to sustain population persistence, even if resistant individuals exist.