Since 2006, white-nose syndrome (WNS) has spread rapidly and caused dramatic declines in North American bat populations. Bat mortality and spatial spread have been primarily studied at separate scales, but the mechanisms linking these processes will largely determine the future state of bat populations. Building upon increased knowledge about the dynamics of WNS within individual hibernacula, we develop a stochastic model for within-cave dynamics that includes infection risk from bat-to-bat contact and fungal spores present in the environment, and also accounts for the influence of infection severity on disease-induced mortality. The individual hibernacula are part of a metapopulation that undergoes reproduction and redistribution between caves in the next winter. The stochastic process of disease spread to previously uninfected caves is assumed to be dependent on the size of the bat metapopulation, based on the hypothesis that disease spread occurs during bat movements between caves during fall swarming. We use published data to explore a range of parameter sets and identify plausible parameter sets from which influential variables and scenarios for future bat declines can be assessed.
We found a limited set of plausible parameter values for which the model simulations matched observations of over-winter survival of infected bats, WNS prevalence in infected hibernacula, and the rate of spread between caves. These parameters suggest this multi-scale model can account for observed dynamics and that infection rates from contact between bats may be overshadowed by infection from contaminated surfaces. We also find that stochasticity in disease dynamics significantly slows the rate of population decline and increases the range of possible outcomes. The overall picture is one of severe declines, but simulations using each plausible parameter set resulted in large differences in final metapopulation size and the rate of decline, as well as the proportion of caves without bats after 10 years. To our knowledge, this is the first model linking the emerging mechanistic understanding of WNS disease processes within caves to the dynamics of the entire metapopulation. The model structure allows examination of important questions about how density-dependent transmission, the evolution of resistance, and metapopulation dynamics can account for observations of small but persistent bat populations following WNS epidemics.