When populations become small, their probability of extinction typically goes up, because demographic and environmental stochasticity are more likely to set the population on an irreversible decline. However, when one population goes locally extinct, a species is not necessarily lost; the area might be re-colonized by migrants from a different population later, if other populations exist. Metapopulation theory tells us that a balance between population extinctions and re-colonizations in heterogeneous patches that are linked by dispersal can allow a species to persist regionally, even when it goes extinct locally.
What happens when we add infectious diseases into our host metapopulation model? Connectivity might be detrimental to regional persistence when infectious diseases are introduced, because pathogens in one population can invade the other populations via host dispersal, whereas pathogens are limited to a single population when populations aren’t linked via dispersal. Or…not?
Heard et al. (2015) recently published a quite complicated and fancy metapopulation model that suggests that connectivity actually increases the probability of metapopulation persistence in an Australian frog species endangered by the fungal pathogen (Bd), which causes the disease chytridiomycosis. From survey work, they knew that the prevalence of Bd in growling glass frogs was lower in warm and/or salty wetlands. They could also show that the probability of a local extinction in any given frog population increased with the prevalence of Bd in the frog population. By linking local extinction risk to Bd prevalence and microclimate, they could create metapopulation models using known dispersal distances for the growling glass frog, and they could run simulations regarding metapopulation persistence under scenarios where they eliminated frog dispersal among populations or not. They had two important findings. First, if you ignore the fact that Bd prevalence varies with microclimate, the probability of metapopulation persistance is predicted to be much lower than it actually is. The warm and/or salty wetlands act as important low Bd prevalence frog population refugia that can seed the other populations in a metapopulation when they go locally extinct, such that microclimate variability increases persistence. Second, “re-seeding” can only happen if dispersal occurs among populations, so connectivity increases metapopulation persistence in this system.
One lingering question is whether this system is a good example of the role of connectivity in all host metapopulations plagued by infectious diseases. Heard et al. (2015) argue that Bd is basically everywhere already – and there to stay – because it can be maintained in both environmental reservoirs and reservoir hosts. Therefore, they suggest that for growling glass frogs, dispersal of hosts among populations doesn’t really play a role in disease dynamics. In systems where the pathogen is not yet widespread (i.e., regions currently being invaded), where reservoirs are less likely to provide long-term maintenance of the pathogen, or where dispersal of reservoir hosts is particularly important to pathogen spread, host dispersal could start to have detrimental impacts on long-term metapopulation persistence. This is cool stuff that deserves more attention!
Heard, G.W., C.D. Thomas, J.A. Hodgson, M.P. Scroggie, D.S. Ramsey, and N. Clemann. 2015. Refugia and connectivity sustain amphibian metapopulations afflicted by disease. Ecology Letters, 18: 853–863.