Using physiology to understand climate-driven changes in disease and their implications for conservation

Abstract

Given that host-parasite interactions are generally mediated by physiological responses, we submit that physiological models could facilitate predicting how host-parasite interactions respond to climate change, and might offer theoretical and terminological cohesion that has been lacking in the climate change-disease literature.

Abstract

Controversy persists regarding the contributions of climate change to biodiversity losses, through its effects on the spread and emergence of infectious diseases. One of the reasons for this controversy is that there are few mechanistic studies that explore the links among climate change, infectious disease, and declines of host populations. Given that host–parasite interactions are generally mediated by physiological responses, we submit that physiological models could facilitate the prediction of how host–parasite interactions will respond to climate change, and might offer theoretical and terminological cohesion that has been lacking in the climate change–disease literature. We stress that much of the work on how climate influences host–parasite interactions has emphasized changes in climatic means, despite a hallmark of climate change being changes in climatic variability and extremes. Owing to this gap, we highlight how temporal variability in weather, coupled with non-linearities in responses to mean climate, can be used to predict the effects of climate on host–parasite interactions. We also discuss the climate variability hypothesis for disease-related declines, which posits that increased unpredictable temperature variability might provide a temporary advantage to pathogens because they are smaller and have faster metabolisms than their hosts, allowing more rapid acclimatization following a temperature shift. In support of these hypotheses, we provide case studies on the role of climatic variability in host population declines associated with the emergence of the infectious diseases chytridiomycosis, withering syndrome, and malaria. Finally, we present a mathematical model that provides the scaffolding to integrate metabolic theory, physiological mechanisms, and large-scale spatiotemporal processes to predict how simultaneous changes in climatic means, variances, and extremes will affect host–parasite interactions. However, several outstanding questions remain to be answered before investigators can accurately predict how changes in climatic means and variances will affect infectious diseases and the conservation status of host populations.