Temperature is an important physical driver of all consumer-resource interactions, but theoretical and empirical advances in the thermal biology of parasitism has tended to trail behind advances in predator-prey thermal biology. Many of the core principles and approaches developed for predator-prey thermal biology translate well to parasitism, including the need to simultaneously account for thermal responses of parasite and host, the importance of performance curve asymmetries, and the potential for Metabolic Theory to provide a more mechanistic framework for modeling thermal performance. In both interaction types, enemies and victims can have plastic responses that complicate predictions in variable-temperature environments, and heterogeneous environments provide opportunities for victims to seek thermal refuges or dampen negative effects of temperature variability. However, parasitism also poses unique challenges due to the intimacy and duration of their interaction with hosts, smaller sizes and faster biological rates than hosts, and potentially opposite predictions for evolution of enemy and victim thermal traits due to a reversal of the “life-dinner principle”.
Results/Conclusions
I will illustrate consequences for the thermal biology of parasitism, presenting recent examples from my lab and the primary literature. Internal parasites are constrained to experience the same thermal variation as their victims, unlike predators which can select different thermal environments from prey. Hosts have also evolved diverse physiological mechanisms to resist parasitism, unlike prey responses to predators which are largely limited by muscle performance. These characteristics make it uniquely challenging to obtain separate measurements of parasite and host thermal performance curves, though approaches based on Metabolic Theory provide possible solutions. Unlike predators, parasites are largely subject to their victims’ thermoregulatory decisions, though physiological intimacy provides unique opportunities to “hijack” host thermoregulation. Unlike many predators, parasites are smaller than hosts with correspondingly faster biological rates, potentially leading to opposite predictions for relative sensitivity to changing temperatures at various time scales. Parasites also rely on and do not immediately kill hosts, opposite the classic “life-dinner principle” thought to drive evolution of asymmetric thermal performance curves in predators and prey. I will conclude by emphasizing the potential value of insights gained by following the work of thermal biologists studying various types of consumer-resource interactions.