COS 289-5 - Ongoing transmission explains elevated Bd infection intensities in a population-level controlled temperature experiment

Abstract: Amphibian populations are threatened by the temperature dependent disease chytridiomycosis, caused by the pathogen Batrachochytrium dendrobatidis (Bd). There has been extensive research into how temperature affects Bd infection in individual amphibians, but less is known about how these patterns scale up to disease dynamics in whole populations. The goals of our study were (1) to develop and parameterize a Metabolic Theory (MT) based model of temperature-dependent individual Bd dynamics and (2) to test whether and how this individual-level model can be scaled up to predict population-level transmission dynamics at different temperatures. Our approach was to conduct controlled temperature experiments measuring Bd infection load dynamics at both individual and population levels for the model species Xenopus laevis. We conducted a controlled temperature lab experiment to measure Bd infection on individually housed frogs at one of four temperatures (10, 15, 20, or 25 °C). We also conducted a large-scale controlled temperature mesocosm experiment tracking population-level Bd transmission dynamics for small populations of frogs maintained at one of three temperatures (10, 15, or 20 °C). In both experiments, frogs quickly developed high levels of infection; however, frogs experienced >1000× higher overall Bd loads in the population-level mesocosm experiment, especially in the 10 °C treatment. Here we show that a MT-based model describing thermal mismatches between pathogen and host thermal performance curves successfully described temperature dependent Bd infection dynamics at both the individual and population levels. The observed elevation of Bd infection intensities at the population level was predicted by an individual-based model with essential nesting, that directly scaled up MT-based thermal mismatches and allowed for the possibility of transmission-intensity feedbacks. This is contrary to a core assumption of most population-level disease models that assume individual infection intensities are independent from ongoing transmission dynamics. In conclusion, our empirical studies and theoretical models demonstrate the potential power of MT-based thermal mismatches to describe temperature dependent infection dynamics at both individual and population levels, and lay the groundwork for a potential paradigm-shift in disease ecology where individual infection intensities may be affected by ongoing transmission from other infected hosts.