Abstract

The complexity of host–parasite interactions makes it difficult to predict how host–parasite systems will respond to climate change. In particular, host and parasite traits such as survival and virulence may have distinct temperature dependencies that must be integrated into models of disease dynamics. Using experimental data from Daphnia magna and a microsporidian parasite, we fitted a mechanistic model of the within-host parasite population dynamics. Model parameters comprising host aging and mortality, as well as parasite growth, virulence, and equilibrium abundance, were specified by relationships arising from the metabolic theory of ecology. The model effectively predicts host survival, parasite growth, and the cost of infection across temperature while using less than half the parameters compared to modeling temperatures discretely. Our results serve as a proof of concept that linking simple metabolic models with a mechanistic host–parasite framework can be used to predict temperature responses of parasite population dynamics at the within-host level.

Highlights

  • The effects of global environmental change on infectious disease dynamics have broad consequences that span human health [1], food security [2], and conservation [3]

  • Host–parasite interactions are impacted by temperature, and climate change is altering the nature of these interactions

  • We fitted thermal relationships based on the metabolic theory of ecology to separate host and parasite traits, including host mortality and aging as well as parasite

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Summary

Introduction

The effects of global environmental change on infectious disease dynamics have broad consequences that span human health [1], food security [2], and conservation [3]. Temperature influences the traits that mediate the impact of infection on host survival, such as parasite development rate [9] and virulence [10], as well as the resistance [11] and tolerance [12] of hosts to parasites. Each of these traits may have distinct temperature responses, and it is the antagonistic and synergistic interactions among the temperature responses of host and parasite traits that determine the net consequences of temperature changes on disease dynamics [13]

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