Anthropogenic climate change is expected to increase not only mean temperatures but also the magnitude and pattern of thermal variability, including the frequency, duration, and predictability of extreme events. While the effects of elevated mean temperatures on disease dynamics are well studied, far less is known about how different patterns of temperature variability shape host-parasite interactions, despite theoretical predictions from the climate variability hypothesis. Here, we used a controlled experimental system (Daphnia magna and two microsporidian parasites, Ordospora colligata and Hamiltosporidium tvaerminnensis) to disentangle the effects of thermal variability. Across two experiments conducted under different thermal regimes, we exposed hosts to cyclic (predictable) and random (unpredictable) heatwaves. Contrary to predictions from the climate variability hypothesis, temperature variability did not uniformly increase infection risk. Instead, infection outcomes depended on the mean temperature, duration of the heatwaves, the pattern of thermal variation, and parasite identity. At lower temperatures (Experiment 1), thermal variability had minimal effects on infection. At higher mean temperatures (Experiment 2), parasites responded in distinct ways: H. tvaerminnensis spore production was sensitive to the pattern of heat events, whereas O. colligata responded primarily to heatwave duration. These results demonstrate that climatic variability can differentially alter host-parasite interactions rather than exerting consistent directional effects on disease, with the effects of temperature variability depending on both species identity and thermal regime. Taken together, these findings suggest that increasing climatic variability may influence parasite communities and disease outcomes under the ongoing global change.
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Viktoria et al. (2026) studied this question.
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