Rozmann, V.; OKeeffe, F.; Officer, M.; Luijckx, P.; Piggott, J. J.

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 clear 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 structure from mean temperature. Across two experiments, we exposed hosts to cyclic (predictable) and random (unpredictable) heatwaves under both non-stressful and stressful mean temperature regimes. Contrary to predictions from the climate variability hypothesis, temperature variability did not uniformly increase infection risk. Instead, infection outcomes depended on the interaction between mean temperature, duration of the heatwaves, the pattern of thermal variation, and parasite identity. Under non-stressful mean temperatures, thermal variability had negligible effects on infection. In contrast, under stressful mean temperatures, parasites responded in distinct ways: H. tvaerminnensis infection was sensitive to the predictability 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. By showing that parasite-specific sensitivities to the pattern of thermal variation emerge under thermal stress, our study highlights a mechanism by which increasing climatic variability may reshape parasite communities and disease outcomes in a warming world.