Short-term temperature fluctuations increase disease in a Daphnia-parasite infectious disease system

• Published in: PLoS biology 2023-09, Vol.21 (9), p.e3002260-e3002260
• Main Authors: Krichel, Leila, Kirk, Devin, Pencer, Clara, Hönig, Madison, Wadhawan, Kiran, Krkosek, Martin
• Format: Article
• Language: English
• Subjects: Acclimation; Acclimatization; Biology and Life Sciences; Climate change; Climatic changes; Daphnia; Disease control; Disease spread; Disease transmission; Ecological research; Ecologists; Ecology; Ecology and Environmental Sciences; Environmental aspects; Fluctuations; Health risks; Host-parasite relationships; Hypotheses; Infections; Infectious diseases; Medicine and Health Sciences; Metabolism; Microsporidia; Parasites; Parasitic diseases; Physical Sciences; Physiological aspects; Predictions; Research and Analysis Methods; Risk factors; Simulation; Stochasticity; Temperature; Temperature effects; Thermal response
• ISSN: 1545-7885; 1544-9173; 1545-7885
• DOI: 10.1371/journal.pbio.3002260

Climate change has profound effects on infectious disease dynamics, yet the impacts of increased short-term temperature fluctuations on disease spread remain poorly understood. We empirically tested the theoretical prediction that short-term thermal fluctuations suppress endemic infection prevalence at the pathogen’s thermal optimum. This prediction follows from a mechanistic disease transmission model analyzed using stochastic simulations of the model parameterized with thermal performance curves (TPCs) from metabolic scaling theory and using nonlinear averaging, which predicts ecological outcomes consistent with Jensen’s inequality (i.e., reduced performance around concave-down portions of a thermal response curve). Experimental observations of replicated epidemics of the microparasite Ordospora colligata in Daphnia magna populations indicate that temperature variability had the opposite effect of our theoretical predictions and instead increase endemic infection prevalence. This positive effect of temperature variability is qualitatively consistent with a published hypothesis that parasites may acclimate more rapidly to fluctuating temperatures than their hosts; however, incorporating hypothetical effects of delayed host acclimation into the mechanistic transmission model did not fully account for the observed pattern. The experimental data indicate that shifts in the distribution of infection burden underlie the positive effect of temperature fluctuations on endemic prevalence. The increase in disease risk associated with climate fluctuations may therefore result from disease processes interacting across scales, particularly within-host dynamics, that are not captured by combining standard transmission models with metabolic scaling theory.