Short-term temperature fluctuations increase disease in a Daphnia-parasite infectious disease system.
Autor: | Krichel L; Department of Ecology and Evolutionary Biology, University of Toronto, Toronto, Canada., Kirk D; Department of Biology, Stanford University, Stanford, California, United States of America., Pencer C; Department of Ecology and Evolutionary Biology, University of Toronto, Toronto, Canada., Hönig M; Department of Ecology and Evolutionary Biology, University of Toronto, Toronto, Canada.; Department of Anthropology, Washington State University, Pullman, Washington, United States of America., Wadhawan K; Department of Ecology and Evolutionary Biology, University of Toronto, Toronto, Canada.; School of Biological Sciences, University of Edinburgh, Edinburgh, United Kingdom., Krkošek M; Department of Ecology and Evolutionary Biology, University of Toronto, Toronto, Canada. |
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Jazyk: | angličtina |
Zdroj: | PLoS biology [PLoS Biol] 2023 Sep 08; Vol. 21 (9), pp. e3002260. Date of Electronic Publication: 2023 Sep 08 (Print Publication: 2023). |
DOI: | 10.1371/journal.pbio.3002260 |
Abstrakt: | 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. Competing Interests: The authors have declared that no competing interests exist. (Copyright: © 2023 Krichel et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.) |
Databáze: | MEDLINE |
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