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Warmer does not have to mean sicker: Temperature and predators can jointly drive timing of epidemics

机译:温暖不一定意味着生病:温度和掠食者可以共同推动流行的时机

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Ecologists and epidemiologists worry that global warming will increase disease prevalence. These fears arise because several direct and indirect mechanisms link warming to disease, and because parasite outbreaks are increasing in many taxa. However, this outcome is not a foregone conclusion, as physiological and community-interaction-based mechanisms may inhibit epidemics at warmer temperatures. Here, we explore this thermal-cormmunity-ecology-based mechanism, centering on fish predators that selectively prey upon Daphnia infected with a fungal parasite. We used an interplay between a simple model built around this system's biology and laboratory experiments designed to parameterize the model. Through this data-model interaction, we found that a given density of predators can inhibit epidemics as temperatures rise when thermal physiology of the predator scales more steeply than that of the host. This case is met in our fish-Daphnia-fungus system. Furthermore, the combination of steeply scaling parasite physiology and predation-induced mortality can inhibit epidemics at lower temperatures. This effect may terminate fungal epidemics of Daphnia as lakes cool in autumn. Thus, predation and physiology could constrain epidemics to intermediate temperatures (a pattern that we see in our system). More generally, these results accentuate the possibility that warmer temperatures might actually enhance predator control of parasites.
机译:生态学家和流行病学家担心全球变暖会增加疾病的流行率。这些担忧之所以出现,是因为几种直接和间接的机制将变暖与疾病联系在一起,并且由于许多分类单元中的寄生虫暴发正在增加。然而,由于生理和基于社区互动的机制可能会抑制温度升高的流行病,因此这一结果尚未成定局。在这里,我们探索这种基于热-联合-生态学的机制,集中在选择性捕食被真菌寄生虫感染的水蚤的鱼类捕食者上。我们使用了围绕该系统生物学构建的简单模型与旨在对该模型进行参数化的实验室实验之间的相互作用。通过这种数据模型的交互作用,我们发现,当掠食者的热生理学规模比宿主更陡峭时,随着温度升高,一定密度的掠食者可以抑制流行病。我们的鱼-水蚤-真菌系统遇到了这种情况。此外,陡峭的寄生虫生理学和捕食引起的死亡率的结合可以在较低温度下抑制流行病。随着秋季湖泊的降温,这种作用可能会终止水蚤的真菌流行。因此,捕食和生理可能会将流行病限制在中间温度(我们在系统中看到的一种模式)。更一般而言,这些结果加剧了温度升高实际上可能会增强食肉动物对寄生虫的控制的可能性。

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