Temperature Drives Epidemics in a Zooplankton-Fungus Disease System: A Trait-Driven Approach Points to Transmission via Host Foraging

Temperature Drives Epidemics in a Zooplankton-Fungus Disease System: A Trait-Driven Approach Points to Transmission via Host Foraging
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温度驱动浮游动物-真菌疾病系统中的流行病:一种特征驱动的方法表明通过宿主觅食传播

DOI:
10.1086/696096
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发表时间:
2018
期刊:
The American Naturalist
影响因子:
--
通讯作者:
S. Hall
S. Hall
中科院分区:
--
文献类型:
--
作者:
Marta S. Shocket;Alexander T. Strauss;J. Hite;Maja B. Sljivar;D. Civitello;M. Duffy;C. Cáceres;S. Hall

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气候变暖可能会对传染病产生特殊的影响,导致一些传染病增加,而另一些则减少或在地理上发生变化。一个机制框架可以更好地预测这些不同的温度疾病结果。然而,由于不同宿主和寄生虫性状的非线性和(有时)相反的热响应,以及由于用观察和实验验证模型预测的困难,这样的框架仍然具有挑战性。我们在浮游动物-真菌(Daphnia dentifera metschnikowia bicuspidata)系统中解决了这些挑战。我们检验了气温升高促进疾病传播并产生更大流行病的假设。在湖泊中,秋天开始得更早、更温暖的流行病会变得更大。在中观实验中,温度升高会产生更大的流行病。一个用性状分析参数化的机制模型显示,这种模式主要是由传播率(β)的温度依赖性引起的,受宿主觅食(因此暴露于寄生虫)率(f)的增加所控制。在性状分析中,寄生虫的产生似乎对形状流行病也有充分的反应;然而,这一特性在中游实验和湖泊调查中被证明对热不敏感。因此,在温暖的环境中,宿主的觅食增加提高了传播率,通过可能普遍的、基于暴露的变温动物机制产生更大的流行病。这种机制方法突出了基于特征的框架将如何增强对传染病对变暖世界的反应的预测性洞察力。
Climatic warming will likely have idiosyncratic impacts on infectious diseases, causing some to increase while others decrease or shift geographically. A mechanistic framework could better predict these different temperature-disease outcomes. However, such a framework remains challenging to develop, due to the nonlinear and (sometimes) opposing thermal responses of different host and parasite traits and due to the difficulty of validating model predictions with observations and experiments. We address these challenges in a zooplankton-fungus (Daphnia dentifera–Metschnikowia bicuspidata) system. We test the hypothesis that warmer temperatures promote disease spread and produce larger epidemics. In lakes, epidemics that start earlier and warmer in autumn grow much larger. In a mesocosm experiment, warmer temperatures produced larger epidemics. A mechanistic model parameterized with trait assays revealed that this pattern arose primarily from the temperature dependence of transmission rate (β), governed by the increasing foraging (and, hence, parasite exposure) rate of hosts (f). In the trait assays, parasite production seemed sufficiently responsive to shape epidemics as well; however, this trait proved too thermally insensitive in the mesocosm experiment and lake survey to matter much. Thus, in warmer environments, increased foraging of hosts raised transmission rate, yielding bigger epidemics through a potentially general, exposure-based mechanism for ectotherms. This mechanistic approach highlights how a trait-based framework will enhance predictive insight into responses of infectious disease to a warmer world.
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