Parasite exposure and host susceptibility jointly drive the emergence of epidemics
Parasite exposure and host susceptibility jointly drive the emergence of epidemics
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DOI：
10.1002/ecy.3245
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发表时间：
2020-12-27
期刊：
影响因子：
4.8
通讯作者：
Caceres, Carla E.
中科院分区：
文献类型：
--
作者：
Merrill, Tara E. Stewart;Hall, Spencer R.;Caceres, Carla E.
寄生虫传播被认为取决于寄生虫暴露和宿主对感染的易感性;然而，这两个因素对流行病的相对贡献仍不清楚。我们利用水生宿主和其真菌寄生虫之间的相互作用来评估寄生虫暴露和宿主易感性如何相互作用以驱动流行病。在六湖，我们追踪了从疫情前到疫情出现的以下因素：（1）寄生虫接触（通过真菌孢子攻击野生捕获的宿主来观察），（2）宿主易感性（实验测量为产生最终感染所需的真菌孢子数量），（3）宿主易感性特征（屏障抗性和内部清除率，两者都用实验测定法定量），和（4）寄生虫流行率（从野生捕获的宿主观察测量）。在6个月内跟踪这些因素，并在近7，000个野生捕获的宿主中提供了有关流行病驱动因素的关键信息。我们发现，流行病严重依赖于暴露和易感性的相互作用;只有当宿主人口的暴露水平超过其个人的恢复能力时，流行病才会出现。此外，我们发现宿主的内部清除特性（血细胞反应）在调节流行病方面至关重要。我们的研究提供了寄生虫暴露和宿主易感性如何相互作用以抑制或驱动自然系统中的疾病的经验证明，并表明流行病可以通过这两个过程中的传染性来延迟。最后，我们的研究结果强调了个体宿主特征如何扩大规模以影响广泛的流行病学模式。
Parasite transmission is thought to depend on both parasite exposure and host susceptibility to infection; however, the relative contribution of these two factors to epidemics remains unclear. We used interactions between an aquatic host and its fungal parasite to evaluate how parasite exposure and host susceptibility interact to drive epidemics. In six lakes, we tracked the following factors from pre-epidemic to epidemic emergence: (1) parasite exposure (measured observationally as fungal spores attacking wild-caught hosts), (2) host susceptibility (measured experimentally as the number of fungal spores required to produce terminal infection), (3) host susceptibility traits (barrier resistance and internal clearance, both quantified with experimental assays), and (4) parasite prevalence (measured observationally from wild-caught hosts). Tracking these factors over 6 months and in almost 7,000 wild-caught hosts provided key information on the drivers of epidemics. We found that epidemics depended critically on the interaction of exposure and susceptibility; epidemics only emerged when a host population's level of exposure exceeded its individuals' capacity for recovery. Additionally, we found that host internal clearance traits (the hemocyte response) were critical in regulating epidemics. Our study provides an empirical demonstration of how parasite exposure and host susceptibility interact to inhibit or drive disease in natural systems and demonstrates that epidemics can be delayed by asynchronicity in the two processes. Finally, our results highlight how individual host traits can scale up to influence broad epidemiological patterns.