Alexander T. Strauss, J. Hite, D. Civitello, Marta S. Shocket, C. Cáceres, S. Hall
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Exposure rate (foraging, F) frequently decreased with parasite density (Z), and per-parasite susceptibility (U) frequently decreased with parasite encounters (F × Z). Consequently, infection rates (F × U × Z) often peaked at intermediate parasite densities. Moreover, host genotypes varied substantially in these responses. Exposure rates remained constant for some genotypes but decreased sensitively with parasite density for others (up to 78%). Furthermore, genotypes with more sensitive foraging/exposure also foraged faster in the absence of parasites (suggesting ‘fast and sensitive’ versus ‘slow and steady’ strategies). These relationships suggest that high densities of parasites can inhibit transmission by decreasing exposure rates and/or per-parasite susceptibility, and identify several intriguing axes for the evolution of host defence.","PeriodicalId":20609,"journal":{"name":"Proceedings of the Royal Society B","volume":"128 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2019-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"18","resultStr":"{\"title\":\"Genotypic variation in parasite avoidance behaviour and other mechanistic, nonlinear components of transmission\",\"authors\":\"Alexander T. Strauss, J. Hite, D. Civitello, Marta S. Shocket, C. Cáceres, S. Hall\",\"doi\":\"10.1098/rspb.2019.2164\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Traditional epidemiological models assume that transmission increases proportionally to the density of parasites. However, empirical data frequently contradict this assumption. 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Exposure rates remained constant for some genotypes but decreased sensitively with parasite density for others (up to 78%). Furthermore, genotypes with more sensitive foraging/exposure also foraged faster in the absence of parasites (suggesting ‘fast and sensitive’ versus ‘slow and steady’ strategies). 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引用次数: 18
摘要
传统的流行病学模型假定传播与寄生虫密度成正比。然而,经验数据经常与这一假设相矛盾。一般的机制模型可以解释为什么传播非线性地依赖于寄生虫密度,从而确定宿主的潜在防御策略。例如,宿主可以在较高的寄生虫密度下降低暴露率(通过行为回避),或者在遇到更多寄生虫时降低每只寄生虫的易感性(例如通过更强的免疫反应)。为了说明这一点,我们拟合了19个基因型的牙水蚤宿主在营养获得性寄生虫双尖蚤的梯度上的机制传播模型。暴露率(F)随寄生虫密度(Z)而降低,单个寄生虫易感性(U)随寄生虫接触(F × Z)而降低。因此,感染率(F × U × Z)通常在中等寄生虫密度时达到峰值。此外,宿主基因型在这些反应中有很大差异。某些基因型的暴露率保持不变,但其他基因型的暴露率随寄生虫密度而敏感下降(高达78%)。此外,具有更敏感的觅食/暴露的基因型在没有寄生虫的情况下也觅食得更快(这表明“快速和敏感”相对于“缓慢和稳定”策略)。这些关系表明,高密度的寄生虫可以通过降低暴露率和/或单个寄生虫的易感性来抑制传播,并确定了宿主防御进化的几个有趣轴。
Genotypic variation in parasite avoidance behaviour and other mechanistic, nonlinear components of transmission
Traditional epidemiological models assume that transmission increases proportionally to the density of parasites. However, empirical data frequently contradict this assumption. General yet mechanistic models can explain why transmission depends nonlinearly on parasite density and thereby identify potential defensive strategies of hosts. For example, hosts could decrease their exposure rates at higher parasite densities (via behavioural avoidance) or decrease their per-parasite susceptibility when encountering more parasites (e.g. via stronger immune responses). To illustrate, we fitted mechanistic transmission models to 19 genotypes of Daphnia dentifera hosts over gradients of the trophically acquired parasite, Metschnikowia bicuspidata. Exposure rate (foraging, F) frequently decreased with parasite density (Z), and per-parasite susceptibility (U) frequently decreased with parasite encounters (F × Z). Consequently, infection rates (F × U × Z) often peaked at intermediate parasite densities. Moreover, host genotypes varied substantially in these responses. Exposure rates remained constant for some genotypes but decreased sensitively with parasite density for others (up to 78%). Furthermore, genotypes with more sensitive foraging/exposure also foraged faster in the absence of parasites (suggesting ‘fast and sensitive’ versus ‘slow and steady’ strategies). These relationships suggest that high densities of parasites can inhibit transmission by decreasing exposure rates and/or per-parasite susceptibility, and identify several intriguing axes for the evolution of host defence.