Trait-mediated indirect effects, predators, and disease: test of a size-based model

Trait-mediated indirect effects, predators, and disease: test of a size-based model
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DOI:
10.1007/s00442-013-2673-0
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发表时间:
2013-11-01
期刊:
影响因子:
2.7
通讯作者:
Caceres, Carla E.
Caceres, Carla E.
中科院分区:
环境科学与生态学2区
文献类型:
--
作者:
Bertram, Christopher R.;Pinkowski, Mark;Caceres, Carla E.

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野生动物疾病的日益流行凸显了发现流行病驱动因素的必要性。捕食者可以通过密度介导的效应直接影响疾病的流行(例如,扑杀受感染的宿主导致疾病流行率降低)。然而,捕食者的性状介导的间接效应(TMIE)也能强烈影响疾病,但先验预测 TMIE 是否会增加或减少疾病患病率可能具有挑战性,特别是因为单个捕食者可能会引发对疾病患病率产生相反影响的反应。在这里,我们将实验室实验与浮游动物宿主、真菌寄生虫、多种捕食者系统中基于大小的 TMIE 机械模型配对。利它素可以增加或减少宿主水蚤的体型,具体取决于捕食者。这些大小的变化可能会影响真菌疾病的关键特征,因为感染风险和孢子产量随着体型的大小而增加。对于六种宿主基因型,我们测量了决定疾病传播指数的五种性状 (R (0))。尽管宿主体型和疾病特征对无脊椎动物捕食者Chaoborus产生的利它素没有反应,但来自鱼类的信号降低了未感染宿主的体型和出生率以及受感染宿主的孢子产量。这些结果支持鱼类的尺寸模型;出生和孢子产量反应应该会抑制疾病传播。然而,鱼类利好素并没有降低感染风险,因此与大小模型的预测相矛盾。暴露于利他素会增加宿主每个孢子的敏感性,抵消大小驱动的孢子暴露减少。因此,综合相关性状,鱼类利好素对 R (0) 指标没有净影响。这一结果强调需要将基于 TMIE 的捕食者反应纳入疾病传播涉及的所有关键特征中。
Increasing prevalence of wildlife disease accentuates the need to uncover drivers of epidemics. Predators can directly influence disease prevalence via density-mediated effects (e.g., culling infected hosts leading to reduced disease prevalence). However, trait-mediated indirect effects (TMIEs) of predators can also strongly influence disease-but predicting a priori whether TMIEs should increase or decrease disease prevalence can be challenging, especially since a single predator may elicit responses that have opposing effects on disease prevalence. Here, we pair laboratory experiments with a mechanistic, size-based model of TMIEs in a zooplankton host, fungal parasite, multiple predator system. Kairomones can either increase or decrease body size of the host Daphnia, depending on the predator. These changes in size could influence key traits of fungal disease, since infection risk and spore yield increase with body size. For six host genotypes, we measured five traits that determine an index of disease spread (R (0)). Although host size and disease traits did not respond to kairomones produced by the invertebrate predator Chaoborus, cues from fish reduced body size and birth rate of uninfected hosts and spore yield from infected hosts. These results support the size model for fish; the birth and spore yield responses should depress disease spread. However, infection risk did not decrease with fish kairomones, thus contradicting predictions of the size model. Exposure to kairomones increased per spore susceptibility of hosts, countering size-driven decreases in exposure to spores. Consequently, synthesizing among the relevant traits, there was no net effect of fish kairomones on the R (0) metric. This result accentuates the need to integrate the TMIE-based response to predators among all key traits involved in disease spread.