Program in Ecology, Evolution and Conservation Biology, University of Illinois at Urbana-Champaign, Urbana, IL, 61801, USA,
Oecologia. 2013 Nov;173(3):1023-32. doi: 10.1007/s00442-013-2673-0. Epub 2013 May 8.
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.
野生动物疾病的发病率不断上升，这凸显了揭示传染病驱动因素的必要性。捕食者可以通过密度介导的效应（例如，清除感染宿主，从而降低疾病的发病率）直接影响疾病的发病率。然而，捕食者的特征介导的间接效应（TMIEs）也可能强烈影响疾病——但预测 TMIEs 是否应该增加或减少疾病的发病率可能具有挑战性，尤其是因为单一捕食者可能会引起对疾病发病率产生相反影响的反应。在这里，我们将实验室实验与一个基于机制的、基于大小的浮游动物宿主、真菌寄生虫、多种捕食者系统的 TMIE 模型配对。信息素可以根据捕食者的不同而增加或减少宿主桡足类的体型。这些体型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会随着体型的增加而增加。对于六种宿主基因型，我们测量了五个决定疾病传播指数（R0）的特征。尽管宿主大小和疾病特征没有对无脊椎动物捕食者 Chaoborus 产生的信息素产生反应，但来自鱼类的线索降低了未感染宿主的体型和出生率以及感染宿主的孢子产量。这些结果支持鱼类的体型模型；出生和孢子产量的反应应该会降低疾病的传播。然而，鱼类信息素并没有降低感染风险，因此与体型模型的预测相矛盾。信息素的暴露增加了宿主对每一个孢子的易感性，抵消了因体型变化而导致的对孢子暴露的减少。因此，综合考虑所有相关特征，鱼类信息素对 R0 指标没有净效应。这一结果凸显了在疾病传播涉及的所有关键特征中，整合基于 TMIE 的捕食者反应的必要性。
