Schoebel Corine N, Auld Stuart K J R, Spaak Piet, Little Tom J
Department of Biodiversity and Conservation Biology, Swiss Federal Research Institute WSL, Birmensdorf, Switzerland; Eawag, Dübendorf, Switzerland; and Institute of Integrative Biology, ETH, Zürich, Switzerland.
Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, United Kingdom; School of Natural Sciences, University of Stirling, Stirling, United Kingdom.
PLoS One. 2014 Apr 15;9(4):e94569. doi: 10.1371/journal.pone.0094569. eCollection 2014.
Host density can increase infection rates and reduce host fitness as increasing population density enhances the risk of becoming infected either through increased encounter rate or because host condition may decline. Conceivably, potential hosts could take high host density as a cue to up-regulate their defence systems. However, as host density usually covaries with food availability, it is difficult to examine the importance of host density in isolation. Thus, we performed two full-factorial experiments that varied juvenile densities of Daphnia magna (a freshwater crustacean) and food availability independently. We also included a simulated high-density treatment, where juvenile experimental animals were kept in filtered media that previously maintained Daphnia at high-density. Upon reaching adulthood, we exposed the Daphnia to their sterilizing bacterial parasite, Pasteuria ramosa, and examined how the juvenile treatments influenced the likelihood and severity of infection (Experiment I) and host immune investment (Experiment II). Neither juvenile density nor food treatments affected the likelihood of infection; however, well-fed hosts that were well-fed as juveniles produced more offspring prior to sterilization than their less well-fed counterparts. By contrast, parasite growth was independent of host juvenile resources or host density. Parasite-exposed hosts had a greater number of circulating haemocytes than controls (i.e., there was a cellular immune response), but the magnitude of immune response was not mediated by food availability or host density. These results suggest that density dependent effects on disease arise primarily through correlated changes in food availability: low food could limit parasitism and potentially curtail epidemics by reducing both the host's and parasite's reproduction as both depend on the same food.
宿主密度可提高感染率并降低宿主健康水平，因为种群密度增加会通过提高接触率或因宿主状况可能下降而增加感染风险。可以想象，潜在宿主可能会将高宿主密度作为上调其防御系统的一个信号。然而，由于宿主密度通常与食物可利用性共同变化，所以很难单独研究宿主密度的重要性。因此，我们进行了两项全因子实验，分别独立改变大型溞（一种淡水甲壳类动物）的幼体密度和食物可利用性。我们还设置了一个模拟高密度处理组，将幼体实验动物饲养在先前维持大型溞高密度的过滤介质中。成年后，我们让大型溞接触其杀菌性细菌寄生虫——枝原体巴氏杆菌，并研究幼体处理如何影响感染的可能性和严重程度（实验一）以及宿主的免疫投入（实验二）。幼体密度和食物处理均未影响感染的可能性；然而，幼体期营养良好的宿主在被寄生前比营养较差的宿主产生更多后代。相比之下，寄生虫的生长与宿主幼体资源或宿主密度无关。接触寄生虫的宿主比对照组有更多的循环血细胞（即存在细胞免疫反应），但免疫反应的强度不受食物可利用性或宿主密度的介导。这些结果表明，密度依赖性对疾病的影响主要通过食物可利用性的相关变化产生：低食物供应可能会限制寄生作用，并可能通过减少宿主和寄生虫的繁殖来遏制流行病，因为两者都依赖于相同的食物。
