Dissertation Research: A mechanistic basis for the effects of toxins on epidemic disease in Daphnia

生态学家、自然保护区管理者和自然资源保护主义者都越来越担心野生动物种群中的疾病爆发（流行病）似乎正在增加。 与此同时，这些野生动物种群的环境越来越受到化学品的污染。 这两者之间有联系吗？污染物会增加疾病吗？如果是这样的话，污染物和传染病是否共同威胁着宿主种群的持续存在？ 在一些案例研究中，污染物水平与疾病流行率的增加存在令人担忧的相关性。 然而，其他例子显示了相反的模式，因此污染不一定会加剧疾病。这种特殊的结果使得很难概括污染物？疾病链接 本研究的目的是使用实验和理论模型来确定这些明显的特质结果的基础一般生理过程。 我的目标是提出一个能更好地预测化学污染对疾病的影响的理论。为了建立这个更普遍的理论，本研究集中在一个案例研究上。 它集中在铜，一种重金属，对淡水无脊椎动物，Daphnia dentifera，及其真菌寄生虫，Metschnikowia bicuspidata的影响，以解决几个关键问题。首先，铜暴露如何影响个体的疾病特征，如感染易感性和寄生虫在宿主内复制？ 第二，这些改变的特征将如何影响宿主种群中的流行病？接下来，这项研究将量化宿主防御铜和疾病的遗传变异。 这种变异如何影响流行病期间宿主的生态和进化反应？最后，本研究将从生理学的角度研究为什么铜会影响这些关键的宿主和寄生虫特征。明确关注生理机制的理论将大大增强未来将其他化学污染物与不同系统中的流行病联系起来的预测。不同的宿主-疾病系统对不同污染物的特异性反应抑制了这一重要生态问题的合成。这个跨学科计划通过创建一个预测性的一般框架来解决这个具有挑战性的问题，该框架结合了毒理学，能量学，社区生态学和进化生物学的技术和理论。 有了这样的理论，我们将更好地理解污染物和疾病如何以及何时共同威胁自然群落中的宿主持久性。

Ecologists, natural area managers, and conservationists alike have become increasingly concerned that disease outbreaks (epidemics) seem to be increasing in wildlife populations. At the same time, the environments of these wildlife populations are increasingly contaminated with chemicals. Could these two be linked: could pollutants increase disease? If so, do pollutants and infectious disease jointly threaten the persistence of host populations? In some case studies, pollutant levels are worryingly correlated with increased disease prevalence. However, other examples show the opposite patterns, so contamination does not necessarily exacerbate disease. Such idiosyncratic outcomes make it hard to generalize about contaminant ? disease links. This research aims to use experiments and theoretical models to identify general physiological processes that underlie these apparent idiosyncratic outcomes. I aim to produce theory than can better predict implications of chemical contamination for disease.To create this more general theory, this research focuses on a case study. It centers on the effects of copper, a heavy metal, on a freshwater invertebrate, Daphnia dentifera, and its fungal parasite, Metschnikowia bicuspidata, to address several key questions. First, how does copper exposure affect disease traits of individuals such as susceptibility to infection, and parasite within-host replication? Second, how will these altered traits influence epidemics in host populations? Next, this research will quantify genetic variation for host defense against copper and disease. How does this variation affect ecological and evolutionary response of hosts during epidemics? Finally, this research will examine, from a physiological perspective, why copper influences these critical host and parasite traits. Theory that explicitly focuses on physiological mechanisms will greatly enhance future predictions linking other chemical pollutants to epidemics in diverse systems. Synthesis of this import ecological issue has been inhibited by the idiosyncratic response of different host-disease systems to different contaminants. This interdisciplinary program tackles this challenging problem by creating a predictive, general framework that combines techniques and theory from toxicology, energetics, community ecology and evolutionary biology. Armed with such theory, we will better understand how and when how pollutants and disease jointly threaten host persistence in natural communities.