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

Indiana University, Bloomington IN

Investigators

Abstract

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.