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.
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? This project addressed these critical environmental issues using a case study of the effects of heavy metal contamination on a freshwater invertebrate, Daphnia dentifera, and its fungal parasite, Metschikowia bicuspidata. First, we found that exposure to a common heavy metal pollutant, copper, increased the susceptibility of hosts to infection but decreased the reproduction of parasites within infected hosts. With long term pollution, the decrease in parasite reproduction was larger than the increase in susceptibility. Therefore, we predicted that disease outbreaks in chronically polluted populations would be smaller. We confirmed this prediction with an experiment containing replicated populations of Daphnia. Epidemics were smaller in polluted environments, and they caused less harm to the Daphnia populations. Our first study found that copper pollution increased the susceptibility of Daphnia to infection by increasing the rate that they contacted parasites. We explored the generality of this effect by testing two other metal pollutants (Zinc and Cadmium) for similar effects on susceptibility. We found the opposite effect for these two pollutants – exposure reduced susceptibility of Daphnia to fungal infection because it reduced the rate of contact to the parasite. While we found some evidence of genetic variation among Daphnia in contact rates to parasites, these differences were small relative to the changes caused by pollution. Finally, we explored, from a physiological perspective, why copper pollution decreased the production of parasites within infected hosts. We combined two physiological models that track the growth, development, and reproduction of organisms. The two models focus on the physiological effects of pollutants and parasites, separately. By combining these perspectives, we found that many different types of pollutants should reduce parasite reproduction within infected Daphnia. However, we also found that some pollutants should cause infected Daphnia to die earlier, while others would cause them to live longer (relative to pollution-free scenarios). Therefore, pollution should generally reduce fungal disease outbreaks in Daphnia because it decreases parasite reproduction.
