Infectious diseases represent a global concern for public health in the 21st century. Furthermore, human, livestock, and wildlife health are tightly linked because many of the most impactful human diseases are vector-borne or zoonotic (i.e., involve at least one nonhuman host). Thus, a deep understanding of parasite spread among wildlife hosts could enhance predictions and management of human risk of infection. My proposed research addresses this critical issue by focusing on a major human parasite, Schistosoma mansoni, which cycles between humans and snails (Biomphalaria spp.). The central goal of my proposal is to build and test new theory to predict the production of Schistosoma cercariae (the free-living stage which infects humans) by dynamic snail populations. The density of Schistosoma cercariae in aquatic habitats is a major determinant of human exposure risk. Thus, our work could help mitigate a central problem in global public health. Individual-level traits like host susceptibility and parasite reproduction drive populatio-level disease dynamics. However, snails and schistosomes are not uniform entities that exist in constant environments. Instead, their traits can vary dramatically and the environment is heterogeneous. Thus, integrating the intrinsic traits of hosts and parasites (e.g., body size and underlying physiology) with the influence of external factors (e.g., resource availability and population density) could greatly enhance predictions of human infection risk. Overall, my project tests the hypothesis that (algal) resource availability and the size-structure of snail populations powerfully determine the production of Schistosoma cercariae by snail populations. We will use experiments and mathematical models to link body size and resource availability to several key traits of snails and, ultimately, population dynamics of schistosomes. First, we will construct and test metabolic theory that aims to predict how cercarial production by infected snails depends sensitively on time, host body size, and resource availability. Second, snail risk of infection by schistosomes depends sensitively on body size. We will test a size-explicit framework to enhance predictions of snail infections by focusing on the two key processes that drive transmission: exposure to parasites and susceptibility to infection given exposure. Third, we will combine these models to produce a highly detailed, yet parsimonious agent-based model for the dynamics of Schistosoma in snail populations. We will then test the predictive power of this model under more natural conditions using a mesocosm experiment in which we track snail infections and the density of Schistosoma cercariae through time. Ultimately, this approach enables us to rigorously test our central hypothesis that snail size and resource availability drive schistosome dynamics and human risk at the population level. Moreover, this work initiates a highly integrative and novel perspective on the ecological dynamics of a major human parasite and its intermediate host. Consequently, this project could significantly contribute to both fundamental research on host - parasite interactions and an important applied problem in global human health.
Currently, more than 200 million humans worldwide are infected with schistosomes, flatworms in the genus Schistosoma, and approximately 20 million humans suffer from severe schistosomiasis. Human- parasitic schistosomes cycle between humans and freshwater snails. Humans become infected after exposure to larval parasites (cercariae) that were produced by infected snails in freshwater habitats. This project aims to construct novel theory that integrates physiology, ecology, and epidemiology to predict the production of Schistosoma mansoni cercariae by snail populations, a major determinant of human risk for schistosome infection.
| Civitello, David J; Fatima, Hiba; Johnson, Leah R et al. (2018) Bioenergetic theory predicts infection dynamics of human schistosomes in intermediate host snails across ecological gradients. Ecol Lett 21:692-701 |
| Cohen, Jeremy M; Civitello, David J; Brace, Amber J et al. (2016) Spatial scale modulates the strength of ecological processes driving disease distributions. Proc Natl Acad Sci U S A 113:E3359-64 |
| Jayawardena, Uthpala A; Rohr, Jason R; Navaratne, Ayanthi N et al. (2016) Combined Effects of Pesticides and Trematode Infections on Hourglass Tree Frog Polypedates cruciger. Ecohealth 13:111-22 |
| Rohr, Jason R; Civitello, David J; Crumrine, Patrick W et al. (2015) Predator diversity, intraguild predation, and indirect effects drive parasite transmission. Proc Natl Acad Sci U S A 112:3008-13 |
| Civitello, David J; Cohen, Jeremy; Fatima, Hiba et al. (2015) Biodiversity inhibits parasites: Broad evidence for the dilution effect. Proc Natl Acad Sci U S A 112:8667-71 |
| Civitello, David J; Cohen, Jeremy; Fatima, Hiba et al. (2015) Reply to Salkeld et al.: Diversity-disease patterns are robust to study design, selection criteria, and publication bias. Proc Natl Acad Sci U S A 112:E6262 |
| Gervasi, Stephanie S; Civitello, David J; Kilvitis, Holly J et al. (2015) The context of host competence: a role for plasticity in host-parasite dynamics. Trends Parasitol 31:419-25 |
