Disease transmission in multi-host communities

Understanding the impact of multi-host interactions on parasite transmission is crucial for prediction of disease emergence in communities. Important questions include what ecological contexts amplify or dilute parasite transmission? What emergence thresholds exist and how do they influence outbreak dynamics in multi-host disease systems?

I have developed a theoretical framework for how competition and contact patterns drive parasite transmission outcomes in multi-species communities.


The dilution effect hypothesis has been investigated in many empirical systems, including Lyme disease in small mammals, West Nile Virus in wild birds and mosquitoes, trematodes in amphibians, hantavirus in rodents and yellow barley virus in plant systems.

Biodiversity may buffer against the risk of transmission of zoonotic infectious diseases to humans in many contexts. Empirical studies have found negative associations between host biodiversity and disease risk (termed the “dilution effect”) .The frequency of opportunities for transmission is key to the severity of directly transmitted disease outbreaks in multi-host communities. Transmission opportunities for generalist microparasites often arise from competitive and trophic interactions. Additionally, contact heterogeneities within and between species either hinder or promote transmission. However, general theory incorporating competition and contact heterogeneities for disease-diversity relationships is under-developed. In collaboration with Andrew Park and John Vinson at the University of Georgia, I have developed a formal framework to explore disease-diversity relationships for directly transmitted parasites that infect multiple host species, including influenza viruses, rabies virus, distemper viruses and hantaviruses. We explicitly included host regulation through intraspecific and interspecific competition. We examined how these factors interact with frequency-dependent and density-dependent transmission, along with traits of the hosts in the assemblage.

I derived an analytical relationship describing the propensity for parasite fitness to decrease in species assemblages relative to in single host species. This relationship reveals that increases in biodiversity do not necessarily suppress frequency-dependent pathogen transmission and regulation of hosts via interspecific competition does not always lead to a dilution effect. Incorporating competition and contact heterogeneities into simple mathematical models changes predictions for how increasing species richness alters parasite fitness in multispecies communities. Adding more species can either increase or decrease parasite fitness, depending on ecological context and the traits of the species in an assemblage. Further, we showed the propensity for amplification of disease risk in multispecies communities may have different drivers; for example, the life history traits of species in the assemblage may promote transmission, or strong interspecific contact may promote transmission, depending on ecological context. Our approach explicitly shows that species identity and ecological interactions between hosts together determine microparasite transmission outcomes in multispecies communities. Contact patterns and competition need to be included as components of predictive models for disease-diversity relationships.

What is the role of environmental transmission, combined with multi-host transmission, in parasite invasion and persistence? Study systems to examine this question include Ranavirus, a pathogen that infects amphibians globally, and Leptospirosis, an emerging zoonotic disease.

Understanding drivers of Ranavirus outbreaks.

Ranavirus is a multi-host pathogen that infects amphibians globally. I am examining the relative roles of multiple hosts and the environment in Ranavirus transmission by comparing dynamics and epidemic thresholds in single-host and multi-host mathematical models parameterized with empirical data. In the first stage of this project, I have developed a mathematical model for Ranavirus transmission in wood frogs, an abundant species in the Eastern United States that is highly susceptible to Ranavirus. The model combines direct and environmental transmission and incorporates a realistic infectious period distribution informed by empirical data. The model shows that direct contact drives epidemic dynamics in wood frogs, rather than necrophagy or environmental transmission. The second stage of the project will involve building multi-host models, informed by experiments, to make predictions for Ranavirus transmission in multi-host amphibian communities. The models will combine interactions between wood frogs and less susceptible species and will shed light on the role of species composition on epidemic thresholds in communities. This project is being pursued in collaboration with Matt Gray (University of Tennessee) and Angela Peace (Texas Tech). Peace and I are leading mathematical analysis and simulations of these simple models.

Ecological dynamics of Leptospirosis.

Leptospirosis is a bacterial infection with a global distribution that infects multiple hosts, including humans. Outbreaks following rainfall events are an issue in countries with poor sanitation. I am collaborating with members of the Leptospirosis NIMBioS working group to develop a multi-host model of leptospirosis transmission. One of the potential goals of the model is to understand the contributions of different host species and the environment to transmission dynamics.