Research Area

My research focuses on both the mechanisms leading to and the consequences of aggregation in free-living and host-parasite systems. The term aggregation simply describes the nearly ubiquitous phenomenon in nature that many hosts (patches) have few parasites (free-living individuals) while few hosts (patches) have many parasites (free-living individuals). Despite the relative simplicity of the pattern, there are many, many potential mechanisms that can generate these aggregated distributions in nature and the resulting aggregation patterns can have significant implications for the dynamics of host-parasite systems and the scaling of biodiversity.

The first component of my work explores how and when we can identify mechanisms from aggregated host-parasite distributions. For example, if I go out and sample H hosts that contain a total of P parasites, can I reliably infer anything about the mechanisms acting on this host-parasite system based on how these P parasites are distributed amongst these H hosts? Using tools from macroecology, probability theory, and combinatorics, I am developing statistical models that allow us to identify when particular mechanisms such as parasite-induced host mortality or host heterogeneity are having a disproportionate effect on the distribution of P parasites among H hosts.

The second component of my work takes a more dynamic approach to parasite aggregation where I have been part of a collaboration in developing host-parasite Integral Projection Models that explicitly model the dynamics of the host-parasite distribution through time. For many fungal diseases, such as amphibian chytrid fungus, explicitly tracking the fungal load distribution can better capture host-parasite dynamics as the vital rates of the hosts (e.g. growth, survival, loss of infection, reproduction, etc.) are heavily dependent on how infected the hosts are. I am using these types of models to answer empirically-motivated questions about how fluctuating environments, transmission dynamics, and genetic variation in host resistance affect parasite-induced host extinction in amphibian-chytrid fungus systems.