Research Interests:

I am interested in the evolutionary ecology of zoonotic and wildlife disease--very broadly, how parasites get around, stick around, and kill. I am especially interested in the importance of rare events in transmission and persistence, in the role of seasonality in disease dynamics, and looking at infectious disease in a community context. I prefer to work on problems that are relevant to theoretical and applied problems. I also try to integrate experiments, surveys, and a variety of quantitative tools to look at a problem from multiple angles.

I am working on several new projects. Here are two:

• Range expansion of blacklegged ticks (Ixodes scapularis), vector of Lyme disease and other emerging infectious diseases. As recently as the 1960's blacklegged ticks were (apparently) restricted to island refuges off the New England coast, but they are now ubiquitous throughout much of the Northeast. How did these ticks move so far so quickly? What stops their continued expansion? How will they respond to a changing climate? I'm planning some ecologically relevant, manipulative experiments to help determine how (or whether) winter temperatures limit ticks, which may help answer that last question about climate change. I'm also trying to find data to help test alternate models of range expansion so that we can better predict (and prepare for) the future spread of these and other vectors of zoonotic disease.
• Ranavirus infections and chytridiomycosis in the amphibians of New York State. Ranaviruses and the fungal pathogen, Batrachochytrium dendrobatidis (Bd), are two important emerging pathogens in amphibians. Bd has been associated with amphibian declines and extinctions around the world. Ranavirus epidemics decimate amphibians in natural populations and aquaculture. Little is known, however, about these important pathogens in amphibian communities in the Northeast. We are just beginning to get the sense that they are common, but which species are most susceptible, which habitats most conducive to epidemics, or even whether we are dealing with one or many types of Bd and ranavirus remains unclear. I have been using samples from road-kill, die-offs, and more active surveillance to begin to address these questions. In the near future I hope to also work out how these pathogens move from one host species to another.

Background:

I conducted my dissertation with Dr. James P. Collins at Arizona State University in Tempe, Arizona. Dr. Collins has been central to a great deal of research on and responses to the global amphibian declines. He led an international research group seeking to understand the role of disease in these declines. He also got me interested in infectious disease.

My dissertation research focused on the transmission, persistence, and virulence of a lethal virus of tiger salamanders, Ambystoma tigrinum virus (ATV), which we have been developing into a model system for understanding how infectious disease operates in amphibian populations. One of the more interesting results of my research was figuring out how a lethal virus can persist in hosts with a strongly seasonal life history. I even coined a term, intraspecific reservoir to describe how one life history stage acts as a reservoir for another. I am also interested in the evolution of parasite virulence. I suspect, however, that the often assumed, but rarely tested trade-off between virulence and transmission does not operate in this system (manuscript in review).

I spent two years as a postdoctoral associate at the Cary Institute of Ecosystem Studies, Millbrook, New York working with Dr. Richard S. Ostfeld on the Lyme disease system. I am very interested in what makes some individuals more infectious than others. I used the long-term small mammal trapping data that Dr. Ostfeld and his team had been collecting for well over a decade to figure out which mice and chipmunks fed more ticks (and were thus more likely to be infected with the Lyme disease agent, Borrelia burgdorferi, and to infect naive ticks). The results are complex, but strongly indicate that there is no particular group or type of mice or chipmunks that are necessarily "super spreaders." More recent work with my friend and collaborator, Justin Calabrese, shows that natural variation in the distribution of questing ticks and/or host home range sizes can easily account for the aggregation of ticks on some individuals. That is, "super spreaders" may simply be a consequence of normal variability in ecological interactions.

The focus of my postdoctoral research, however, was experimentally testing the "dilution effect" in the Lyme disease system. That is, do more diverse host communities reduce the risk of human infection? There has been a great deal of correlational support for this hypothesis, but few experimental tests, especially at an ecologically relevant scale. We set out to remedy this deficiency. We manipulated small mammal host communities in 30 forest fragments in Dutchess County, removing mice from one fragment and adding them to another (and the same with chipmunks and squirrels). We used mark-recapture methods to measure changes in host density and survival in the presence/absence of competitors, dragged for larval and nymphal ticks to see whether the host community influenced tick population size, and are screening nymphal ticks for the agent of Lyme disease to determine how host community composition changed the probability that a tick-bite is infectious. This work is ongoing, and while some things are becoming apparent--hosts do not seem to compete with each other!--I have more data than answers at this time.

If these kinds of questions interest you, you might consider volunteering in my lab. Just email me and we can talk through some ideas. Or, if you think graduate school is right for you, think about joining my lab.