Postdoctoral associate at the Cary Institute of Ecosystem Studies, Millbrook, New York with Dr. Richard S. Ostfeld.
Ph.D. in biology from Arizona State University with Dr. James P. Collins.
B.A. in biology from Carleton College, Northfield, Minnesota.
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.
Seining for salamander larvae in Arizona.
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 (in press).
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. Dr. Ostfeld is probably best known for his research on the "dilution effect," which is the premise that host community composition can influence the transmission, and therefore dynamics and risk, of infectious disease.
My postdoctoral research focused on experimentally testing the "dilution effect" in the Lyme disease system. We conducted a large-scale manipulation of small mammal host communities in 30 forest fragments in Dutchess County, NY, removing mice from one fragment and adding them to another (and the same with chipmunks and squirrels). While some things are becoming apparent--hosts do not seem to compete with each other!--I have more data than answers at this time. Note, too, that we are continuing this research, applying more effective manipulations and expanding our research to include Anaplasma phagocytophilum and Babesia microti.
I was also very interested in understanding why certain mice and chipmunks feed (and are thus more likely to be infected with the Lyme disease agent, Borrelia burgdorferi, and to infect naive ticks) more ticks 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 test a suite of fairly complex seasonal models of tick burdens. The results are complex, but strongly indicate that there is no particular group or type of mice or chipmunks that are necessarily "super spreaders." (Note: 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.)
Last updated: October 2009