Research Areas
I am a wildlife ecologist with training in zoology and veterinary medicine, and I have conducted research at the intersection of disease ecology, immunological ecology, and physiological ecology. I primarily examine infectious disease dynamics at molecular, cellular, organismal, and population levels, with the primary goal of understanding host-pathogen interactions. As a veterinarian, I possess a deep understanding of the physiological, immunological, and pathological processes involved in a host’s response to disease. As a zoologist and ecologist with veterinary training, I am thus in the unique position of being able to examine disease processes in natural systems from the point of view of internal host dynamics, and to conduct comprehensive immunological studies in wildlife. By studying environmentally transmitted diseases, my work also bridges the gap between internal host ecosystems and the external environment. Overall, I strive to understand why hosts get the diseases they do, when they do. To this end, my research involves three main, complementary themes:
1. Host susceptibility to disease, and how susceptibility and disease dynamics fluctuate seasonally
2. Within-host coinfection and immune trade offs
3. Examining hosts as internal ecosystems
1. Seasonally Driven Host Susceptibility to Disease
I am interested in what makes one host more susceptible to disease than another host in its population. Expanding this to the population level, I am interested in why populations of hosts experience disease outbreaks contained in space and time. I address these issues by examining host physiological and immunological traits in concert with markers of infection, comparing these measures temporally.
My doctoral dissertation research focused on how host susceptibility to anthrax changed seasonally in Etosha National Park, Namibia, a natural, uncontrolled anthrax system in which plains ungulates experience annual, wet season anthrax outbreaks. Given the facts that anthrax can only be transmitted (usually orally) environmentally and that the bacteria exist in the environment as hardy, very long-lived spores that do not appear to undergo appreciable environmental replication, it is unclear why natural anthrax outbreaks occur rather than a more constant incidence of this disease. For this work, I examined seasonal differences in host immune allocation, both generally (likely due to changes in resource abundance) and in association with seasonally-constrained, directly transmitted gastrointestinal (GI) parasites, hormonal changes, and anthrax exposure.
During my postdoctoral research at Princeton University, I studied the seasonality of environmentally transmitted pathogens, focusing primarily on GI parasites in non-human primates in Laikipia Province, Kenya. Using these data sets, I continue to examine the host gut microbiome in concert with seasonal parasite infection intensity fluctuation. In addition, I was a founding member of a multi-institution Parasite Ecology Research Project (PERP) examining the effects of climate change on parasite biodiversity and vulnerability to extinction. By building models using new theories and existing datasets, we investigated how parasites, particularly environmentally transmitted pathogens, may be affected by different climate change scenarios, including how increased seasonal fluctuations or seasonal damping may affect host-pathogen dynamics.
2. Within-Host Coinfection and Immune Trade-Offs
Macroparasites, in particular GI helminths, have been found in many laboratory studies to be immunomodulatory in hosts. These large worms typically skew host immune function toward the Th2-type arm of immunity, which is ineffective in fighting against most microparasite infections (most intracellular bacteria and viruses). Microparasite infections largely require a Th1-type immune response from the host for control and clearance of infection, and these two immune arms are usually mutually exclusive and mutually inhibitory. While these patterns have been demonstrated in many laboratory systems, they have only been shown in a couple of studies in complex natural systems.
For my dissertation research, I found strong evidence that GI parasites skew zebra hosts toward a Th2-type immune response during the wet season, and that this likely contributes to making these hosts more susceptible to fulminant anthrax infection at this time. In addition, I found that GI parasite immunomodulation also correlates with increased host susceptibility to ectoparasite infestations, illustrating that GI parasites are likely the primary drivers of host immunomodulation in this system. While I expected these GI parasite infections in turn to increase host stress in the wet season, I found that stress hormone levels were in no way correlated with GI parasite infection intensities, indicating that these hosts are largely tolerant of their macroparasites despite the number of resources they command.
I continued to examine issues of coinfection trade offs in my postdoctoral work. While my study animals in Etosha were infected with only one or two species of gut macroparasites, my study primates in Kenya experienced more diverse macroparasite coinfections. Thus, I used them to investigate which parasites affect the host microbiome the most, and which parasites drive infection transmission dynamics between troops.
3. Hosts as Internal Ecosystems
The discipline of ecological immunology is still in its infancy; the majority of immunological studies in wildlife to date have measured just one or two basic components of host immunity and host-pathogen interactions. While examining immune function in natural settings is complex due to individual variation, seasonal fluctuations, and innumerable other factors that must be controlled for, I feel strongly that we must ultimately ground-truth the findings from highly controlled laboratory studies in natural systems.
Thus, for my dissertation research, I measured nine measures of immune function, four hormones, several body measurements, infection with three pathogens, and several environmental parameters in my study animals. In addition, I performed the first longitudinal, comprehensive ecological immunology study in the wild, as I resampled my study animals as many times as possible over five seasons to control for individual variation and to examine pathogen and immune changes over time. While I have used these data to examine several hypotheses thus far, I am also interested in quantifying the relationships between all components within these hosts. I am currently working on developing an internal host “food web” using path and cluster analyses; while a few other studies have attempted to quantify the internal host ecosystem, the wealth of data I possess for each of my study animals over time will allow me to create the most comprehensive analysis of internal host ecosystems to date. While this is a valuable exercise in and of itself to both highlight the complexity of the internal host milieu and to drive the further development of these methods, such networks will also help to elucidate complex host-pathogen interactions from a within-host perspective..