I'm a Ph.D. candidate in Genetics in Vaughn Cooper's laboratory at UNH. My research interests are as follows:
Sudden expansion of host range has been the cause of numerous bacterial outbreaks and epidemics and continues to threaten both the immunocompromised and healthy human populations. For this reason, pathogenic microbes that are capable of persisting in multiple hosts and environments are under continued investigation. By identifying factors, genetic or phenotypic, that allow for the expansion of host range, investigators can begin to understand what allows for adaptation to new hosts.
My research focuses on examining the effects of host adaptation on growth in an alternative host. Specifically, I used experimental evolution to adapt B. cenocepacia HI2424 to an Allium cepa onion model and characterized subsequent decreases in virulence in a C. elegans infection model. I used experimental evolution because it remains an effective approach for studying phenotypes associated with adaptation to a specific host, as opposed to other methods that involve heavy interference by the researcher such as a candidate gene approach. By allowing the onion environment to exert selective pressures on bacterial populations, any changes occurring during the experiment are the direct result of adaptation in that environment.
My chosen strain, B. cenocepacia HI2424, was recovered in upstate New York from agricultural soil as a normal member of the soil microbial community. Macrorestriction digestion with pulsed-field gel electrophoresis and multilocus sequence typing classified this isolate as belonging to the PHDC strain lineage within the species B. cenocepacia. This strain, named for its initial identification as the cause of an outbreak in the Philadelphia-DC area of the United States, is widely distributed as a human CF pathogen in 24 US states and parts of Europe. In addition to its relevant strain characterization, the species B. cenocepacia is the Bcc species most often recovered from the lungs of CF patients.
In addition to its clinical relevance, B. cenocepacia HI2424 displays an ability to initially infect both animal and plant hosts. In preliminary experiments, this strain macerated plant tissue in an onion half model and kill nematodes in a liquid C. elegans model of chronic infection. These characteristics make this strain a good candidate for further investigation.
The questions that drive my research are as follows:
1) What phenotypes allow B. cenocepacia to infect such a wide range of plants and animal hosts?
2) If B. cenocepacia is allowed to adapt to a single host, will the bacteria retain its original host range? Does adaptation to a single host limit subsequent host range?
3) If B. cenocepacia virulence increases in one plant species as a result of adaptation, does virulence increase in other plant species?
4) Can attenuation of B. cenocepacia virulence, resulting from host-specific adaptation, be reversed? If so, how rapidly?
