We study the ecological and genetic factors influencing the evolution of facultative bacterial pathogens as well as the disease ecology consequences of these dynamics. Our approach integrates theoretical and quantitative ecology and evolution with microbial genetics using the plant pathogen Agrobacterium tumefaciens as a model.
Cooperation is a key feature of the pathogenesis of many infectious diseases. Virulent agrobacteria manipulate host plants to produce specialized resources, however this is vulnerable to cheating by some avirulent genotypes. We study the evolutionary and epidemiological dynamics that allow for the maintenance of cooperative pathogenesis despite this cheating.
Plasmids play a key role in the ecology and evolution of bacterial populations as they frequently carry genes conferring traits such as antibiotic resistance and pathogenesis. The conjugative systems that they often encode allow for their horizontal transmission to other bacterial cells. Conjugation of the A. tumefaciens‘ virulence plasmid is tightly regulated such that it only occurs when a quorum sensing system is activated in the presence of an infected host. We are working to understand the adaptive significance of this gene regulation.
Faculative pathogens cause many important human and agricultural diseases. Despite this, most epidemiological models do not accurately capture their ecology. These organisms can maintain significant populations in non-host environments and consequently experience heterogeneous selective pressures. We are working to understand how ecological trade offs associated with the complex life history of faculative pathogens can influence pathogen evolution and epidemiology of the disease they cause.