John Stavrinides
Research interests:
Bacterial pathogenesis, host-microbe interactions, genetics and genomics, bioinformatics.
Understanding the host range and virulence potential of bacterial pathogens is central to our ability to predict and control emerging and reemerging infectious diseases. For cross-kingdom pathogens in particular, which have evolved the ability to exploit biologically distinct hosts, knowledge of their specific host affinities and disease strategies is vital to assessing their evolutionary momentum and potential for emergence. The multi-host and cross-kingdom pathogen, Pantoea agglomerans, serves as the ideal study system for examining the underlying genetic basis of bacterial-host interactions, pathogen host range, and the evolution of host-specific adaptation. P. agglomerans is found on plant surfaces in the environment and is known primarily for causing plant disease, yet it is closely related to the human pathogenic E. coli and Salmonella and is fully capable of infecting humans. Cases of bacteremia and septicemia involving P. agglomerans have become increasingly more common in the nosocomial setting, some of which have resulted in human fatalities. We are also currently exploring whether these nosocomial populations are distinct from the environmental populations, or whether there is gene flow between them.
My research uses a combination of genetic, genomic, evolutionary, and bioinformatic approaches to address questions relating to host-specific virulence. Our genetics approach involves genetic screening of P. agglomerans using the nematode, fruit fly, and several plants as hosts, with comparative virulence assays being used to identify common and host-specific disease determinants. As a complement to these genetic studies, we are conducting comparative genomic analyses of Pantoea isolates with different host affinities and pathogenic potential to delineate the specific evolutionary genomic changes that mediate the association between pathogen and host, and to gain a better understanding of host-specific adaptation. By comparing closely related clinical and environmental isolates, it is possible to reconstruct the stepwise evolutionary events that have allowed specific isolates to acclimate to one or many specific hosts. Ultimately, my research has significant implications for understanding the evolutionary processes that govern host-specific virulence and pathogenicity, and the emergence of new infectious agents.