Virulence mechanisms of human respiratory pathogens

Pseudomonas aeruginosa and the Streptococcus Anginosus Group are two major groups of bacterial pathogens associated with lung infections in individuals afflicted with the genetic disease cystic fibrosis (CF). Using genetic, biochemical, and structural approaches, we are interested in understanding how the many virulence factors produced by these bacteria contribute to their ability to cause infectious disease.

 
This is a bacterium

mechanisms of Antibacterial toxin secretion

Antibacterial toxins are secreted by both commensal and pathogenic bacteria to compete for space and nutrients in numerous contexts including the human gut microbiome. We are interested in understanding how antibacterial toxins are transported from one cell to another and how they exert toxicity once delivered to a target cell. An understanding of the molecular principles underlying this process may one day allow for the rational manipulate bacterial populations relevant to human health and/or the environment.

 

exopolysaccharide secretion and bacterial adhesion

Many species of bacteria exist in dense cellular aggregates held together by bacterially produced exopolysaccharides. In this form, bacteria are difficult to eradicate due in part to decreased efficacy of antibiotics. We are interested in determining how bacterial exopolysaccharides are synthesized and exported from the cell. By understanding how this process occurs at the molecular level, we hope to one day be able to inhibit exopolysaccharide secretion under circumstances where it is detrimental to human activities (i.e. biofouling of pipes, colonization of indwelling medical devices, etc.). 

 
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phage susceptibility and resistance in the enterococci

Bacteria possess immune systems that protect against bacteriophage infection using many different mechanisms. Phages, in turn, evolve strategies to overcome these defences yet the mechanisms remain incompletely understood. We are interested in antiphage defence and counter-defence mechanisms in the Gram-positive pathogen Enterococcus faecalis, which we anticipate will be broadly applicable to diverse Gram-positive bacteria.