Shigella species are responsible for bacillary dysentery or shigellosis, a disease estimated to cause nearly 1 million deaths per year. Shigella species are closely related to the pathogenic E. coli, with Shigella and enteroinvasive E. coli being clinically indistinguishable. These pathogens utilise a common infection strategy whereby bacterial effector proteins are delivered directly into the host cell via a type 3 secretion system (T3SS), a strategy also shared by many other pathogenic bacteria (e.g. Salmonella, Yersinia and Vibrio spp).
Research in my laboratory currently focuses on structure/function studies of effector proteins that are common between the extracellular pathogenic E. coli (enteropathogenic and enterohaemorrhagic E. coli) and the intracellular enteroinvasive E. coli and Shigella species. The signalling pathways targeted by effectors that are shared by intracellular and extracellular pathogens represent fundamental processes required for infection such as subversion of cellular trafficking and regulation of apoptosis.