Enteropathogenic E. coli (EPEC) is a major public health concern in developing countries where it causes significant morbidity and mortality in infants. EPEC, along with a few other related pathogens namely enterohemorrhagic E. coli (EHEC), Citrobacter rodentium, rabbit enteropathogenic E. coli (REPEC), and Escherichia albertii constitute a group collectively referred to as attaching and effacing (A/E) pathogens. They are so called because upon infection these pathogens attach intimately to intestinal cells and destroy cellular microvilli. Destruction of the microvilli reduces the ability of the cells to absorb water and nutrients, which ultimately leads to diarrhea. Upon destruction, the infected bacterium recruits the structural proteins from the microvilli and remodels them to form filament-like protrusions that extend out of the infected cell and are crowned on top by the infecting bacterium. This histopathological structure is commonly referred to as attaching and effacing (A/E) pedestal. The ability of EPEC to form A/E lesions and cause disease depends on the presence of a pathogenicity island called locus of enterocyte effacement (LEE). The LEE encodes a type 3-secretion system that connects the cytoplasm of the bacteria to that of the host and enables EPEC to traffic a constellation of factors directly into the host, which aid bacterial colonization and cause disease. My lab is interested in identifying bacterial factors that regulate the LEE and modulate the resulting pathogenicity of EPEC. Identification of such virulence factors and their mechanism of action is essential for the development of effective therapeutic measures to combat EPEC infections, especially in light of the emergence of highly drug-resistant strains of EPEC. We use a highly interdisciplinary approach by incorporating tools and techniques from bioinformatics, genetics, and biochemistry to interrogate and characterize such virulence factors.