Although the Gram-negative bacterium Escherichia coli is normally considered to be a harmless commensal of the gastrointestinal flora, there are some exceptions to this rule. In the past few decades it has become increasingly evident that there are serotypes of E. coli that may cause disease in susceptible hosts. Disease states range from the invasive infections of the urinary tract caused by uropathogenic E. coli (UPEC) to the more typical diarrheal disease caused by several groups of E. coli serotypes, including enteropathogenic E. coli (EPEC) and enterohemorrhagic E. coli (EHEC). There is an increasing realization that bacteria–host interactions with pathogenic E. coli are far more complex and intricate than originally imagined. Studying the ways that bacteria such as EHEC and EPEC are able to subvert host cell functions to their own ends can be thought of as a “window” through which we are able to view the inner workings of the eukaryotic cell. In this chapter we examine some of the mechanisms by which EHEC and EPEC are able to coerce their host; we also examine the sequelae of these interactions.

EPEC usually refers to E. coli serotypes O55:[H6], O86:H34, O111:[H2], O114:H2, O119:[H6], O127:H6, O142:H6, and O142:H34, where square brackets indicate the occurrence of nonmotile strains (Nataro and Kaper, 1998). Infection with EPEC typically causes a chronic watery diarrhea, accompanied by a low-grade fever and nausea.