Molecular Pathogenesis of EnteropathogenicEscherichia coli

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Abstract
Escherichia coli can cause gastrointestinal disease by a variety of mechanisms. This chapter focuses on the molecular pathogenesis of one specific category of diarrheagenic E. coli, the enteropathogenic E. coli (EPEC). It discusses the various bacterial factors and genes involved in EPEC pathogenesis as well as the specific changes that occur in the host cell in response to EPEC infection. Some studies report that the ability of EPEC to enter cell cultures exceeds that of Enteroinvasive E. coli (EIEC), but other investigators argue that the methodology of some invasion assays gives artificially elevated invasion levels for strongly adherent bacteria such as EPEC. As for many other bacterial pathogens, expression of EPEC virulence factors is regulated by a trans-acting regulator. The lack of tropomyosin accumulation with EPEC compared with the accumulation with Salmonella typhimurium suggests that the cytoskeletal rearrangement caused by EPEC forms a relatively inert, stable cytoskeletal structure that the bacterium rests on but does not promote an actin-myosin-tropomyosin-mediated event involved in mechanical bacterial uptake. Activation of protein kinase C induces rapid changes in intestinal water and electrolyte secretion in vivo and in vitro, thereby suggesting another possible intracellular mediator of the secretory response to EPEC infection. Several EPEC mutants were examined for their abilities to induce phosphorylation of Hp90. A strain cured of the 60-MDa plasmid encoding bundle-forming pilus (BFP) could still phosphorylate Hp90.