Adherence of DiarrheagenicEscherichia coliStrains to Epithelial Cells

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Abstract
An important early step in the colonization of the human gastrointestinal tract by bacteria is the adhesion of the organ- ism to the host surface. Although adhesion is essential to maintain members of the normal microflora in the intestine, it is also the critical early phase in all diarrheal infections caused by pathogenic Escherichia coli strains. It is important, there- fore, to fully understand the mechanisms underlying E. coli adhesion and in that way to be able to develop methods of maintaining the intestinal normal microflora and to prevent pathogenic E. coli from initiating an infectious process. Great progress has been made in recent years in the iden- tification of the adherence factors of different diarrheagenic E. coli strains (Table 1). These protein structures are associated with the bacterial surface and can be subdivided into fimbrial and nonfimbrial adhesins (Fig. 1). In this minireview, we will discuss recent advances in the identification and characteriza- tion of previously known and novel adhesion factors from the six major categories of diarrheagenic E. coli strains: entero- pathogenic E. coli (EPEC), enterohemorrhagic E. coli (EHEC), enterotoxigenic E. coli (ETEC), enteroaggregative E. coli (EAEC), enteroinvasive E. coli (EIEC), and diffusely ad- hering E. coli (DAEC). EPEC AND EHEC STRAINS EPEC and EHEC strains are implicated in diarrhea and/or dysentery in humans. EPEC is a major etiological agent of infant diarrhea in developing countries. EHEC, a food-borne pathogen of worldwide importance, can cause nonbloody di- arrhea, but the most serious manifestation of disease is bloody diarrhea that can progress to a fatal illness due to acute kidney failure (hemolytic uremic syndrome), particularly in children (reviewed in reference 88). EPEC is an inhabitant of the small intestine, while EHEC colonizes primarily the large human intestine. These two E. coli pathotypes are distinct from other pathogenic E. coli strains because they produce a distinct his- topathological lesion on intestinal epithelial cells known as the attaching and effacing (A/E) lesion. A/E lesions are marked by localized degeneration of the intestinal brush border surface, loss of epithelial microvilli, and assembly of highly organized pedestal-like actin structures in the epithelial cells at the sites

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