Typical Enteropathogenic Escherichia Coli Research Articles

A localized adherence-like pattern as a second pattern of adherence of classic enteropathogenic Escherichia coli to HEp-2 cells that is associated with infantile diarrhea.

Escherichia coli strains that cause nonbloody diarrhea in infants are known to present three distinct patterns of adherence to epithelial cells, namely, localized (LA), diffuse (DA), and aggregative (AA) adherence. Strains with LA (typical Enteropathogenic Escherichia coli [EPEC]) are well recognized as a cause of secretory diarrhea, but the role of strains with DA (DAEC) is controversial, and strains with AA (EAEC) have been more frequently related to persistent diarrhea whereas its relationship with acute diarrhea is not well defined. To determine the relationship of the different types of E. coli adherence patterns with acute diarrhea (lasting less than 14 days) and persistent diarrhea (lasting more than 14 days) in São Paulo, Brazil, we studied stool specimens from 40 infants under 1 year of age with diarrhea and 40 age-matched control infants without any gastrointestinal symptoms. Twenty-eight (35.0%) of eighty cases yielded adherent E. coli (HEp-2 cells). Strains with localized and aggregative adherence were associated with acute and persistent diarrhea. A total of 11.2% of the adherent strains were typical EPEC serotypes and hybridized with the enteroadherence factor probe; 5.0% were EAEC and hybridized with the EAEC probe. DAEC strains were isolated from 10.0% of patients and 7.5% of controls and did not hybridize with the two probes used (daaC and AIDA-I). Strains with a localized adherence-like pattern (atypical EPEC) were found significantly more frequently (P = 0.028) in cultures from children with diarrhea (17.5%) than in controls (2.5%).

Enteropathogenic Escherichia coli.

Abstract Enteropathogenic Escherichia coli (EPEC) strains are a leading cause of diarrhea among infants in developing countries. These bacteria spread via fecal–oral transmission and colonize the small intestine. Typical EPEC differs from atypical strains in that they possess the bfp operon and generate a type IV-B class of fimbriae known as the bundle-forming pilus (BFP). EPEC uses BFP to attach to intestinal epithelium. Upon attachment, EPEC translocates effector proteins into the host cell via a type 3 secretion system, which is encoded on a pathogenicity island known as the locus of enterocyte effacement. Translocated effectors modulate the host response in a number of ways, including subversion of immune responses and hijacking of the cytoskeletal system. By inducing actin rearrangement, EPEC causes the formation of actin pedestals onto which it sits, and leads to the effacement of microvilli, giving this bacterium a characteristic attaching and effacing phenotype. EPEC infections are typically self-limiting, with rehydration therapy constituting primary treatment, but they can be protracted and lethal. Breastfeeding provides a great protective effect, validating the use of a vaccine to induce a humoral response in mother or child as a potential means of preventative action. This chapter provides a detailed discussion on EPEC pathogenesis and host cell responses and summarizes the current detection and treatment options available.