The presence of the pathogenicity island (PAI) O122 genes, efa1 (lifA), sen, pagC, nleB, and nleE, in typical and atypical enteropathogenic Escherichia coli (EPEC) strains was investigated. The simultaneous occurrence of all genes was statistically associated with diarrhea due to atypical EPEC. Detection of the complete PAI O122 could aid in the identification of potential pathogenic strains of atypical EPEC.Enteropathogenic Escherichia coli (EPEC) and Shiga toxin (Stx)-producing E. coli (STEC) are important human enteropathogens (9). EPEC is further subgrouped into typical (tEPEC) and atypical (aEPEC) EPEC (8, 21). tEPEC strains are major causative agents of acute diarrhea in infants in developing countries, whereas aEPEC strains affect children and adults worldwide (5,7,9,21). The main difference between tEPEC and aEPEC is the presence of the EPEC adherence factor (EAF) plasmid in tEPEC (8,21). This plasmid encodes the bundle-forming pilus (BFP), which mediates localized adherence to intestinal cells (9), which is an essential property to differentiate tEPEC from aEPEC strains (1,7,21).Formation of the attaching-and-effacing (AE) lesion is the major virulence mechanism of EPEC and an additional virulence property of enterohemorrhagic E. coli (EHEC) strains, a subset of STEC strains (9). This lesion consists of intimate bacterial adherence to the intestinal epithelial cells, cytoskeleton remodeling, and microvillus effacement (9). The genes encoding the AE lesion are located in a pathogenicity island (PAI) known as the locus of enterocyte effacement (LEE) (9). Despite the recognized importance of AE lesion formation, other putative virulence genes among AE-producing E. coli strains have been described. Efa1 (EHEC factor for adherence) is an adhesin originally described in some EHEC strains (16). The efa1 gene is almost identical to lifA, an EPEC gene encoding lymphostatin (LifA) (13). LifA inhibits the proliferation of mitogen-activated lymphocytes and the synthesis of proinflammatory cytokines (13). Efa1/LifA contributes to EPEC adherence to epithelial cells and is critical for intestinal colonization by Citrobacter rodentium, which is an AE lesion-producing bacterial pathogen of mice (12). Although, in the prototype EHEC O157:H7 strain EDL933, efa1 (lifA) lacks the 3Ј region (efaC), the adherence ability of this strain is preserved (20).efa1 (lifA) is outside the LEE and inside PAI O122 (16). This island also harbors genes which are very similar to pagC of Salmonella enterica serovar Typhimurium, sen of Shigella flexneri, and two C. rodentium non-LEE genes, nleB and nleE. PagC is required for bacterial survival within macrophages and is immunogenic to humans, while sen encodes an S. flexneri enterotoxin (10). NleB is linked to colonization and disease in mice (11), and NleE induces polymorphonuclear (PMN) transepithelial migration and is involved in the blockage of 24). Afset et al. (2) found that, of 182 virulence genes searched for among aEPEC strains, 12 were statistically associated with diarrhea, includi...