Typical and atypical enteropathogenic Escherichia coli (EPEC) strains differ in several characteristics. Typical EPEC, a leading cause of infantile diarrhea in developing countries, is rare in industrialized countries, where atypical EPEC seems to be a more important cause of diarrhea. For typical EPEC, the only reservoir is humans; for atypical EPEC, both animals and humans can be reservoirs. Typical and atypical EPEC also differ in genetic characteristics, serotypes, and virulence properties. Atypical EPEC is more closely related to Shiga toxin–producing E. coli (STEC), and like STEC these strains appear to be emerging pathogens.

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Enteropathogenic Escherichia coli (EPEC) has been associated with infantile diarrhea and mortality in humans in developing countries. While diarrhea is also a major problem among primates kept in captivity, the role of E. coli is unclear. This study was designed to characterize diarrheagenic E. coli recovered from the feces of 56 New World nonhuman primates, primarily marmosets (Callithrix spp.). Seventeen of the 56 primates had signs of diarrhea and/or enteritis. E. coli recovered from feces from these animals was tested by PCR for genes encoding virulence factors of diarrheagenic E. coli and for patterns of adherence to HeLa cells. In addition, isolates were characterized by the fluorescence actin staining test and by their ability to induce attaching and effacing lesions. PCR for the eae gene was positive in 10 of the 39 (27%) apparently healthy animals and in 8 of the 17 (47%) animals with diarrhea and/or enteritis. Colonies of eae ؉ E. coli were serotyped and examined by PCR for genes encoding EPEC virulence markers. The eae ؉ E. coli isolates recovered from both healthy and sick nonhuman primates demonstrated virulence-associated attributes similar to those of EPEC strains implicated in human disease and are designated monkey EPEC. The results presented here indicate that EPEC may be a significant pathogen for nonhuman primates, deserving further investigation. The similarities between the affected animals investigated in this study and human EPEC infections suggest that marmosets may represent an important model for EPEC in humans.

The complete nucleotide sequence was determined for pMAR7, an enteropathogenic Escherichia coli (EPEC) adherence factor (EAF) plasmid that contains genes encoding a type IV attachment pilus (Bfp) and the global virulence regulator per. Prototypic EAF plasmid pMAR7 is self-transmissible, unlike the smaller EAF plasmid pB171, which has no genes encoding conjugative functions. The tra locus, a highly conserved 33-kb segment found in pMAR7, is similar to the tra (conjugation) region of the F plasmid. ISEc13 copies flanking the pMAR7 tra region could potentially mobilize or delete the tra genes. Hybridization of 134 EPEC strains showed that a complete tra region is present only in strains of the EPEC1 clonal group. This study confirms EPEC's potential for dissemination of virulence attributes by horizontal transfer of the EAF plasmid.Enteropathogenic Escherichia coli (EPEC) are an important cause of acute and persistent diarrhea in infants in developing countries. EPEC strains produce a characteristic intestinal histopathology called the attaching-and-effacing (A/E) lesion, which is characterized by intimate bacterial adherence to the epithelial membrane, effacement of the microvilli, and striking cytoskeletal changes (18). The A/E phenotype is encoded by a 35-kb chromosomal pathogenicity island (PAI) known as the locus of enterocyte effacement (LEE) (17). The LEE encodes a type III secretion system that translocates virulence effector proteins into host epithelial cells and the surface protein intimin, mediating intimate adherence to host cells (reviewed in reference 12). The A/E histopathology and the presence of LEE are also characteristic of other diarrheagenic strains, including enterohemorrhagic E. coli (EHEC).The large plasmid pMAR2, the first genetic element implicated in EPEC disease, is present in the prototypic EPEC strain E2348/69 (O127:H6) (2). Adherence of EPEC to HEp-2 epithelial cells and in vivo adherence to piglet intestinal epithelium was shown to be dependent on this self-transmissible plasmid. Transfer of this plasmid to a nonadherent E. coli K-12 strain conferred the ability to adhere to epithelial cells. Of 32 adherent strains with classical EPEC serotypes, 31 possessed similar large plasmids, subsequently named EAF for EPEC adherence factor plasmids. Adult volunteers developed diarrhea in nine of ten cases challenged with wild-type E2348/69 (13) but in only two of nine controls who ingested the plasmidcured derivative. Antibodies to an outer membrane protein expressed by the parent strain were detected after treatment with wild type but not the plasmid-cured derivative. Expression of the protein, later identified as intimin (11), was also linked to the plasmid. A 1-kb region of pMAR2, called the EAF probe, was the first molecular diagnostic tool for EPEC (19).The type IV pilus named the bundle-forming pilus (BFP) (8) encoded in a 14-gene locus, was the first virulence factor to be identified for the EAF plasmid (24, 25). The rope-like filaments of BFP connect EPEC bacteria into microcolonies i...