**4. Enteropathogenic** *E. coli* **(EPEC)**

## **4.1 An overview of EPEC**

Enteropathogenic *E. coli* (EPEC) is a pathotype that causes infrequent diarrheal diseases in adults and has also been implicated in gastroenteritis outbreaks in children in health care settings [104, 105]. EPEC was the first pathotype described in 1955 to refer to *E. coli* causing infantile diarrheal and implicated in a few outbreaks between the 1940s and 1950s [106]. Infection from this pathotype is frequent in children under two years living in low- and middle-income countries, and is the second leading cause of death among this age group, amounting to about 1.5 million deaths annually [105]. Like other DEC, the onset of EPEC-related diarrheal is characterized by acute watery stool which if it persists could result in loss of electrolytes and malabsorption of nutrients in children [3, 107]. Infection caused by EPEC strains is not limited to humans as they have also been implicated as a causative agent of diarrheal illness in young calves (**Figure 2**) [108].

EPEC strains are previously classified solely based on the combination of the three immunogenic structures O, H, and K antigens but the diversity observed for these antigens rendered serotyping unreliable rapid diagnostic tool for this pathotype [17, 107]. However, as recommended in 1987 by World Health Organization, 12 serogroups; O26, O55, O86, O111, O114, O119, O125, O126, O127, O128, O142, and O158 belonged to EPEC pathotype. In addition to six others; O39, O88, O103, O145, O157, and O158 have been classified and belonged to this pathotype although some of these serogroups consist of *E. coli* strains from different serotypes [108, 109]. EPEC strains are classified as either motile (H+ ) or non-motile (H− ). Among EPEC strains with flagellar associated antigens, H2 and H6 are the most frequent, whereas others that are less common include H7, H8, H9, H12, H21, H27, H25, and H34 [3, 107].

*The Biology and the Evolutionary Dynamics of Diarrheagenic* Escherichia coli *Pathotypes DOI: http://dx.doi.org/10.5772/intechopen.101567*

EPEC pathotype is defined based on the carriage of LEE locus that mediates the induction of A/E localized lesions [110], a feature that is shared with some STEC strains. However, the inability to produce Shiga toxins or other enterotoxins differentiate EPEC pathotype from EHEC/STEC strains [3, 10]. Additionally, based on the presence or absence of *E. coli* adherence factor plasmid (pEAF), EPEC pathotype is sub-grouped into two subtypes; typical (tEPEC) and atypical (aEPEC) [111]. Relative to tEPEC that is regarded to be more virulent, aEPEC group is reported to be highly diverse and more prevalent in diarrheal illness in children [111, 112]. Several O and/or H antigens of aEPEC strains are nontypeable. Of the typeable serogroups belonging to this subtype, O51 is the most frequent followed by five others (O145, O26, O55, O111, and O119) [3]. aEPEC O55:H7 is closely related with STEC O157:H7 and from the evolutionary perspective, the latter is believed to have evolved and diverged 400 years ago from the ancestor of the former [113]. EPEC like other diarrheagenic *E. coli* pathotypes is transmitted through the fecal-oral route as well as contact with contaminated surfaces or secretions. While humans are believed to be the major reservoir for tEPEC strains, aEPEC strains are present both in healthy individuals and in animals (**Figure 2**) [111, 112, 114].
