**4.2 Attaching and effacing (A/E) lesion**

The hallmark of EPEC infection is the ability of the organism to attach intimately to epithelial cells and efface microvilli (**Figure 1C**). This effect was first described by Staley et al. [41], although the term attaching and effacing (A/E)

#### **Figure 1.**

*EPEC adhesion to epithelial cells: (A) localized adherence pattern (LA) of typical EPEC on HeLa cells; (B) localized adherence-like (LAL) pattern of atypical EPEC on HeLa cells; (C) attaching and effacing (A/E) of enterocytes by EPEC; and (D) small bowel biopsy of infant infected with typical EPEC O111ab:H2 [36].*

**55**

*Enteropathogenic Escherichia coli*

**4.3 Invasiveness**

**4.4 Biofilm formation**

**4.5 The EAF plasmid**

**4.6 Bundle-forming pilus (BFP)**

**system (TTSS)**

*DOI: http://dx.doi.org/10.5772/intechopen.82861*

was coined by Moon et al. [13]. The A/E characteristic can be observed by electron microscopic examination of cultured epithelial cells exposed to EPEC or of intesti-

Intracellular typical EPEC have been observed both in tissue culture and in small intestinal biopsies from an EPEC-infected infant (**Figure 1D**) [36]. Fletcher et al. [42] and Scaletsky et al. [43] have reported that EPEC O111:NM strains contain plasmid sequences that confer invasiveness upon *E. coli* K12 strains. However, despite their invasive potential in vitro, most EPEC are considered as noninvasive pathogens [44].

Typical EPEC have the ability to form biofilms on abiotic surfaces under static conditions, or on a flow through continuous culture system, and a model of EPEC biofilm formation has been proposed [45]. Biofilm formation requires adhesive structures as type 1 pili, antigen 43, BFP, and the EspA filament (see below) as participants in bacterial aggregation during biofilm formation on abiotic surfaces [45]. Atypical EPEC strains have also been shown to adhere to abiotic surfaces (polystyrene and glass) [46, 47]. The non-fimbrial adhesin curli and the T1P were shown to mediate binding to these surfaces in some atypical EPEC at different temperatures [48, 49].

Typical EPEC strains possess a large virulence plasmid called the EPEC adherence factor (EAF) plasmid [9], which varies in sequence among different EPEC strains but is somewhat conserved [12]. The EAF plasmid pMAR2 is found among strains of the EPEC1 lineage, whereas pB171 is more common among EPEC2 strains [50, 51]. Two sets of genes located on the EAF plasmid are important for pathogenicity: the *bfp* gene cluster encoding BFP [38] and the *per* locus encoding a transcriptional activator called plasmid-encoded regulator (Per) [51]. Both BFP and PerA have been shown to contribute to virulence in human volunteers [52]. Between pMAR2 and pB171, the *bfp* and *per* loci share 99% sequence similarity [50]. Studies of comparison genomics of the EAF plasmids from varied EPEC phylogenomic lineages demonstrated significant plasmid

Typical EPEC strains produce a type IV pilus, the bundle-forming pili (BFP), which interconnects bacteria within microcolonies, promoting their stabilization and producing the LA phenotype [38]. The BFP is encoded by an operon of 14 genes contained on the EAF plasmid, with *bfpA* encoding the major structural subunit (bundlin) [54]. These 14 *bfp* genes are highly conserved among EPEC1 and EPEC2 strains. Some O128:H2 and O119:H2 EPEC strains that contain part of the *bfpA* gene have the rest of the *bfp* gene cluster deleted and replaced with an IS*66* element [55, 56].

**4.7 The locus of enterocyte effacement (LEE) and the type III secretion** 

The locus of enterocyte effacement (LEE) is a 35.6-kb pathogenicity island of EPEC containing genes necessary for the formation of the A/E lesion [57]. The EPEC LEE contains at least 41 open reading frames that are organized into five operons

diversity among isolates within the same phylogenomic lineage [53].

nal biopsies from infants or animals infected with EPEC [24].

was coined by Moon et al. [13]. The A/E characteristic can be observed by electron microscopic examination of cultured epithelial cells exposed to EPEC or of intestinal biopsies from infants or animals infected with EPEC [24].
