*7.2.1 Colonization and adherence*

DAEC pathotype carries genes that encode Afa/Dr adhesins [3, 177]. Afa/ Dr family includes Afa, Dr, and F1845 adhesins that are both afimbrial (such as AfaE-I and AfaE-III), and fimbrial (such as F1845 and Dr) adhesive structures on the bacterial surface encoded by the *afa*, *dra*, and *daa* operons, respectively [177, 181]. These adhesins have been found not only in DAEC but also in UPEC (Uropathogenic *E. coli*), indicating that strains that produce Afa/Dr adhesins may cause both intestinal and extraintestinal infections. Afa/Dr adhesins bind to human decay-accelerating factor (hDAF) and carcinoembryonic antigen-related cell adhesion molecules that induce receptor clustering resulting in a partial internalization of bacterial cells (**Figure 3**). These adhesins can induce the production of cytokine IL-8 and result in intestinal inflammation, loss of microvilli structure, and watery diarrhea [177]. There are two different subclasses of atypical DAEC; a subclass that contains all the adhesins typical of the Afa/Dr family of adhesins in another *E. coli* pathotype such as diffusely adherent EPEC, while the other subclass does not bind hDAF and expresses a different array of adhesins on its surface, including AfaE-VII, AfaE-VIII, AAF-I, AAF-II, and AAF-III and still able to induce proinflammation [177].

The prevalence of the genes constituting the operons that encode the Afa/Dr adhesins have been reported to vary in DAEC pathotype. In a study, the prevalence of the Afa/Dr adhesin family encoding genes *afaE-1, afaE-2, afaE-3*, *afaE-5* and *daaE* were reported in 64.3%, 14.2%, 28.6%, 21.5% and 21.5% of DAEC isolates, respectively [182], while in another study [183], the prevalence of these genes were 44%, 10%, 2%, 2% and 6%, respectively.
