a ∣ Enterotoxigenic Escherichia coli (ETEC) becomes anchored to enterocytes of the small bowel through colonization factors (CFs) and an adhesin that is found at the tip of the flagella (EtpA). Tighter adherence is mediated through Tia and TibA. Two toxins, heat-labile enterotoxin (LT) and heat-stable enterotoxin (ST), are secreted and cause diarrhoea through cyclic AMP (cAMP)- and cyclic GMP (cGMP)-mediated activation of cystic fibrosis transmembrane conductance regulator (CFTR). b ∣ Enteroagreggative E. coli (EAEC) attaches to enterocytes in both the small and large bowels through aggregative adherence fimbriae (AAF) that stimulate a strong interleukin-8 (IL-8) response, allowing biofilms to form on the surface of cells. Plasmid-encoded toxin (Pet) is a serine protease autotransporter of the Enterobacteriaceae (SPATE) that targets α-fodrin (also known as SPTAN1), which disrupts the actin cytoskeleton and induces exfoliation. c ∣ Diffusely adherent E. coli (DAEC) forms a diffuse attaching pattern on enterocytes of the small bowel, which is mediated through afimbrial (Afa) and fimbrial adhesins, which are collectively known as Afa–Dr fimbriae. Most Afa–Dr fimbriae bind to complement decay-accelerating factor (DAF); a subset of Afa–Dr fimbriae bind to receptors in the carcinoembryonic-antigen-related cell-adhesion molecule (CEACAM) family. The autotransported toxin Sat has been implicated in lesions of tight junctions (TJs) in Afa–Dr-expressing DAEC, as well as in increased permeability. Polymorphonuclear leukocyte (PMN) infiltration increases surface localization of DAF. For full details, see main text. AMP, antimicrobial peptides; Gsα, stimulatory guanylyl-nucleotide-binding (G) protein α-subunit; MAPK, mitogen-activated protein kinase; PKA, protein kinase A.