Enterotoxigenic E.
coli                                                                                             255
Fig. 14.5 Mechanism of action for enterotoxigenic            LT increases cAMP level, while ST increases cGMP, and
Escherichia coli (ETEC)-mediated diarrhea. After arrival     both mediate phosphorylation of CFTR (cystic fibrosis
in the intestine, ETEC binds to the epithelial cells using   transmembrane conductance regulator), a chloride ion
colonization factors (CFs) and/or TibA and produces sev-     transporter protein, which increases Cl− secretion in crypt
eral toxins including LT-I, LT-II, STa, STb, EAST1, and      cells and decreases absorption of Na+ and Cl− by absorp-
ClyA. Mechanism of action of LT-I and STa is presented.      tive cells
human and animal origin. The toxin activates                 Symptoms
cGMP, induces fluid accumulation, and possibly
plays a role in the onset of diarrhea. In addition,          ETEC infection does not show any apparent his-
ETEC also produces EatA, a serine protease                   tological changes in the mucosal layer, and there
autotransporter, which plays a role in pathogene-            is little or no inflammation in the intestine. The
sis by damaging the epithelial cell surface. Some            symptoms may include watery diarrhea, vomit-
strains of ETEC may secrete ClyA, a cholesterol-            ing, sunken eyes, massive dehydration, and a col-
dependent cytolysin (CDC), and form pore in the              lapse of the circulatory system. Diarrhea lasts for
cell membrane. It binds to cholesterol on the                3–4 days and is self-limited. Diarrhea may be
membrane and shows lytic activity against eryth-             lethal in young children and infants, with a mor-
rocytes, macrophages, and HeLa cells.                        tality rate of less than 1%.