Table 58-7.

Section of Intestine Most Commonly Affected, Type of Intestinal Lesion(s), Invasiveness, Virulence Characteristics, and Mechanism of Diarrhea of Enteric Escherichia coli Infecting Dogs

	Disease Localization	Intestinal Lesions	Invasion of Intestinal Epithelial Cells	Virulence Characteristics
Enteropathogenic E. coli (EPEC)	Small and large intestine	Effacement of microvilli and pedestal formation Mucosal inflammation	Variable	Adherence factor plasmid contains genes encoding bundle-forming pili Locus for enterocyte effacement contains bacterial genes encoding intimin (eae), a type III secretory apparatus, translocated intimin receptor, and EPEC-secreted proteins	Malabsorption, water and electrolyte secretion, increased permeability of tight junctions, and mucosal inflammation
Enterotoxigenic E. coli (ETEC)	Small intestine	Minimal histologic changes or inflammation	Noninvasive	Heat-labile toxins stimulate adenylyl cyclase activity by activational adenosine diphosphate-ribosylation of Gsα, thereby increasing the synthesis of cyclic adenosine monophosphate Heat-stabile toxins bind to and activate membrane-bound guanylyl cyclase, thereby increasing the synthesis of cyclic guanosine monophosphate	Secretory diarrhea (“traveler's diarrhea” in people): stimulate Cl− secretion by crypt epithelium and inhibit NaCl absorption by villous epithelium
Enterohemorrhagic E. coli (EHEC) and E. coli 0127:H7	Large intestine	Edema and submucosal hemorrhage, arteritis, and microvascular thrombosis of intestinal arterioles	Noninvasive	Shiga-like verotoxins inhibit protein synthesis resulting in cell death	Hemorrhagic colitis Hemolytic uremic syndrome