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Enterotoxigenic E. coli (ETEC) and heat-labile E. coli (HL-ETEC) are the major etiological agents of traveler’s diarrhea (TD). ETEC and HL-ETEC enterotoxin (ET) enter the small intestine, where it binds to receptors on epithelial cells. The ET receptors belong to a family of G-protein coupled receptors, the guanylyl cyclase (GC) receptors. The enterotoxin-GC-receptor complex cause an increase in the intracellular concentration of cGMP. cGMP is normally broken down by the enzyme phosphodiesterase, which mediates the hydrolysis of the ester bond. By replacing the phosphodiesterase with an inactive mutant (or by inhibiting the native phosphodiesterase), cGMP levels can be maintained. This results in an increase in the motility of the cilia and activation of the Na+/K+-ATPase pump on the membrane of the intestinal cells. Activation of the Na+/K+-ATPase pumps causes loss of sodium and water, and the resulting watery diarrhea (Pajon et al. (1996) J Clin Invest