e presence of an infectious agent in the gut causes local irritation of the small intestine walls. is increases the peristaltic action of the intestinal smooth muscles, increasing the speed of transit of the gut contents and not allowing enough time for absorption. rough a variety of dierent mechanisms, pathogens increase secretions of electrolytes and water into the small intestine, and some also reduce absorption. Cholera toxin, for instance, promotes secretion into the gut by stimulating adenylyl cyclase activity in the intestinal epithelial cells. It does so by causing a persistent activation of Gs subunits through an inhibition of the inbuilt GTPase activity, which ordinarily returns the subunit to its inactive state (see Chapter 2, Section 2.2.4). e result is an increase in cellular cyclic AMP levels which, through activation of protein kinase A, massively increases the conductance of Cl– into the gut lumen. Other diarrhoea-inducing microbes act through other mechanisms to increase Cl– secretion, or to reduce Na+ absorption. Importantly, particularly in terms of therapy, microbes which induce diarrhoea, including cholera toxin, do not aect SGLT-1 (see Box 13.1).