The causative agent Vibrio cholerae is ingested in faecally contaminated water or food. The bacteria attach by means of adhesins to the intestinal mucosa, where, without actually penetrating the cells, they release the cholera exotoxin. This comprises an 'A' and several 'B' subunits; the former is the active ingredient, while the latter attach to epithelial cells by binding to a specific glycolipid in the membrane. This allows the passage of the 'A' subunit into the cell, where it causes the activation of an enzyme called adenylate cyclase (Figure 7.12). This results in uncontrolled production of cyclic AMP, causing active secretion of chloride and water into the intestinal lumen. The outcome of this is huge fluid loss (10 l or more per day) through profuse and debilitating diarrhoea. In the young, old and sick, death through dehydration and salt depletion can follow within a very short time. If proper liquid and electrolyte replacement therapy is available, recovery rates can be very high. Although it is now very rare in the developed world (in 2002, only two cases were reported in the USA), cholera is a major killer in the third world. It is easily preventable by means of clean water supplies and improved
Figure 7.12 The action of the cholera exotoxin. Activation of the enzyme adenylate cyclase results in elevated levels of cyclic AMP and the secretion of electrolytes out of the epithelial cells lining the intestine and into the lumen. This is followed by water loss, resulting in debilitating dehydration sanitation, however when these services break down, for example during war or after an earthquake, cholera outbreaks quickly follow.
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