Throughout the world and especially in developing countries acute diarrhoea1 diseases are the single major cause of morbidity and mortality both in humans and farm animals. Bacteria are among the chief causal agents of acute diarrhoeas and although fluid secretion can result from an increase in luminal osmolarity or hydrostatic pressure, the majority of bacterial enteropathogens appear to cause fluid loss by stimulating enterocytes to actively secrete electrolytes. Based on their ability to cause histological damage to the host intestinal epithelium, enteropathogenic bacteria can be classified as invasive or non-invasive strains. Invasive strains damage the host mucosa and cause diarrhoea by cytotoxic destruction of enterocytes and/or the induction of inflammatory responses; some strains also elaborate enterotoxins. The molecular mechanisms underlying the cytotoxic and diarrhoeagenic effects of these bacteria are not well understood, but in contrast, in recent years major advances have been made in elucidating the molecular mechanisms by which non-invasive bacteria elicit their enteropathogenic effects. These bacteria cause diarrhoea by elaborating one or more enterotoxins without histological damage to the host mucosa. The mechanisms by which these enterotoxins and their intracellular mediators regulate ion transport will be reviewed here (for the sake of brevity literature cited includes recent reviews).