In developing countries many enteric infections are caused by acid-sensitive pathogens. Failure of the gastric acid barrier to infection has been reported in cholera but gastric acid secretion has been little studied in other enteric infections. We therefore studied basal and stimulated gastric acid in 185 Bangladeshi men admitted to hospital for the treatment of enteric infection. Patients with dysentery (amoebiasis, n=24 and shigellosis, n= 19) and culture-negative diarrhoea (n=69) had similar mean gastric acid levels (basal, 3-5 mmol/h; stimulated, 11-17 mmol/h), which remained stable in those patients studied throughout 12 weeks of convalescence. In contrast, patients with secretory diarrhoea caused by cholera or enterotoxigenic Escherichia coli (ETEC) had low gastric acid levels (P