Fimbriae of Human Enterotoxigenic Escherichia Coli and Control of their Expression

Abstract

One of the major causes of diarrhoea in infants in developing countries and in travellers to the Third World is enterotoxigenic Escherichia coli (ETEC) (1–4). Infection is acquired by ingesting contaminated food or water. Two virulence attributes of ETEC are essential for pathogenicity, namely enterotoxin production and the ability to adhere to and to colonize the epithelium of the small intestine. Bacterial growth in situ and elaboration of enterotoxin(s) leads to increased water and electrolyte secretion into the intestinal lumen and thus the diarrhoeic response and dehydration. Individual strains of ETEC may produce either heatlabile enterotoxin (LT) or heat-stable enterotoxin (ST), or both. The heat-labile toxin resembles the enterotoxin of Vibrio cholerae in molecular weight, serological properties and mode of action (5, 6). The heat-stable toxin is a polypeptide of low molecular weight which is poorly antigenic (6). Two types of ST have been identified, STa or ST1 being produced by human ETEC strains. LT and ST activate adenylate cyclase and guanylate cyclase, respectively (6).