The haemolytic uraemic syndrome, first described in 1955 by Gasser, is the number one cause of acute renal failure in infants. There are three types of the haemolytic uraemic syndrome: the seasonal epidemic form with prodromic diarrhoea and generally favourable outcome which usually occurs in infants, a less typical form without signs of digestive tract involvement and no seasonal prevalence which occurs more readily in older children and sometimes in families has a less favourable prognosis, and finally drug- or disease-related forms. Currently, overall mortality due to haemolytic uraemic syndrome has been reduced to about 4%, usually as a result of damage to the central nervous system. Several microorganism, including Shigella dysenteriae, Salmonella typhi, Campylobacter jejuni, Streptococcus pneumoniae, Rickittsiae and certain viruses (Coksackiae, Influenzae, Epstein-Barr) have been identified as causative agents. In 1983, digestive tract infection due to an Escherichia coli strain producing verotoxin was identified as capable of producing haemolytic uraemic syndrome and more rarely thrombopenic thrombotic purpura. The germ produces two exotoxins (whose effect is accentuated by the E. coli lipopolysaccharide endotoxin) which lead to the glomerular microangiopathy causing haemolytic uraemic syndrome. Diagnosis is based on identification (monoclonal antibodies, ELISA, PCR) of the verotoxins themselves or the two encoding genes in stool samples. Symptomatic treatment is essential but the effectiveness of antibiotics is still debated. Theoretically, antibiotics could worsen the syndrome by increasing endotoxin release from lysed bacteria, but inversely they could also prevent the syndrome if given early enough. Further research is required to acquire precise epidemiological data and identify animal reservoirs of verotoxin producing E. coli.