RECENT ADVANCES Advances in haemolytic uraemic syndrome

The purpose of this review is to draw together recent advances in the pathogenesis of haemolytic uraemic syndrome (HUS) induced by verocytotoxin, including information from the successful Third International Symposium on Verocytotoxin Producing Escherichia coli, “VTEC’97”, in Baltimore.However, the highly publicised outbreaks of verocytotoxin producing Escherichia coli (VTEC) infection in Japan and Scotland in 1996 demand a brief epidemiological preface. These two epidemics were caused by the VTEC serotype O157. Reinforced by the recommendations of the Advisory Committee on the Biological Safety of Food in 1995, local public health laboratories in the UK have been routinely screening diarrhoeal faecal samples for this pathogen and the number of positive isolates reported to the Central Public Health Laboratory Service has soared. It is not known whether this reflects a true increase in VTEC related disease or is simply the result of more extensive investigation. The family of verocytotoxins closely resembles shiga toxin, the exotoxin of Shigella dysenteriae type I. The terms shiga-like toxin and verocytotoxin are synonymous, although there is pressure from US groups to standardise to the former. VT-2 is the toxin most closely associated with HUS in Europe and North America. Unlike the shiga toxin itself, the verotoxins are plasmid encoded and thus this important pathogenic property can be transferred between E coli strains, with potentially serious epidemiological consequences. Experience suggests that this has not yet happened in the UK. In the epidemiological survey conducted in Britain and Ireland in the late 1980s, 2 serotype O157 was the main, but by no means the only, culprit, and other VTEC serotypes were also involved. Children presenting with diarrhoea associated HUS at the Birmingham Children’s Hospital since 1990, however, have all had evidence of O157 either by stool culture or serology. Non-O157 serotypes are of major significance in other parts of the world—for example, O111 in Australia. Worryingly, Schmidt et al documented an outbreak of colitis and HUS at a German kindergarten in which the infective cause was a VT-2 producing Citrobacter freundii that had contaminated parsley used in a salad. It appears that the VT-2 plasmid can jump species! For all these reasons a further period of surveillance in the UK is called for. From February 1997 for a period of three years paediatricians have again been asked to report cases of HUS to the surveillance unit of the Royal College of Paediatrics and Child Health using the monthly orange card scheme. This is linked to VTEC surveillance operated through public health laboratories. Because of the importance of recognising outbreaks early, paediatricians are also being encouraged to report immediately by telephone. Parallel studies are in progress in other countries.