An outbreak of Escherichia coli O157:H7 infection occurred in July 1996 in Sakai City. About 5000 children were infected, 122 of whom developed hemolytic uremic syndrome (HUS). In this outbreak, almost all patients were administrated some type of antibiotics. The effects of antibiotics on E. coli O157 associated hemorrhagic colitis (HC) have been controversial. In this study, we focused on the effects of antibiotics on development of HUS in the HUS in the Sakai outbreak. We retrospectively determined the antibiotics administrated within three days after the onset of HC, clinical courses, and laboratory data of 301 patients who were hospitalized and identified as Escherichia coli O157 infection by stool culture, from results of questionnaires sent by the Osaka Prefecture Medical Association to hospitals in Osaka Prefecture. The antibiotics used could be identified for 216 patients. The incidence of HUS among these patients was 11.6%. They were divided into 19 groups based on the type of antibiotics administrated. The incidence of HUS in the new quinolone (3.7%) group was low, but was high in the intravenous cephalosporin (18.2%) group. The differences in the incidence of HUS among the 19 antibiotic groups was significant (p < 0.05) on analysis of covariance which eliminated the contributions of variables including age, sex and laboratory data. These findings indicate that the suitable antibiotics can prevent the development of E. coli O157-associated HUS.

The activity of alpha-L-iduronidase was determined in leukocytes from two patients with the Hurler syndrome, five obligatory heterozygotes, one patient with the Hunter syndrome, and ten normal individuals. It was found that the determination of alpha-L-iduronidase in leukocytes was a useful method for differential diagnosis between the Hurler and Hunter syndromes. Heterozygotes of the Hurler syndrome showed approximately 50% level of alpha-L-iduronidase activity in leukocytes as compared with that of normal individuals. This suggests that the determination of alpha-L-iduronidase activity may be available for the carrier detection of the Hurler syndrome.

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