Hemolytic uremic syndrome in pediatric intensive care units in são paulo, Brazil.

The hemolytic uremic syndrome (HUS) caused by Shiga toxin-producing Escherichia coli (STEC) is one of the most frequent causes of pediatric acute renal failure. The aim of this study was to report the clinic and microbiologic features associated with 13 post-diarrheal HUS cases identified in pediatric intensive care units in the city of São Paulo, Brazil, from January 2001 to August 2005. Epidemiologic, clinic, and laboratorial information, along with fecal and serum samples, were collected for identifying the genetic sequences of Stx and for studying antibodies directed against LPS O26, O111 and O157. STEC was isolated from three patients, and serotypes O26:H11, O157:H7 and O165:H- were identified. In nine patients, high levels of IgM against LPS O111 (n=2) and O157 (n=7) were detected. Dialysis was required in 76.9% of the patients; arterial hypertension was present in 61.5%, neurological complications were observed in 30.7%, and only one patient died. During a 5-year follow-up period, one patient developed chronic kidney disease. The combined use of microbiologic and serologic techniques provided evidence of STEC infection in 92.3% of the HUS cases studied, and the importance of O157 STEC as agents of HUS in São Paulo has not been previously highlighted.

Human colostrum contains IgA antibodies reactive to colonization factors I and II of enterotoxigenic Escherichia coli.

Diarrhea is an important cause of morbidity and mortality amongst infants of low socio-economic levels in developing countries and in travelers who visit such areas. Enterotoxigenic E. coli strains express two sets of virulence-associated factors: enterotoxins (heat-stable toxins or heat-labile toxins) and colonization factors. Studies have shown that breast-feeding protects infants against infectious diseases, such as diarrhea, as it presents a great variety of immunological components. The aim of this study was to analyze the reactivity of immunoglobulin A from human colostrum to colonization factor antigens I and II. The colostrum ability in preventing enterotoxigenic E. coli adhesion to Caco-2 cells was also evaluated. Colostrum samples were collected from 32 healthy women, and a human colostrum pool was prepared. Enterotoxigenic E. coli strains expressing colonization factor antigens I and II were utilized. The colostrum pool and individual samples showed variable antienterotoxigenic E. coli immunoglobulin A titers, that were reactive with colonization factor antigen I and CS1/CS3 (colonization factor antigen II). The human colostrum pool and individual samples inhibited enterotoxigenic E. coli colonization factor antigen I and II adhesion to Caco-2 cells, at variable levels, and this ability was a result of immunoglobulin A antibodies reactive to these colonization factors. The immunoglobulin A-depleted pool lost this inhibitory ability. As bacterial adhesion is the initial mechanism of enterotoxigenic E. coli infection, breast-feeding could protect the offspring against diarrhea caused by this agent.