Streptococcus intermedius: A Cause of Lobar Pneumonia with Meningitis and Brain Abscesses

the 14 cases involving E. coli, results of evaluation for stx1, stx2, and eae genes were positive for 6 of 6, 3 of 5, and 2 of 3, respectively. Of the 6 cases of E. coli with known serotypes, 5 were non-O157. Thus, the phenotypic and genetic profiles of our strain (not serotypable; stx2 positive; stx1 and eae negative) seem to be atypical. The lack of diarrhea in the patient we described might be related to the absence of the eae gene in our strain, given that this gene encodes for intimin, an adhesive protein that facilitates colonization of intestinal epithelium and subsequent disease [4]. The transient increase of serum creatinine levels following antibiotic therapy for UTI does not allow us to conclude with certainty that ofloxacin was responsible. However, this observation is in agreement with results of a recent in vitro study showing that quinolones may induce the stx2 gene [5]. The presence of the stx2 gene in our strain might also explain the severity of the HUS, given that the association of stx2 with severity of the disease has been previously reported [6]. The case described herein of a STEC UTI associated with HUS underscores the importance of direct detection of Shiga toxins in urinary E. coli strains and suggests that quinolones should perhaps be avoided as therapy for UTI in this context. Many authors attributed the adverse effect of antimicrobial agents in HUS with diarrhea to the release of Shiga toxins. Our observation seems to support this position.