INTRODUCTION: Extended-spectrum-β-lactamases (ESBL) are plasmid-encoded enzymes that confer resistance to multiple antimicrobials. ESBL-producing enterobacteria that cause bacteremia limit therapeutic options and increase mortality. OBJECTIVE: To perform a clinical and molecular description of bacteremia caused by ESBL-producing enterobacteria. METHOD: We retrospectively studied the cases of bacteremia due to ESBL-producing Escherichia coli, Klebsiella pneumoniae and Proteus spp in adults admitted to a university hospital during the years 2004-2007. We reviewed the clinical records and antimicrobial susceptibility patterns. Molecular typing was performed by polymerase chain reaction and study of clonality by pulsed-field electrophoresis. RESULTS: We found a prevalence of 9.8% ESBL in enterobacteria causing bacteremia. Decreased susceptibility to quinolones and aminoglycosides was observed, without resistance to carbapenems. The predominant ESBL types were CTX-M (96%), TEM (62%) and GES (28%). 79% of the strains presented more than one type of ESBL. Clinical analysis revealed high prevalence of risk factors, previous use of antimicrobials and of invasive devices. There was no significant clonality. CONCLUSION: The presence of ESBLs in bloodstream infections is a clinical problem that must be considered when choosing empiric therapy.
INTRODUCTION: Extended-spectrum-β-lactamases (ESBL) are plasmid-encoded enzymes that confer resistance to multiple antimicrobials. ESBL-producing enterobacteria that cause bacteremia limit therapeutic options and increase mortality. OBJECTIVE: To perform a clinical and molecular description of bacteremia caused by ESBL-producing enterobacteria. METHOD: We retrospectively studied the cases of bacteremia due to ESBL-producing Escherichia coli, Klebsiella pneumoniae and Proteus spp in adults admitted to a university hospital during the years 2004-2007. We reviewed the clinical records and antimicrobial susceptibility patterns. Molecular typing was performed by polymerase chain reaction and study of clonality by pulsed-field electrophoresis. RESULTS: We found a prevalence of 9.8% ESBL in enterobacteria causing bacteremia. Decreased susceptibility to quinolones and aminoglycosides was observed, without resistance to carbapenems. The predominant ESBL types were CTX-M (96%), TEM (62%) and GES (28%). 79% of the strains presented more than one type of ESBL. Clinical analysis revealed high prevalence of risk factors, previous use of antimicrobials and of invasive devices. There was no significant clonality. CONCLUSION: The presence of ESBLs in bloodstream infections is a clinical problem that must be considered when choosing empiric therapy.