Molecular epidemiology and risk factors of bloodstream infections caused by extended-spectrum β-lactamase-producing Klebsiella pneumoniae A case–control study

SummaryObjectivesTo study the prevalence, risk factors, outcome, and molecular epidemiology in patients with bacteremia caused by extended-spectrum β-lactamase (ESBL)-producing Klebsiella pneumoniae (Kp) (cases), in comparison with patients with bacteremia caused by a susceptible Kp (controls).MethodsThis was a retrospective case–control study including all episodes of Kp bacteremia for the period 1993 to 2002 at a referral hospital for adults in Mexico. ESBL production was tested for by E-test. All isolates were typed by pulsed field gel electrophoresis (PFGE). A subset of isolates underwent plasmid analysis, conjugal transfer of cefotaxime resistance to Escherichia coli J53-2, isoelectric focusing bioassay, colony-blot hybridization, PCR, and sequencing.ResultsOf the 121 patients with bacteremia due to Kp included in the study, 17 (14.0%) had an ESBL-Kp isolate (cases). Multivariate analysis identified prior use of cephalosporins (OR 7.6, 95% CI 1.1–53.5; p=0.039) and stay in the intensive care unit (ICU; OR 5.6, 95% CI 1.1–27.9; p=0.033) as significant risk factors. No differences were observed in hospital stay or mortality after the event. Multi-drug resistance was more frequent in ESBL-Kp. There was no clonal predominance. A distinct β-lactamase profile was identified, which included a combination of TEM-1 (pI 5.4) and SHV-5 (pI 8.2) in 13/17 ESBL-Kp isolates. Cefotaxime resistance was transferred by conjugation in 14/17 isolates with a >120-kb plasmid encoding ESBL.ConclusionsThe prevalence of ESBL-Kp was found to be lower than that previously reported in Latin America. ESBL-Kp bacteremia was not associated with a worse clinical outcome. We were able to identify a plasmid-mediated horizontal dissemination over the 10-year period