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Mortality and molecular epidemiology associated with extended-spectrum β-lactamase production in Escherichia coli from bloodstream infection

Authors Leistner R, Sakellariou C, Gürntke S, Kola A, Steinmetz I, Kohler C, Pfeifer Y, Eller C, Gastmeier P, Schwab F

Received 2 November 2013

Accepted for publication 10 December 2013

Published 13 March 2014 Volume 2014:7 Pages 57—62


Checked for plagiarism Yes

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Peer reviewer comments 4

Rasmus Leistner,1 Christian Sakellariou,1 Stephan Gürntke,1 Axel Kola,1 Ivo Steinmetz,2 Christian Kohler,2 Yvonne Pfeifer,3 Christoph Eller,3 Petra Gastmeier,1 Frank Schwab1

1Institute of Hygiene and Environmental Medicine, National Reference Center for the Surveillance of Nosocomial Infections, Charité Universitätsmedizin Berlin, Berlin, Germany; 2Friedrich Löffler Institute of Medical Microbiology, Universitätsmedizin Greifswald, Greifswald, Germany; 3Robert Koch Institute, FG13 Nosocomial Pathogens and Antibiotic Resistance, Wernigerode, Germany

Background: The rate of infections due to extended-spectrum β-lactamase (ESBL)-producing Escherichia coli is growing worldwide. These infections are suspected to be related to increased mortality. We aimed to estimate the difference in mortality due to bloodstream infections (BSIs) with ESBL-positive and ESBL-negative E. coli isolates and to determine the molecular epidemiology of our ESBL-positive isolates.
Materials and methods: We performed a cohort study on consecutive patients with E. coli BSI between 2008 and 2010 at the Charité University Hospital. Collected data were ESBL production, basic demographic parameters, and underlying diseases by the Charlson comorbidity index (CCI). The presence of ESBL genes was analyzed by polymerase chain reaction (PCR) and sequencing. Phylogenetic groups of ESBL-positive E. coli were determined by PCR. Risk factors for mortality were analyzed by multivariable regression analysis.
Results: We identified 115 patients with BSI due to E. coli with ESBL phenotype and 983 due to ESBL-negative E. coli. Fifty-eight percent (n=67) of the ESBL-positive BSIs were hospital-acquired. Among the 99 isolates that were available for PCR screening and sequencing, we found mainly 87 CTX-M producers, with CTX-M-15 (n=55) and CTX-M-1 (n=21) as the most common types. Parameters significantly associated with mortality were age, CCI, and length of stay before and after onset of BSI.
Conclusion: The most common ESBL genotypes in clinical isolates from E. coli BSIs were CTX-M-15 (58%) and CTX-M-1 (22%). ESBL production in clinical E. coli BSI isolates was not related to increased mortality. However, the common occurrence of hospital-acquired BSI due to ESBL-positive E. coli indicates future challenges for hospitals.

Keywords: BSI, mortality, ESBL-genotype, sepsis

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