Abstract
We conducted a prospective study to assess the risk factors, molecular epidemiology and outcome of bloodstream infection (BSI) due to Enterococcus faecium in hospitalized cancer patients. Between 2006 and 2012, a significant increase in vancomycin-susceptible E. faecium BSI was observed among cancer patients. Comparison of 54 episodes of BSI due to E. faecium with 38 episodes of BSI due to E. faecalis showed that previous use of carbapenems was the only independent risk factor for E. faecium acquisition (OR 10.24; 95% CI, 1.35-77.66). All E. faecium isolates were susceptible to glycopeptides, whereas 97% showed high-level resistance to ampicillin and ciprofloxacin. All 30 isolates available for genotyping belonged to the hospital-associated E. faecium lineages 17, 18 and 78. After 2009, most of the isolates belonged to ST117 (lineage 78). Patients with E. faecium BSI were more likely to receive inadequate initial empirical antibiotic therapy than patients with E. faecalis BSI, and time to adequate empirical antibiotic therapy was also longer in the former group. No significant differences were found between the two groups regarding early and overall case-fatality rates. Independent risk factors for overall case-fatality were current corticosteroids (OR 4.18; 95% CI, 1.34-13.01) and intensive care unit admission (OR 9.97; 95% CI, 1.96-50.63). The emergence of E. faecium among cancer patients is a concern since there are limited treatment options and it may presage the emergence of vancomycin-resistant enterococci. A rationale approach that combines infection control with antimicrobial stewardship.
Highlights
Enterococci are part of the normal human microbial flora
Thirteen episodes of enterococcal bloodstream infection (BSI) were not included in the study because they were caused by species other than E. faecium or E. faecalis (E. gallinarum 6, E. casseliflavus 2, E. avium 2, E. hirae 1, E. durans and E. raffinosus 1)
54 episodes of BSI caused by E. faecium and 38 by E. faecalis were included in the study
Summary
Enterococci are part of the normal human microbial flora. Historically, the majority of invasive enterococcal infections were caused by Enterococcus faecalis, followed by Enterococcus faecium [1]. The epidemiology of invasive enterococcal infections appears to be changing worldwide, and a number of trends have been recognized, notably, the global emergence of enterococci as important nosocomial pathogens and the emergence of resistance to commonly used antimicrobial agents, including penicillins, aminoglycosides and glycopeptides [1]. An increase in the number of E. faecium strains in hospitals in different countries has been documented during the last decade [2,3,4] These isolates had in common the antibiotic resistance traits (to ampicillin, quinolones and to glycopeptides in some cases) and several virulence factors that might have contributed to the success of E. faecium as a leading nosocomial pathogen [4,5]. These strains were initially classified within a single clonal complex 17, it appears that the genetic diversity of this CC allows the classification of all isolates in three main lineages (17, 18, and 78), which is a more accurate representation of the recent evolution of these isolates[6]
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