Abstract

BackgroundTo analyze the clinical characteristics and outcomes of carbapenem-resistant Klebsiella pneumoniae (CRKp) and carbapenem-susceptible K. pneumoniae (CSKp) bloodstream infections (BSIs), and to study the risk factors for development of CRKp BSI and K. pneumoniae BSI-related mortality.MethodsA retrospective case control study of patients with K. pneumoniae BSI was conducted in the intensive care unit of the First Affiliated Hospital, Medical of College, Zhejiang University from January 2013 to December 2014. Carbapenem resistance was defined in accordance with the Clinical and Laboratory Standards Institute 2016 guidelines. Risk factors for the development of CRKp BSI and risk factors for mortality due to K. pneumoniae BSI were assessed. Virulence genes were detected by polymerase chain reaction assay.ResultsIn total, 48 patients were enrolled in the study, including 31 (65%) patients with CRKp BSI and 17 (35%) patients with CSKp BSI. CSKp infection was associated with more severe clinical symptoms, particularly a higher serum creatinine level (165.06 ± 127.01 in the CSKp group vs. 93.77 ± 84.35 μmol/L in the CRKp group, p = 0.039), but there was no significant difference in prognosis between the CSKp and CRKp groups. On multivariate analysis, indwelling central venous catheter (p = 0.045) was the only factor independently associated with CRKp bacteremia. However, the mortality of K. pneumoniae BSI patients was not correlated with carbapenem resistance. In addition, the isolates had diverse clonality and different origins. The frequency of detection of the allS and magA virulence genes was higher in the CSKp group than in the CRKp group (alls p = 0.04; magA p = 0.047).ConclusionsPatients in the CSKp group experienced more severe clinical symptoms, although mortality did not differ significantly between the CRKp and CSKp groups. An indwelling central venous catheter was the only factor independently associated with CRKp BSI. The mortality of patients with K. pneumoniae BSI was not associated with carbapenem resistance. The frequency of virulence genes was higher in the CSKp group than in the CRKp group.

Highlights

  • To analyze the clinical characteristics and outcomes of carbapenem-resistant Klebsiella pneumoniae (CRKp) and carbapenem-susceptible K. pneumoniae (CSKp) bloodstream infections (BSIs), and to study the risk factors for development of CRKp BSI and K. pneumoniae BSI-related mortality

  • An indwelling central venous catheter was the only factor independently associated with CRKp BSI, partly consisted with the past studies [35, 36]

  • We identified several differences between the CRKp and CSKp groups, and explored the impact of carbapenem resistance and bacterial virulence genes on the outcomes of patients with K. pneumoniae BSIs.These data can lay the groundwork for future research in this field

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Summary

Introduction

To analyze the clinical characteristics and outcomes of carbapenem-resistant Klebsiella pneumoniae (CRKp) and carbapenem-susceptible K. pneumoniae (CSKp) bloodstream infections (BSIs), and to study the risk factors for development of CRKp BSI and K. pneumoniae BSI-related mortality. Klebsiella pneumoniae, a member of the family Enterobacteriaceae, is a causative organism of various infections, including serious community-onset infections, such as necrotizing pneumonia, pyogenic liver abscesses, and endogenous endophthalmitis [1, 2]; and nosocomial infections, urinary tract infections (UTIs), respiratory tract infections, and bloodstream infections (BSIs) [1, 3, 4]. Due to abuse of antimicrobial agents in developing countries, the incidence of carbapenemresistant Enterobacteriaceae (CRE) is of considerable concern. K. pneumoniae is the most prevalent Enterobacteriaceae species, accounting for 71.9% of 242 CRE strains in a retrospective study conducted in a tertiary hospital in Hangzhou, China [5]. 48-like) is the most common mechanism of resistance among K. pneumoniae isolates. Other mechanisms include alterations in outer membrane permeability, mediated by loss of porins and the upregulation of efflux systems [7]

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