Infections caused by extended-spectrum beta-lactamase-producing Enterobacterales after rectal colonisation with ESBL-producing Escherichia coli or Klebsiella pneumoniae.

2019 
Abstract Objectives Infections due to extended-spectrum beta-lactamase-producing Enterobacterales (ESBL-E) are considered infections with a high public health burden. In this study, we aimed to identify incidences of and risk factors for healthcare-associated infections (HAI) after rectal colonisation with ESBL-producing Escherichia coli (ESBL-EC) or Klebsiella pneumoniae (ESBL-KP). Methods This prospective cohort study was performed in 2014 and 2015. Patients colonised with ESBL-EC or ESBL-KP were monitored for subsequent HAI with ESBL-E, and other pathogens. In case of an ESBL-E infection, rectal and clinical isolates were compared using pulsed-field gel electrophoresis (PFGE), and whole-genome sequencing (WGS) for ESBL-KP isolates. Proportional hazard models were applied to identify risk factors for HAI, and to analyse competing risks. Results Among all patients admitted to the hospital during the study period, 13.6% were rectally screened for third-generation cephalosporin-resistant Enterobacterales (3GCREB). 2386 rectal carriers of ESBL-EC, and 585 of ESBL-KP were included in the study. Incidence density (ID) for HAI with ESBL-E was 2.74 per 1000 patient days at risk (95%CI 2.16 – 3.43) among carriers of ESBL-EC, while it was 4.44 per 1000 patient days at risk (95%CI 3.17 – 6.04) among carriers of ESBL-KP. In contrast, ID for HAI with other pathogens was 4.36 per 1000 patient days at risk (95%CI 3.62 – 5.21) among carriers of ESBL-EC, and 5.00 per 1000 patient days at risk (95%CI 3.64 – 6.69) among carriers of ESBL-KP. Cox proportional hazard regression analyses identified colonisation with ESBL-KP (HR = 1.58, 95%CI 1.068 – 2.325) compared to ESBL-EC as independent risk factor for HAI with ESBL-E. The results were consistent over all competing risk analyses. Conclusions Clinicians should be aware of the increased risk of ESBL-E infections among patients colonised with ESBL-KP compared to ESBL-EC that might be caused by underlying diseases, higher pathogenicity of ESBL-KP and other factors.
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