Association Between Rectal Colonization with Highly Resistant Gram-negative Rods (HRGNRs) and Subsequent Infection with HRGNRs
Abstract
Objective
Rectal colonization with Highly Resistant Gram-negative Rods (HR-GNRs) probably precedes infection. We aimed to assess the association between rectal HR-GNR colonization and subsequent HR-GNR infection in clinical patients during a follow-up period of one year in a historical cohort study design.
Methods
Rectal HR-GNR colonization was assessed by culturing. Subsequent development of infection was determined by assessing all clinical microbiological culture results extracted from the laboratory information system including clinical data regarding HR-GNR infections. A multivariable logistic regression model was constructed with HR-GNR rectal colonization as independent variable and HR-GNR infection as dependent variable. Gender, age, antibiotic use, historic clinical admission and previous (HR-GNR) infections were included as possible confounders.
Results
1133 patients were included of whom 68 patients (6.1%) were colonized with a HR-GNR. In total 22 patients with HR-GNR infections were detected. Urinary tract infections were most common (n = 14, 63.6%), followed by bloodstream infections (n = 5, 22.7%) and other infections (n = 8, 36.4%). Eight out of 68 HR-GNR colonized patients (11.8%) developed a subsequent HR-GNR infection compared to 14 out of 1065 HR-GNR negative patients (1.3%), resulting in an odds ratio (95% CI) of 7.1 (2.8–18.1) in the multivariable logistic regression analyses.
Conclusions
Rectal colonization with a HR-GNR was a significant risk factor for a subsequent HR-GNR infection. This implies that historical colonization culture results should be considered in the choice of empirical antibiotic therapy to include coverage of the cultured HR-GNR, at least in critically ill patients.
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Full Scientific Study
Date
January 25, 2019
Conference or Journal
PLOS One
Author(s)
Dennis Souverein
Sjoerd M. Euser
Bjorn L. Herpers
Jan Kluytmans
John W. A. Rossen
Jeroen W. Den Boer