CLABSI caused by CRKP is associated with high mortality. Identification of the genetic basis for carbapenem resistance is crucial for selecting the proper antimicrobial therapy, and testing for bacterial clonality. We aimed to study the genetic basis of CRKP causing CLABSI in3 ICUs, and use ERIC PCR to test for their clonality.
The study was conducted in a tertiary care hospital in Egypt from 1/1/2016 to 31/12/2017 after approval by the Institution Review Board. We enrolled all patients with CVCs in 3 ICUs. At least 2 sets of blood cultures were collected from each febrile patient by BACT/ALERT system (Bio Merieux, France), before starting antibiotic. The pathogens and their antimicrobial susceptibility were detected by the VITEK 2 system (Bio Merieux, France). Phenotypic detection of carbapenemase activity was done by modified Hodge (MHT) Test and Carba-NP Test. Multiplex PCR was done to identify the carbapenemase genes. Molecular typing of carbapenem-resistant isolates was performed by ERIC–PCR.
We enrolled 1210 patients admitted for17785 ICU days. Central catheters were utilized in 53.3% of patients for a total of 11014 central line days. Out of 130 Gram- negative CLABSI pathogens detected, we identified carbapenem resistance in 57 (43.8%); of which K. pneumoniae was the predominant pathogen (27 out of 57, 47.4%). By MHT and carba-NP, 63.79% of K. pneumoniae isolates were carbapenemase producers. Multiplex PCR revealed blaNDM in 48.14% and blaKPC in 33.33% of the K. pneumoniae isolates, whereas blaOXA-48 was not detected. ERIC-PCR analysis of 27 CRKP isolates showed genetic relatedness among only 5 KPC-positive and 2 producers, while most isolates were polyclonal.
We detected high rate of carbapenem resistance among K.pneumoniae causing CLABSI showing blaNDM in 48.14% and blaKPC in 33.33%; and they were mostly polyclonal.
A. El Kholy,