1.Genetic Homology Analysis of Bloodstream Infection Secondary to Intestinal Colonization with Carbapenem-Resistant Klebsiella Pneumoniae
Xinyue LI ; Hongjuan ZHANG ; Xiaoyan ZHU ; Meijia HUANG ; Yunmin XU ; Xundie LI ; Xinyi ZHENG ; Shaoxuan LI ; Bin SHAN
Medical Journal of Peking Union Medical College Hospital 2025;16(5):1138-1147
To investigate the genetic relatedness between carbapenem-resistant A retrospective analysis was conducted on clinical data from patients screened for carbapenem-resistant Among 12 878 patients screened for CRE, 60 (0.47%) were identified with intestinal CRKP colonization. Of these, 6 (10.0%) developed bloodstream infections, with an all-cause mortality rate of 66.7% (4/6) during hospitalization. The predominant strain type among paired isolates was ST11-KL64 producing KPC-2, accounting for 91.7%(11/12) of cases. Except for one patient(with a categorical agreement of 82.6%), colonizing and bloodstream isolates from the same patient showed complete agreement (100% categorical agreement) in antimicrobial susceptibility profiles for all antibiotics except tigecycline. Intraclass correlation coefficients for biofilm formation and siderophore production were both > 0.75 of all paired strains, indicating high phenotypic consistency. Except for one patient, core genome single nucleotide polymorphism (SNP) analysis and phylogenetic reconstruction revealed high genetic homology between colonizing and bloodstream isolates from the same patient (SNP difference < 10). Clonal relatedness was also observed among colonizing strains from different departments (SNP difference < 120). Although the intestinal colonization rate of CRKP is low, it poses a high mortality risk once bloodstream infection occurs. The high consistency in antimicrobial resistance profiles, biofilm formation, siderophore production, and genomic homology between colonizing and bloodstream isolates suggests that intestinal colonization is the direct source of subsequent invasive infection. Enhanced early screening, dynamic monitoring, risk-stratified prevention, and optimized intervention strategies are recommended to reduce the risk of CRKP infection and mortality.

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