Colistin is the last line of defense for carbapenem-resistant Enterobacteriaceae (CRE) or Acinetobacter baumannii infection [1]. Recently, a plasmid-mediated colistin resistance mechanism (mcr-1 gene) was identified in human, animal, and environmental isolates in China, and the worldwide spread of the mcr-1 gene has continuously been reported [2]. This colistin resistance mechanism has mainly been found in isolates linked to community-associated infections or from animals [2]. However, mcr-1-encoding plasmid-mediated colistin-resistant Escherichia coli isolates were detected in a Danish patient with a bloodstream infection [3]. This possibility raises major public health concern for the emerging threats of CRE, given the limited therapeutic options, clinical severity, and poor outcomes. The aim of this study was to evaluate the recent epidemiology of colistin resistance in bloodstream E. coli, including mcr-1-mediated colistin resistance in Korea.

Clinical non-duplicated E. coli isolates (n=1,193), included in this study, were previously isolated from the blood of patients and stored in skim milk at -70℃ until the tests at a tertiary teaching hospital in Seoul, Korea during 2014–2015. To detect colistin-resistant isolates, test organisms were screened on Mueller-Hinton agar (Oxoid, Basingstoke, UK) containing colistin (0, 1, 2, and 4 µg/mL) with the E. coli ATCC25922 strain. One isolate was grown on an agar plate with a concentration of 4 µg/mL colistin and the minimal inhibitory concentration (MIC) of colistin, determined by E-test (bioMérieux, Marcy l’E’toile, France) was 6 µg/mL, indicating that the isolate was resistant to colistin, according to the EUCAST resistance criteria (>2 µg/mL) [4]. The mcr-1 gene was not detected following repeated PCR in this isolate [2]. The overall prevalence of colistin resistance in E. coli isolates from the blood was 0.15% (1/644) in 2015 and 0% (0/549) in 2014.

In this study, only one isolate was found to be resistant to colistin, but the resistance was not conferred by the mcr-1 gene. Although the mechanism underlying resistance in this isolate is currently unclear, lipopolysaccharide (LPS) modification via diverse routes is a well-known mechanism of colistin-resistance in Gram negative bacilli, and polymyxin-resistant mutants of E. coli show a higher rate of substitution of the ester-linked phosphate group in the lipid A portion of LPS [5]. Other possible colistin resistance mechanisms are overexpression of efflux pump systems and overproduction of the capsule polysaccharide [5].

In conclusion, the prevalence of colistin resistance in E. coli isolates from the blood of patients with bloodstream infection in Korea was very low, and the mcr-1 gene was not detected. Colistin susceptibility appears to be well conserved in E. coli causing blood-stream infections in Korea. However, the incidence of community-associated E. coli bacteremia continues to rise in Korea [6]. Therefore, the inflow of plasmid-mediated colistin via the mcr-1 gene should be closely monitored in E. coli blood isolates.