The impact of vancomycin-resistant Enterococcus (VRE) screening policy change on the incidence of healthcare-associated VRE bacteremia.

OBJECTIVE: To evaluate the impact of a vancomycin-resistant Enterococcus (VRE) screening policy change on the incidence of healthcare-associated (HA)-VRE bacteremia in an endemic hospital setting. DESIGN: A quasi-experimental before-and-after study. SETTING: A 1,989-bed tertiary-care referral center in Seoul, Republic of Korea. METHODS: Since May 2010, our hospital has diminished VRE screening for admitted patients transferred from other healthcare facilities. We assessed the impact of this policy change on the incidence of HA-VRE bacteremia using segmented autoregression analysis of interrupted time series from January 2006 to December 2014 at the hospital and unit levels. In addition, we compared the molecular characteristics of VRE blood isolates collected before and after the screening policy change using multilocus sequence typing and pulsed-field gel electrophoresis. RESULTS: After the VRE screening policy change, the incidence of hospital-wide HA-VRE bacteremia increased, although no significant changes of level or slope were observed. In addition, a significant slope change in the incidence of HA-VRE bacteremia (change in slope, 0.007; 95% CI, 0.001-0.013; P = .02) was observed in the hemato-oncology department. Molecular analysis revealed that various VRE sequence types appeared after the policy change and that clonally related strains became more predominant (increasing from 26.1% to 59.3%). CONCLUSIONS: The incidence of HA-VRE bacteremia increased significantly after VRE screening policy change, and this increase was mainly driven by high-risk patient populations. When planning VRE control programs in hospitals, different approaches that consider risk for severe VRE infection in patients may be required.

Sequence type 17 is a predictor of subsequent bacteremia in vancomycin-resistant Enterococcus faecium-colonized patients: a retrospective cohort study.

BACKGROUND: Sequence type (ST) 17 vancomycin-resistant Enterococcus faecium (VREF) is frequently isolated in nosocomial settings. The aim of this study was to identify whether ST17 contributes to subsequent bacteremia more often than other STs among hospitalized patients carrying VREF. METHODS: A retrospective cohort study was conducted in patients carrying ST17 VREF and those with non-ST17 VREF. Rectal screening according to hospital policy was used to identify patients with VREF. Subsequent VREF bacteremia events within a year of detection of colonization were recorded. Cox regression analysis was used to adjust the covariates involved in determining the association between ST17 and subsequent bacteremia events. RESULTS: The cohorts comprised 52 patients with ST17 and 169 patients with non-ST17 VREF. One-year VREF bacteremia-free rates were 85.9% and 90.2%, respectively. In multivariate analysis, ST17 was associated with subsequent bacteremia at an adjusted hazard risk (aHR) of 4.02 (95% confidence interval [CI], 1.32-12.29). Liver transplantation (aHR, 40.08; 95% CI, 4.87-329.76) and hematologic malignancy (aHR, 20.97; 95% CI, 4.87-87.82) were also significant. All cases of subsequent bacteremia in ST17 VREF carriers were caused by ST17; however, subsequent bacteremia in non-ST17 carriers was often caused by ST17 or another ST variant. CONCLUSIONS: A specific genotype, ST17 is a predictor of subsequent bacteremia in hospitalized patients carrying VREF. Patients with a hematologic malignancy and those receiving a liver transplant are also at high risk. More targeted strategies may be needed to prevent VREF infection in hospitals.

Emergence of vancomycin-resistant Enterococcus faecium ST1421 lacking the pstS gene in Korea.

Although multilocus sequence typing (MLST) has been used to study molecular epidemiology and to explore the population structure of Enterococcus faecium, vancomycin-resistant E. faecium (VREF) strains lacking the pstS gene that were non-typable using conventional MLST methods were reported recently. We found nationwide emergence of VREF isolates lacking pstS in Korea and hereby report the molecular characteristics of these isolates. Forty-six VREF isolates lacking the pstS gene were identified among 300 VREF rectal isolates collected from hospitalized patients between 2014 and 2015. MLST was performed and clonal relatedness was determined by pulsed-field gel electrophoresis (PFGE). Four VREF ST1421 isolates were whole-genome sequenced. Among the VREF rectal isolates lacking pstS, 98% were classified as ST1421, which has identical allelic profiles to ST17 for all housekeeping genes except pstS. PFGE pattern analyses revealed 32 pulsotypes. All isolates harbored Tn1546 components with various transposase and insertion sequences. The whole-genome sequencing of four VREF ST1421 isolates showed that the pstS gene region was deleted at various locations with considerable inversion. The pstS gene was also depleted in 12.1% of 33 VREF clinical isolates in 2006-2007 and in 11.8% of 59 clinical isolates in 2012-2013. VREF ST1421 strains lacking the pstS gene have emerged in Korea. The emergence and spread of pstS-deleted VREF strains pose a serious challenge for epidemiological investigation. Alternative molecular typing methods to MLST will be increasingly necessary.

Resistance mechanisms and clinical characteristics of linezolid-resistant Enterococcus faecium isolates: A single-centre study in South Korea.

OBJECTIVES: This study aimed to determine the prevalence of linezolid-resistant (LR) vancomycin-resistant enterococci and to investigate the mechanisms of linezolid resistance with clinical and microbiological characterisation. METHODS: All vancomycin-resistant Enterococcus faecium (VREF) isolated from blood and rectal swab cultures during 2012-2015 were tested for linezolid resistance. LR-VREF isolates were tested for antimicrobial susceptibility, glycopeptide resistance genes and virulence genes. Multilocus sequence typing (MLST) and pulsed-field gel electrophoresis (PFGE) were performed. Isolates were tested for known mechanisms of linezolid resistance. RESULTS: Among 389 VREF isolates, 7 (1.8%) were found to be resistant to linezolid. All LR-VREF isolates carried the vanA gene. Five isolates had both hyl and esp genes. The isolates were susceptible to tigecycline, daptomycin and quinupristin/dalfopristin, except for one isolate with daptomycin resistance. Two LR-VREF isolates recovered from patients with previous linezolid exposure contained the G2576T mutation in 23S rRNA and exhibited high-level resistance to linezolid (MIC>64mg/L). The other five isolates recovered from linezolid-naïve patients revealed no known linezolid resistance mechanism and exhibited low-level resistance to linezolid (MICs=8-16mg/L). Plasmid-mediated genes encoding cfr or optrA were not detected. LR-VREF isolates were represented by six different sequence types, belonging to hospital lineages, and were assigned to seven PFGE types. CONCLUSIONS: The prevalence of LR-VREF in this centre was low. Both linezolid exposure and horizontal transmission appear to be responsible for acquisition of LR-VREF in hospitalised patients. Prudent use of linezolid and improved infection control strategies are needed to limit the spread of LR-VREF.

Detection of clonal KPC-2-producing Klebsiella pneumoniae ST258 in Korea during nationwide surveillance in 2011.

This study analysed the characteristics and genetic similarity of recent Klebsiella pneumoniae carbapenemase (KPC-2)-producing Klebsiella pneumoniae isolates from Korea. Recent laboratory surveillance detected an increase in carbapenemase-producing Enterobacteriaceae in Korea. A total of 6 KPC-2-producing K. pneumoniae were identified from 277 Enterobacteriaceae clinical isolates. All were sequence type (ST) 258 and they had the same pulsotype. They had high MICs for carbapenems and multi-drug resistance. TEM-1, SHV-11 and OXA type ß-lactamases were detected in all isolates, whereas CTX-M type ß-lactamases and plasmid-mediated AmpC ß-lactamase (PABL) were not present. A conjugation experiment failed, but blaKPC-2-harbouring plasmids from the six isolates were used to transform Escherichia coli DH5-α by electroporation. Each of the transformants harboured a blaKPC-2-positive approximately 95 kb plasmid, which was typed in the IncFII incompatibility group and co-harboured TEM-1 and OXA-9 ß-lactamases. They shared the same restriction profile. This study confirms the emergence of clonal ST258 KPC-2-producing K. pneumoniae in some regions of Korea.

Dissemination of genetically related IMP-6-producing multidrug-resistant Pseudomonas aeruginosa ST235 in South Korea.

The present study aimed to describe the prevalence and molecular epidemiology of metallo-ß-lactamase (MBL)-producing Pseudomonas aeruginosa isolates obtained from non-tertiary care hospitals and geriatric hospitals in South Korea. Of the 644 isolates, 224 were carbapenem-resistant, amongst which 41 (18.3%) were MBL-producers and the major MBL type was IMP-6 (35 isolates). IMP-6-producing isolates were multidrug-resistant and showed higher minimum inhibitory concentrations for meropenem than imipenem. All of the IMP-6-producing isolates had class 1 integrons with amplification sizes of 4.5 kb/5.5 kb (34 isolates) or 3.0 kb (1 isolate); 4.5 kb/5.5 kb integrons had bla(IMP-6)-qac-aacA4-bla(OXA-1)-aadA1 (5.5 kb) and aadB-cmlA-bla(OXA-10)-aadA1 (4.5 kb). Pulsed-field gel electrophoresis (PFGE) analysis indicated that all IMP-6-producing P. aeruginosa from various geographic areas had nearly identical patterns with >85% similarity. All IMP-6-producing isolates showed high genetic similarity to those obtained from tertiary care hospitals and had the same integron type, indicating the spread of these strains to the three types of hospitals nationwide. These data show the wide spreading of clonally related IMP-6-producing P. aeruginosa (sequence type 235) through tertiary, non-tertiary and geriatric hospitals in South Korea. Continuous monitoring and thorough infection control should be performed in all types of hospitals to prevent further spreading of MBL-producing P. aeruginosa.