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Purpose. The aim of the present study was to investigate the dissemination of carbapenem-resistant Klebsiella pneumoniae (CRKP) isolates in integrated intensive care units (IICUs) and emergency ICUs (EICUs) for controlling the spread of CRKP in different ICUs of the hospital. Methodology. From January 2016 to April 2017, a total of 46 non-duplicate CRKP isolates were consecutively isolated from a tertiary hospital. The production of carbapenemases was determined by the modified carbapenem inactivation method (mCIM) test. The resistance and virulence-associated genes were detected by PCR and DNA sequencing. A hypermucoviscosity phenotype was identified by the string test. Bacterial clonal relatedness of the CRKP isolates tested was determined by multi-locus sequence typing (MLST) and PFGE. Results. All CRKP isolates showed multiple drug resistance. All CRKP isolates harboured bla KPC-2-encoding carbapenemase and at least one of the other β-lactamase genes tested, with positive rates of 89.1 % (41/46) for bla CTX-M-65. qnrS was found among 76.1 % (35/46) of the CRKP isolates. A hypermucoviscosity phenotype was found in only two (4.3 %, 2/46) CRKP isolates. The virulence-associated genes with positive rates of more than 90 % among the 46 isolates tested included wabG (100 %, 46/46), ycf (100 %, 46/46), ureA (95.6 %, 44/46) and fim H (95.6 %, 44/46). MLST results showed that 46 CRKP isolates belonged to ST11 (95.6 %, 44/46) and ST86 (4.4 %, 2/46). PFGE patterns showed four clusters. Conclusion. The CRKP ST11 clone with co-production of CTX-M-65 and KPC-2 disseminated in ICUs of this tertiary teaching hospital in central China. The emergence of CRKP with a hypermucoviscosity phenotype in ICUs should be of particular concern.

Between September 2013 and March 2016, 26 (1.95 %) of 1333 Staphylococcus aureus clinical isolates from a Chinese hospital were found to be resistant to mupirocin, including 18 (1.35 %) with high-level mupirocin resistance and 8 (0.6 %) with low-level mupirocin resistance. Among the 18 isolates with high-level mupirocin resistance, 17 were associated with plasmid-mediated mupA. Meanwhile, the 8 isolates with low-level mupirocin resistance were shown to have a V588F mutation in ileS. A total of 14 sequence types (STs) and 18 spa types were identified. All four isolates with t062 belonged to ST965. Three ST5-MRSA-SCCmec II were linked to t311, which was not previously reported. Furthermore, ST764-MRSA-SCCmec II-t002, exclusively found in Japan before, was identified in this study. In conclusion, we observed relatively low prevalence of mupirocin resistance among S. aureus with considerable heterogeneity in East China. Newly emerging MRSA clones with high-level mupirocin resistance should be of concern.

Introduction. Resistance to rifampin (RIF) in Mycobacterium tuberculosis infection is associated with mutations in the rpoB gene coding for the β-subunit of RNA polymerase. The contribution of various rpoB mutations to the development and level of RIF resistance remains elusive. Hypothesis/Gap Statement. Various rpoB mutations may be associated with differential levels of RIF resistance. Aim. This study aimed to investigate the relationship between specific rpoB mutations and the MICs of RIF and rifabutin (RFB) against M. tuberculosis . Methodology. Of the 195 clinical isolates, 105 and 90 isolates were randomly selected from isolates resistant to RIF and sensitive to RIF, respectively. The MICs of 12 agents for M. tuberculosis isolates were determined using commercial Sensititre M. tuberculosis MIC plates and the broth microdilution method. Strains were screened for rpoB mutations by DNA extraction, rpoB gene amplification and DNA sequence analysis. Results. One hundred isolates (95.24 %) were found to have mutations in the RIF-resistance-determining region (RRDR) of the rpoB gene. Three rpoB mutations were identified in 90 RIF-susceptible isolates. Out of 105 isolates, 86 (81.90 %) were cross-resistant to both RIF and RFB. The most frequent mutation occurred at codons 450 and 445. We also found a novel nine-nucleotide (ATCATGCAT) deletion (between positions 1543 and 1551) in the rpoB gene in two strains (1.90 %) with resistance to RIF, but susceptibility to RFB. In addition, the mutation frequency at codon 450 was significantly higher in RIF-resistant/RFB-resistant (RIFR/RFBR) strains than in RIFR/RFBS strains (75.58 % versus 21.05 %, PR/RFBR strains than in RIFR/RFBS strains (1.16 % versus 26.32 %, P Conclusion. Our data support previous findings, which reported that various rpoB mutations are associated with differential levels of RIF resistance. The specific mutations in the rpoB gene in RIFR/RFBR isolates differed from those in the RIFR/RFBS isolates. A novel deletion mutation in the RRDR might be associated with resistance to RIF, but not to RFB. Further clinical studies are required to investigate the efficacy of RFB in the treatment of infections caused by M. tuberculosis strains harbouring these mutations.