Genetic alterations responsible for reduced susceptibility to vancomycin in community-associated MRSA strains of ST72
- Authors
- Baek, Jin Yang; Chung, Doo Ryeon; Ko, Kwan Soo; Kim, So Hyun; Yang, Soo-Jin; Kang, Cheol-In; Peck, Kyong Ran; Song, Jae-Hoon
- Issue Date
- Sep-2017
- Publisher
- OXFORD UNIV PRESS
- Citation
- JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY, v.72, no.9, pp 2454 - 2460
- Pages
- 7
- Journal Title
- JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY
- Volume
- 72
- Number
- 9
- Start Page
- 2454
- End Page
- 2460
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/3978
- DOI
- 10.1093/jac/dkx175
- ISSN
- 0305-7453
1460-2091
- Abstract
- Objectives: We previously reported the first case of vancomycin treatment failure due to development of vancomycin-intermediate resistance in a patient with an MRSA of ST72, a community genotype in Korea. We investigated two isogenic MRSA strains from this patient, who experienced treatment failure with vancomycin and rifampicin. Methods: We tracked the genetic alterations that confer reduced susceptibility to vancomycin on those two isogenic MRSA strains by WGS. Results: Five non-synonymous mutations were identified, including rpoB (H481Y), dprA (G196C), femA (F92C), vraR (E127K) and agrC (E391stop). We further studied the role of a mutation of vraR in reduced susceptibility to vancomycin. Introduction of the mutated vraR (E127K) into a vancomycin-susceptible Staphylococcus aureus strain resulted in an increase in vraSR mRNA expression and vancomycin MIC and development of the heteroVISA phenotype, which was confirmed by the population analysis profile (PAP)/AUC. Electron microscopy showed increased cell wall thickness in the strains with mutated vraR. Conclusions: Based on the genomic data, molecular experiments and PAP and cell wall analyses, we propose that a single mutation of vraR is associated with the reduced susceptibility to vancomycin in MRSA and further treatment failure.
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