Single-nucleotide polymorphisms in a vancomycin-resistant Staphylococcus aureus strain based on whole-genome sequencing
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ORIGINAL PAPER
Single‑nucleotide polymorphisms in a vancomycin‑resistant Staphylococcus aureus strain based on whole‑genome sequencing Jung Wook Kim1 · Kwang Jun Lee1 Received: 21 October 2019 / Revised: 2 February 2020 / Accepted: 11 May 2020 © The Author(s) 2020
Abstract The emergence of vancomycin-resistant Staphylococcus aureus (VRSA) threatens global health. The mechanism of vancomycin resistance of VRSA without vanA gene acquisition was not fully elucidated. Therefore, we aimed to determine the mechanism of vancomycin resistance of VRSA besides that by vanA gene acquisition. In this study, we obtained vancomycinresistant strains (V036-V64; MIC = 64 µg /ml) from susceptible strain (V036; MIC = 0.5 µg /ml) by exposure of vancomycin in vitro and examined the phenotypic characteristics and antibiotic susceptibility profiles of the resistant strain (V036-V64). To identify the genetic variations caused vancomycin resistance, we determined the complete genome sequences of V036 and V036-V64 and analyzed for single-nucleotide polymorphisms (SNPs) between two strains. Morphologically, V036-V64 had a twofold thicker cell wall compared with V036. Linezolid, rifampicin, and ceftaroline had similar MIC ranges against V036-V64 and V036, but V036-V64 showed lower susceptibilities to daptomycin and telavancin. We detected eight singlenucleotide polymorphisms differing between V036-V64 and V036: rimM (G16D), ssaA2 (G128A), rpsK (P60R), rpoB (R917C), walK (T492R), d-alanyl-d-alanine carboxypeptidase (L307I), vraT (A152V), and chromosome segregation ATPase (T440I). This study demonstrates that, under selective pressure, by the accumulation of mutations in genes related to cell wall synthesis, vancomycin-susceptible S. aureus can develop thicker cell walls and, hence, develop high vancomycin resistance. Thus, we highlight a novel vanA-negative mechanism for VRSA emergence. Keywords Staphylococcus aureus · Vancomycin · VRSA
Introduction Methicillin-resistant Staphylococcus aureus (MRSA) is a major cause of nosocomial and community-associated infections throughout the world. MRSA can cause a variety of problems, from skin infections, sepsis, and pneumonia to bloodstream infections. Vancomycin is the main Communicated by Erko Stackebrandt. Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00203-020-01906-y) contains supplementary material, which is available to authorized users. * Kwang Jun Lee [email protected] 1
Division of Antimicrobial Resistance, Center for Infectious Diseases Research, National Institute of Health, Korea Centers for Disease Control and Prevention, Osong Health Technology Administration Complex, 187, Osongsaengmyeong 2‑ro, Osong‑eup, Heungdeok‑gu, Cheongju‑si, Republic of Korea
antimicrobial agent available to treat serious infections with MRSA. However, the intensive use of vancomycin over the years in healthcare premises has led to the development of strains with reduced vancomycin susceptibility. Staphylococcus aureus strains with reduced vancomycin
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