Evidence map›Paper›PMID 32535788›Full record

ArticleArchives of microbiology2020

Single-nucleotide polymorphisms in a vancomycin-resistant Staphylococcus aureus strain based on whole-genome sequencing.

Jung Wook Kim, Kwang Jun Lee

Open access · hybridAbstract read
In one paragraph

Article in Archives of microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.2field-weighted citation impact, top 33% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Molecular Mechanisms of Drug Resistance inInternational journal of molecular sciences · 2022
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Characterization of an osteomyelitis case caused by dalbavancin, ceftaroline, and vancomycin non-susceptible methicillin-resistant Staphylococcus aureus.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2021
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Jung Wook KimDivision 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.
Kwang Jun LeeDivision 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. kwangjun@korea.kr.ORCID http://orcid.org/0000-0002-7831-5905
Korea National Institute of Health · KR

Funding

Korea Centers for Disease Control and Prevention 2016-NI44001-00
6 · The paper itself

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 vancomycin-resistant 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 single-nucleotide 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.

Indexed as

Polymorphism, Single NucleotideWhole Genome SequencingAnti-Bacterial AgentsCell WallHumansMicrobial Sensitivity TestsStaphylococcus aureusVancomycinVancomycin ResistanceAnti-Bacterial AgentsVancomycinStaphylococcus aureusVancomycinVRSA

Identifiers

PMID32535788
PMCPMC7455577
OpenAlexW3034526677

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.