Evidence map›Paper›PMID 28120911›Full record

ArticleScientific reports2017

A potential role of transposon IS431 in the loss of mecA gene.

Aihua Wang, Kai Zhou, Yang Liu, Liang Yang, Qin Zhang, Jing Guan, Nanshan Zhong, Chao Zhuo

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Characterization of SCCAntimicrobial agents and chemotherapy · 2022
    Article
  3. How to survive pig farming: Mechanism of SCCFrontiers in microbiology · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. 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

8 authors at 4 institutions in 2 countries.

Aihua WangState Key Laboratory of Respiratory Diseases, the first affiliated hospital of Guangzhou Medical College, Guangzhou, China.
Kai ZhouState Key Laboratory for Diagnosis and Treatment of Infectious Diseases; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, the First Affiliated Hospital of Medicine School, Zhejiang University, Hangzhou, China.
Yang LiuNational University of Singapore, Singapore.
Liang YangNational University of Singapore, Singapore.
Qin ZhangDaxian people's hospital, Dazhou, China.
Jing GuanState Key Laboratory of Respiratory Diseases, the first affiliated hospital of Guangzhou Medical College, Guangzhou, China.
Nanshan ZhongState Key Laboratory of Respiratory Diseases, the first affiliated hospital of Guangzhou Medical College, Guangzhou, China.
Chao ZhuoState Key Laboratory of Respiratory Diseases, the first affiliated hospital of Guangzhou Medical College, Guangzhou, China.
Guangzhou Medical University · CNNational University of Singapore · SGState Key Laboratory of Diagnosis and Treatment of Infectious DiseasesState Key Laboratory of Respiratory Disease · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acquisition of a vancomycin-resistance-determinant may trigger deletion of the mecA gene. However, the molecular mechanisms involved remain largely unknown. In this study, we successfully produced vancomycin-intermediate-resistant Staphylococcus aureus (VISA) from Methicillin-resistant-S. aureus (MRSA) through serial passages with vancomycin. Five MRSA isolates achieved a vancomycin MIC of >8 mg/ml after 45-day serial exposure to vancomycin. After 20-day passages in media without antibiotics, three of the isolates were restored to pre-induction levels, whilst the remaining 2 (3503-1 and 4126-1) retained a vancomycin MIC >6 mg/ml. The oxacillin MICs for strain 3503-1 and its induced equivalents 3503VR6 and 3503VR10, were 512 μg/ml, <2 μg/ml, and <2 μg/ml, respectively. Oxacillin MICs for 4126-1 and its induced strain 4126VR10 were 512 μg/ml and 128 μg/ml, respectively. Strains 3503-1 and 3503VR6 were sensitive to gentamicin while 4126-1 and 4126VR10 were resistant. PFGE analysis demonstrated that comparing to the parental strain 3503VR6 and 3503VR10 lacked a DNA fragment of 40-kb and 80-kb, respectively. Both deleted regions localized around the transposon IS431. The deletion region of 3503VR10 was further investigated by whole-genome sequencing. We conclude that transition from MRSA to VISA may cause deletion of the mobile genetic element staphylococcal cassette chromosome mec (SCCmec), and possibly be mediated by IS431, resulting in increased susceptibility to oxacillin.

Indexed as

Genes, BacterialChromosomes, BacterialColony Count, MicrobialDNA, BacterialDNA Transposable ElementsElectrophoresis, Gel, Pulsed-FieldMethicillin-Resistant Staphylococcus aureusPolymorphism, Single NucleotideReproducibility of ResultsRNA, Ribosomal, 16SSequence DeletionSyntenyVancomycinVancomycin ResistanceDNA, BacterialDNA Transposable ElementsRNA, Ribosomal, 16SVancomycin

Identifiers

PMID28120911
PMCPMC5264636
OpenAlexW2580249216

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.