Evidence map›Paper›PMID 17923494›Full record

ArticleAntimicrobial agents and chemotherapy2007

Genetic and phenotypic identification of fusidic acid-resistant mutants with the small-colony-variant phenotype in Staphylococcus aureus.

Tobias Norström, Jonas Lannergård, Diarmaid Hughes

Abstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

65 citing papers in PubMed, 108 citations in OpenAlex.

  1. Cryptotanshinone inhibitsVirulence · 2026
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  2. Elongation Factor-G (Antibiotics (Basel, Switzerland) · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Multidrug-ResistantAntibiotics (Basel, Switzerland) · 2025
    Article
  7. Mechanisms of fusidic acid resistance.Biochemical Society transactions · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Profiles of Non-Food science of animal resources · 2022
    Article
  16. The road to success of coagulase-negative staphylococci: clinical significance of small colony variants and their pathogenic role in persistent infections.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2021
    Review
  17. Article
  18. Evaluating the potential efficacy and limitations of a phage for joint antibiotic and phage therapy ofProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  19. Article
  20. Article

5 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Tobias NorströmProgramme for Microbiology, Department of Cell and Molecular Biology, Box 596, Biomedical Center, Uppsala University, Uppsala, Sweden.
Jonas Lannergård
Diarmaid Hughes
Uppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small-colony variants (SCVs) of Staphylococcus aureus are a slow-growing subpopulation whose phenotypes can include resistance to aminoglycosides, defects in electron transport, and enhanced persistence in mammalian cells. Here we show that a subset of mutants selected as SCVs by reduced susceptibility to aminoglycosides are resistant to the antibiotic fusidic acid (FA) and conversely that a subset of mutants selected for resistance to FA are SCVs. Mutation analysis reveals different genetic classes of FA-resistant SCVs. One class, FusA-SCVs, have amino acid substitution mutations in the ribosomal translocase EF-G different from those found in classic FusA mutants. Most of these mutations are located in structural domain V of EF-G, but some are in domain I or III. FusA-SCVs are auxotrophic for hemin. A second class of FA-resistant SCVs carry mutations in rplF, coding for ribosomal protein L6, and are designated as FusE mutants. FusE mutants fall into two phenotypic groups: one auxotrophic for hemin and the other auxotrophic for menadione. Accordingly, we have identified new genetic and phenotypic classes of FA-resistant mutants and clarified the genetic basis of a subset of S. aureus SCV mutants. A clinical implication of these data is that FA resistance could be selected by antimicrobial agents other than FA.

Indexed as

MutationAmino Acid SubstitutionAminoglycosidesAnti-Bacterial AgentsBacterial ProteinsDrug Resistance, BacterialFusidic AcidHeminMicrobial Sensitivity TestsPeptide Elongation Factor GPhenotypePolymerase Chain ReactionRibosomal ProteinsStaphylococcus aureusVitamin K 3VitaminsAminoglycosidesAnti-Bacterial AgentsBacterial ProteinsFusA protein, Staphylococcus aureusFusidic AcidHeminPeptide Elongation Factor Gribosomal protein L6Ribosomal ProteinsVitamin K 3Vitamins

Identifiers

PMID17923494
PMCPMC2168011
OpenAlexW2118977328

What OpenQuestion holds

Textmetadata
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.