Evidence map›Paper›PMID 16940100›Full record

ArticleAntimicrobial agents and chemotherapy2006

Isolates with low-level vancomycin resistance associated with persistent methicillin-resistant Staphylococcus aureus bacteremia.

Benjamin P Howden, Paul D R Johnson, Peter B Ward, Timothy P Stinear, John K Davies

Abstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed
–field-weighted citation impact
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

103 citing papers in PubMed.

  1. Vancomycin pharmacokinetics and pharmacodynamics during short daily hemodialysis.Clinical journal of the American Society of Nephrology : CJASN · 2010
    Trial
  2. Trial
  3. Frontiers in pharmacology · 2026
    Article
  4. Article
  5. Article
  6. Antibiotics (Basel, Switzerland) · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Persistent Methicillin-ResistantAntibiotics (Basel, Switzerland) · 2023
    Review
  12. Article
  13. Article
  14. Knockout ofJournal of bacteriology · 2022
    Article
  15. Adaptive laboratory evolution and independent component analysis disentangle complex vancomycin adaptation trajectories.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Antimicrobial agents and chemotherapy · 2022
    Observational

43 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

5 authors.

Benjamin P HowdenDepartment of Microbiology, Monash University, Clayton, 3800 Victoria, Australia. Ben.Howden@med.monash.edu.au
Paul D R Johnson
Peter B Ward
Timothy P Stinear
John K Davies

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Low-level vancomycin-resistant Staphylococcus aureus (vancomycin-intermediate S. aureus [VISA] and heterogenous VISA [hVISA]) is increasingly reported and leads to glycopeptide treatment failure. Various phenotypic features have been reported for these isolates, but the genetic changes leading to hVISA and VISA have yet to be clearly determined. We assessed phenotypic, antibiotic resistance, and genomic changes by using genomic DNA microarray comparison and sequencing of selected loci in five pairs of clinical hVISA/VISA strains and the initial methicillin-resistant Staphylococcus aureus (MRSA) isolates obtained prior to vancomycin therapy. The isolates were from adult patients in Australia and New Zealand who had persistent MRSA bacteremia (>7 days) while receiving vancomycin therapy. In all cases, the initial isolates were found to be fully vancomycin-susceptible Staphylococcus aureus (VSSA). The hVISA/VISA phenotype was associated with increased cell wall thickness, reduced autolytic activity in four of five hVISA/VISA strains, and a striking reduction in biofilm formation compared to the parent strains in all pairs. All five pairs appeared to be isogenic, and genomic DNA microarray comparison suggested that major genetic changes are not required for the development of the resistant phenotype in these strains. No sequence differences were found in the agr locus or the tcaRA genes for any pair, but a marked reduction in RNAIII expression was found in four pairs. In summary, hVISA/VISA arises from fully VSSA during persistent infection that fails to respond to glycopeptide therapy and is associated with significant phenotypic changes, including a marked reduction in biofilm-forming ability. These clinically derived pairs of isolates will be a useful resource to elucidate the genetic mechanism of resistance in hVISA/VISA strains.

Indexed as

Methicillin ResistanceVancomycin ResistanceBacteremiaBacterial ProteinsBiofilmsDNA, BacterialElectrophoresis, Gel, Pulsed-FieldHumansMicroarray AnalysisMicrobial Sensitivity TestsMicroscopy, ElectronRNA, MessengerStaphylococcus aureusTrans-ActivatorsAgr protein, Staphylococcus aureusBacterial ProteinsDNA, BacterialRNA, MessengerTrans-Activators

Identifiers

PMID16940100
PMCPMC1563555

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.