Evidence map›Paper›PMID 20498310›Full record

ArticleAntimicrobial agents and chemotherapy2010

Cell wall thickening is not a universal accompaniment of the daptomycin nonsusceptibility phenotype in Staphylococcus aureus: evidence for multiple resistance mechanisms.

Soo-Jin Yang, Cynthia C Nast, Nagendra N Mishra, Michael R Yeaman, Paul D Fey, Arnold S Bayer

Abstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

77 citing papers in PubMed, 116 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. DefectivemSphere · 2024
    Article
  5. Article
  6. Genomic Insights intoPathogens (Basel, Switzerland) · 2024
    Article
  7. Article
  8. Phenotypic and genetic characterization of daptomycin non-susceptibleFrontiers in cellular and infection microbiology · 2024
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. The Role ofAntimicrobial agents and chemotherapy · 2022
    Article
  16. Article
  17. Article
  18. Bacterial Targets of Antibiotics in Methicillin-ResistantAntibiotics (Basel, Switzerland) · 2021
    Review
  19. Article
  20. Article

17 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

6 authors at 4 institutions in 1 country.

Soo-Jin YangLos Angeles Biomedical Research Institute, Torrance, California 90502, USA. sjyang@labiomed.org
Cynthia C Nast
Nagendra N Mishra
Michael R Yeaman
Paul D Fey
Arnold S Bayer
The Lundquist Institute · USCedars-Sinai Medical Center · USUniversity of California, Los Angeles · USUniversity of Nebraska Medical Center · US

Funding

Staphylococcal Adaptations to Platelet Microbicidal ProteinR01AI039108 · NIAID · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI BAYER, ARNOLD S · 1997 to 2016
$5.1M
Microbicidal Proteins from PlateletsR01AI039001 · NIAID · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI YEAMAN, MICHAEL R · 2006 to 2010
$1.7M
MICROBICIDAL PROTEINS FROM PLATELETSR29AI039001 · NIAID · LA BIOMED RES INST/ HARBOR UCLA MED CTR · PI YEAMAN, MICHAEL R · 1996 to 2000
$99k
NIAID NIH HHS AI39001NIAID NIH HHS AI39018NIAID NIH HHS R01 AI039001NIAID NIH HHS R01 AI039108NIAID NIH HHS R29 AI039001
6 · The paper itself

Abstract

The mechanism(s) of daptomycin (DAP) resistance (DAPr) is incompletely defined. Thickened cell walls (CWs) acting as either a mechanical barrier or an affinity trap for DAP have been purported to be a major contributor to the DAPr phenotype. To this end, we studied an isogenic set of methicillin-resistant Staphylococcus aureus (MRSA) isolates (pulsotype USA 300) from the bloodstream of a DAP-treated patient with endocarditis in which serial strains exhibited increasing DAPr. Of interest, the DAPr isolate differed from its parental strain in several parameters, including acquisition of a point mutation within the putative synthase domain of the mprF gene in association with enhanced mprF expression, increased synthesis of lysyl-phosphotidylglycerol, an enhanced positive envelope charge, and reduced DAP surface binding. Transmission electron microscopy (TEM) revealed no significant increases in CW thickness in the two DAPr isolates (MRSA 11/21 and REF2145) compared with that in the DAP-susceptible (DAPs) parental strain, MRSA 11/11. The rates of Triton X-100-induced autolysis were also identical for the strain set. Furthermore, among six additional clinically isolated DAPs/DAPr S. aureus strain pairs, only three DAPr isolates exhibited CWs significantly thicker than those of the respective DAPs parent. These data confirm that CW thickening is neither universal to DAPr S. aureus nor sufficient to yield the DAPr phenotype among S. aureus strains.

Indexed as

Drug Resistance, Multiple, BacterialAminoacyltransferasesAnti-Bacterial AgentsBacterial ProteinsBloodCell WallDaptomycinEndocarditis, BacterialHumansMethicillin-Resistant Staphylococcus aureusMicrobial Sensitivity TestsMicroscopy, Electron, TransmissionMutationOctoxynolPhenotypeStaphylococcal InfectionsAminoacyltransferasesAnti-Bacterial AgentsBacterial ProteinsDaptomycinmprF protein, Staphylococcus aureusOctoxynol

Identifiers

PMID20498310
PMCPMC2916340
OpenAlexW2118611827

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.