ReviewArchives of microbiology2026
Vancomycin resistance in gram-positive infections: evolutionary strategies of survival.
Review in Archives of microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- Non-Cytotoxic Benzyl Triphenyl Phosphonium Bromide Is Bactericidal on MRSA and Fully Inhibits Biofilm Formation by MRSA and MRSE.Pharmaceuticals (Basel, Switzerland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vancomycin is a critical glycopeptide antibiotic for treating severe infections caused by Gram-positive bacteria, particularly MRSA and Clostridioides difficile, by inhibiting cell wall synthesis through binding to D-Ala-D-Ala termini of peptidoglycan precursors. Resistance has emerged in Enterococcus spp (VRE) and Staphylococcus spp, (VISA/VRSA) through acquisition of van operons, precursor modification (D-Ala-D-Lac/D-Ser), cell wall thickening, biofilm formation, and regulatory mutations, leading to treatment failures and increased morbidity. Global genomic surveillance reveals ongoing clonal expansion and horizontal spread of resistance determinants. This review comprehensively examines vancomycin's mechanism of action, the evolutionary emergence and genetic basis of resistance, adaptive survival strategies of pathogens, clinical/epidemiological consequences, current alternative therapies, and precision stewardship approaches including area under the concentration-time curve/minimum inhibitory concentration (AUC/MIC)-guided therapeutic drug monitoring (TDM). Most importantly, it highlights the transformative and still under-appreciated role of artificial intelligence in overcoming vancomycin resistance: machine learning accelerates discovery of novel antimicrobial peptides and repurposed drugs, AI-driven surveillance enables real-time resistance detection and outbreak forecasting, and hybrid AI-molecular modeling rationally designs superior vancomycin derivatives with enhanced activity against VRE and VRSA. These rapidly evolving AI-integrated strategies, when combined with strengthened infection control and stewardship, offer the most promising path forward to preserve and extend the clinical utility of vancomycin and related antibiotics.
Indexed as
Identifiers
41563485What OpenQuestion holds
Registered trials
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.