ArticleThe Journal of antimicrobial chemotherapy2023
Resistance to antibacterial antifolates in multidrug-resistant Staphylococcus aureus: prevalence estimates and genetic basis.
Article in The Journal of antimicrobial chemotherapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Breaking resistance: strategies for novel antibacterial therapeutic interventions.Molecular biology reports · 2026Review
- Endophytic fungi as a source of antimicrobial compounds against emerging methicillin-resistantMycology · 2026Review
- Fecal Carriage of Multidrug-ResistantBioMed research international · 2025Article
- Microbial profile and antimicrobial resistance patterns of ocular infection pre/during and post the COVID-19 pandemic.Frontiers in medicine · 2025Article
- Displacement of Hospital-Acquired, Methicillin-ResistantMicroorganisms · 2024Article
- Staph wars: the antibiotic pipeline strikes back.Microbiology (Reading, England) · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectivesAntibacterial antifolate drugs might have a wider role in the management of staphylococcal infection. One factor that could potentially limit their use in this context is pre-existing resistance. Here we explored the prevalence and genetic basis for resistance to these drugs in a large collection (n = 1470) of multidrug-resistant (MDR) Staphylococcus aureus.
methodsStrains were subjected to susceptibility testing to detect resistance to trimethoprim, sulfamethoxazole, co-trimoxazole and the investigational drug, iclaprim. Whole-genome sequences were interrogated to establish the genetic basis for resistance.
resultsAccording to CLSI breakpoints, 15.2% of the strains were resistant to trimethoprim, 5.2% to sulfamethoxazole and 4.1% to co-trimoxazole. Using the proposed breakpoint for iclaprim, 89% of the trimethoprim-resistant strains exhibited non-susceptibility to this agent. Sulfamethozaxole resistance was exclusively the result of mutation in the drug target (dihydropteroate synthase). Resistance to trimethoprim and iclaprim also resulted from mutation in the target (dihydrofolate reductase; DHFR) but was more commonly associated with horizontal acquisition of genes encoding drug-insensitive DHFR proteins. Among the latter, we identified a novel gene (dfrL) encoding a DHFR with ∼35% identity to native and known resistant DHFRs, which was confirmed via molecular cloning to mediate high-level resistance.
conclusionsThis study provides a detailed picture of the genotypes underlying staphylococcal resistance to antifolate drugs in clinical use and in development. Prevalence estimates suggest that resistance to the diaminopyrimidines (trimethoprim/iclaprim) is not uncommon among MDR S. aureus, and considerably higher than observed for sulfamethoxazole or co-trimoxazole.
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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.