ArticleBMC microbiology2013
Staphylococcus aureus but not Listeria monocytogenes adapt to triclosan and adaptation correlates with increased fabI expression and agr deficiency.
Article in BMC microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Treatment ofAntimicrobial agents and chemotherapy · 2025Article
- Reviewing the complexities of bacterial biocide susceptibility and in vitro biocide adaptation methodologies.npj antimicrobials and resistance · 2025Review
- Effect of povidone-iodine and propanol-based mecetronium ethyl sulphate on antimicrobial resistance and virulence in Staphylococcus aureus.Antimicrobial resistance and infection control · 2022Article
- Reduced Susceptibility and Increased Resistance of Bacteria against Disinfectants: A Systematic Review.Microorganisms · 2021Review
- Nonactive-Site Mutations inACS omega · 2020Article
- Antimicrobial Resistance inMicrobiology spectrum · 2018Review
- Fatty Acid Supplementation Reverses the Small Colony Variant Phenotype in Triclosan-Adapted Staphylococcus aureus: Genetic, Proteomic and Phenotypic Analyses.Scientific reports · 2018Article
- Clinical Relevance of Type II Fatty Acid Synthesis Bypass in Staphylococcus aureus.Antimicrobial agents and chemotherapy · 2017Article
- Importance of sigma factor mutations in increased triclosan resistance in Salmonella Typhimurium.BMC microbiology · 2015Article
- Mutations upstream of fabI in triclosan resistant Staphylococcus aureus strains are associated with elevated fabI gene expression.BMC genomics · 2015Article
- Triclosan-induced aminoglycoside-tolerant Listeria monocytogenes isolates can appear as small-colony variants.Antimicrobial agents and chemotherapy · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe ability of pathogens to adapt to the widely used biocide, triclosan, varies substantially. The purpose of the study was to examine bacterial adaptation over an extended period of time to low increments of triclosan concentrations. Focus was two human pathogens, S. aureus and L. monocytogenes that previously have displayed inherent high and low adaptability, respectively.
resultsThree strains of L. monocytogenes and two strains of S. aureus including the community-acquired USA300 were exposed to increasing, sub-lethal concentrations of triclosan in triclosan-containing agar gradients. Following 25 days of exposure on agar plates to sub-lethal concentrations of triclosan with a twofold concentration increase every second day, minimum inhibitory concentration (MIC) for S. aureus increased from 0.125 (8325-4) and 0.0625 (USA 300) mg/L to 4 mg/L. The MIC of all three L. monocytogenes strains was initially 4 mg/L and remained unaltered by the exposure. The adapted S. aureus isolates retained normal colony size but displayed increased expression of fabI encoding an essential enzyme in bacterial fatty acid synthesis. Also, they displayed decreased or no expression of the virulence associated agrC of the agr quorum sensing system. While most adapted strains of USA300 carried mutations in fabI, none of the adapted strains of 8325-4 did.
conclusionsAdaptability to triclosan varies substantially between Gram positive human pathogens. S. aureus displayed an intrinsically lower MIC for triclosan compared to L. monocytogenes but was easily adapted leading to the same MIC as L. monocytogenes. Even though all adapted S. aureus strains over-expressed fabI and eliminated expression of the agr quorum sensing system, adaptation in USA300 involved fabI mutations whereas this was not the case for 8325-4. Thus, adaptation to triclosan by S. aureus appears to involve multiple genetic pathways.
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