ArticleAntimicrobial agents and chemotherapy2008
Identification of the genetic basis for clinical menadione-auxotrophic small-colony variant isolates of Staphylococcus aureus.
Article in Antimicrobial agents and chemotherapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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64 citing papers in PubMed.
- Biological characteristics of a menadione-dependent Staphylococcus aureus small colony variant (SCV) from bovine mastitis and heme promotion of biofilm formation.Archives of microbiology · 2026Article
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- Small-colony variants of Staphylococcus aureus: hidden threat in chronic and recurrent infections.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Resisting the resistance: the antimicrobial peptide DGL13K selects for small colony variants ofJournal of bacteriology · 2025Article
- Detection, Identification and Diagnostic Characterization of the Staphylococcal Small Colony-Variant (SCV) Phenotype.Antibiotics (Basel, Switzerland) · 2023Review
- High-level in vitro resistance to gentamicin acquired in a stepwise manner in Neisseria gonorrhoeae.The Journal of antimicrobial chemotherapy · 2023Article
- Subpopulations in Strains ofAntibiotics (Basel, Switzerland) · 2023Review
- Acute Infection with a Tobramycin-Induced Small Colony Variant of Staphylococcus aureus Causes Increased Inflammation in the Cystic Fibrosis Rat Lung.Infection and immunity · 2022Article
- FunctionalJournal of bacteriology · 2022Article
- Identification of structurally diverse menaquinone-binding antibiotics with in vivo activity against multidrug-resistant pathogens.Nature microbiology · 2022Article
- Microbial Musings - November 2021.Microbiology (Reading, England) · 2022Article
- A functional menadione biosynthesis pathway is required for capsule production byMicrobiology (Reading, England) · 2021Article
- Extracellular DNA released by glycine-auxotrophic Staphylococcus epidermidis small colony variant facilitates catheter-related infections.Communications biology · 2021Article
- Virulence alterations in staphylococcus aureus upon treatment with the sub-inhibitory concentrations of antibiotics.Journal of advanced research · 2021Review
- Inactivation of genes in oxidative respiration and iron acquisition pathways in pediatric clinical isolates of Small colony variant Enterobacteriaceae.Scientific reports · 2021Article
- Designer broad-spectrum polyimidazolium antibiotics.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Controlling the Growth of the Skin Commensal Staphylococcus epidermidis Using d-Alanine Auxotrophy.mSphere · 2020Article
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- Novel Research Models forFrontiers in microbiology · 2020Review
- Proteomic and Metabolomic Analyses of a Tea-Tree Oil-SelectedAntibiotics (Basel, Switzerland) · 2019Article
4 more citing papers are in PubMed but not listed here.
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Abstract
Small-colony variants (SCVs) of Staphylococcus aureus are associated with persistent infections and may be selectively enriched during antibiotic therapy. Three pairs of clonally related S. aureus isolates were recovered from patients receiving systemic antibiotic therapy. Each pair consisted of an isolate with a normal phenotype and an isolate with an SCV phenotype. These SCVs were characterized by reduced susceptibility to gentamicin, reduced hemolytic activity, slow growth, and menadione auxotrophy. Sequencing of the genes involved in menadione biosynthesis revealed mutations in menB, the gene encoding naphthoate synthase, in all three strains with the SCV phenotype. The menB mutations were (i) a 9-bp deletion from nucleotides 55 to 63, (ii) a frameshift mutation that resulted in a premature stop codon at position 230, and (iii) a point mutation that caused the amino acid substitution Gly to Val at codon 233. Fluctuation tests showed that growth-compensated mutants arose in the SCV population of one strain, strain OM1b, at a rate of 1.8 x 10(-8) per cell per generation. Sequence analyses of 23 independently isolated growth-compensated mutants of this strain revealed alterations in the menB sequence in every case. These alterations included reversions to the wild-type sequence and intragenic second-site mutations. Each of the growth-compensated mutants showed a restoration of normal growth and a loss of menadione auxotrophy, increased susceptibility to gentamicin, and restored hemolytic activity. These data show that mutations in menB cause the SCV phenotype in these clinical isolates. This is the first report on the genetic basis of menadione-auxotrophic SCVs determined in clinical S. aureus isolates.
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