ArticleAntimicrobial agents and chemotherapy2009
VanA-type Staphylococcus aureus strain VRSA-7 is partially dependent on vancomycin for growth.
Article in Antimicrobial agents and chemotherapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Vancomycin-resistant Staphylococcus aureus (VRSA) can overcome the cost of antibiotic resistance and may threaten vancomycin's clinical durability.PLoS pathogens · 2024Article
- Fierce poison to others: the phenomenon of bacterial dependence on antibiotics.Journal of biomedical science · 2023Review
- Roles of the Site 2 Protease Eep in Staphylococcus aureus.Journal of bacteriology · 2020Article
- Cationic antimicrobial peptides: alternatives and/or adjuvants to antibiotics active against methicillin-resistant Staphylococcus aureus and multidrug-resistant Pseudomonas aeruginosa.BMC microbiology · 2019Article
- Linezolid dependence in Staphylococcus epidermidis bloodstream isolates.Emerging infectious diseases · 2013Article
- Structural and functional characterization of VanG D-Ala:D-Ser ligase associated with vancomycin resistance in Enterococcus faecalis.The Journal of biological chemistry · 2012Article
- Staphylococcus aureus VRSA-11B is a constitutive vancomycin-resistant mutant of vancomycin-dependent VRSA-11A.Antimicrobial agents and chemotherapy · 2012Article
- Acquired inducible antimicrobial resistance in Gram-positive bacteria.Future microbiology · 2012Review
- Molecular basis of vancomycin dependence in VanA-type Staphylococcus aureus VRSA-9.Journal of bacteriology · 2010Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
VanA-type Staphylococcus aureus strain VRSA-7 was partially dependent on glycopeptides for growth. The vanA gene cluster, together with the erm(A) and the ant(9)-Ia resistance genes, was carried by the ca. 35- to 40-kb conjugative plasmid pIP848 present at five copies per cell. The chromosomal ddl gene had a mutation that led to a N308K substitution in the d-Ala:d-Ala ligase that resulted in a 1,000-fold decrease in activity relative to that of strain VRSA-6. Strain VRSA-7 grown in the absence or in the presence of vancomycin mainly synthesized precursors ending in d-Ala-d-Lac, indicating that the strain relied on the vancomycin resistance pathway for peptidoglycan synthesis. Greatly enhanced growth in the presence of glycopeptides and the absence of mutations in the genes for VanR and VanS indicated the inducible expression of resistance. Thus, a combination of loose regulation of the vanA operon by the two-component system and a gene dosage effect accounts for the partial glycopeptide dependence of VRSA-7. Since peptidoglycan precursors ending in D-Ala-D-Lac are not processed by PBP 2', the strain was fully susceptible to oxacillin, despite the production of a wild-type PBP 2'.
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