ArticleAntimicrobial agents and chemotherapy2015
Characterization of high-level daptomycin resistance in Viridans group Streptococci developed upon in vitro exposure to daptomycin.
Article in Antimicrobial agents and chemotherapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Daptomycin forms a stable complex with phosphatidylglycerol for selective uptake to bacterial membrane.eLife · 2025Article
- Biosynthesis of mitis group streptococcal glycolipids and their roles in physiology and antibiotic susceptibility.bioRxiv : the preprint server for biology · 2024Article
- Antibiotic Resistance to Molecules Commonly Prescribed for the Treatment of Antibiotic-Resistant Gram-Positive Pathogens: What Is Relevant for the Clinician?Pathogens (Basel, Switzerland) · 2024Review
- Membrane Phenotypic, Metabolic and Genotypic Adaptations ofAntibiotics (Basel, Switzerland) · 2023Article
- Article
- Bacterial cell membranes and their role in daptomycin resistance: A review.Frontiers in molecular biosciences · 2022Review
- Development of High-Level Daptomycin Resistance inAntimicrobial agents and chemotherapy · 2021Article
- Evaluating the Rapid Emergence of Daptomycin Resistance inJournal of clinical microbiology · 2021Article
- Streptococcus pneumoniae, S. mitis, and S. oralis Produce a Phosphatidylglycerol-Dependent,mSphere · 2021Article
- Phosphatidylcholine Biosynthesis in Mitis Group Streptococci via Host Metabolite Scavenging.Journal of bacteriology · 2019Article
- Daptomycin Dose-Ranging Evaluation with Single-Dose versus Multidose Ceftriaxone Combinations against Streptococcus mitisAntimicrobial agents and chemotherapy · 2019Article
- Mechanism of High-Level Daptomycin Resistance inmSphere · 2018Article
- Mitochondria-targeted antioxidants as highly effective antibiotics.Scientific reports · 2017Article
- Impact of High-Level Daptomycin Resistance in the Streptococcus mitis Group on Virulence and Survivability during Daptomycin Treatment in Experimental Infective Endocarditis.Antimicrobial agents and chemotherapy · 2017Article
- Streptococcus mitis and S. oralis Lack a Requirement for CdsA, the Enzyme Required for Synthesis of Major Membrane Phospholipids in Bacteria.Antimicrobial agents and chemotherapy · 2017Article
- Perturbations of Phosphatidate Cytidylyltransferase (CdsA) Mediate Daptomycin Resistance in Streptococcus mitis/oralis by a Novel Mechanism.Antimicrobial agents and chemotherapy · 2017Article
- Evolving resistance among Gram-positive pathogens.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2015Review
- Mechanisms of drug resistance: daptomycin resistance.Annals of the New York Academy of Sciences · 2015Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viridans group streptococci (VGS) are part of the normal flora that may cause bacteremia, often leading to endocarditis. We evaluated daptomycin against four clinical strains of VGS (MICs = 1 or 2 μg/ml) using an in vitro-simulated endocardial vegetation model, a simulated bacteremia model, and kill curves. Daptomycin exposure was simulated at 6 mg/kg of body weight and 8 mg/kg every 24 h for endocardial and bacteremia models. Total drug concentrations were used for analyses containing protein (albumin and pooled human serum), and free (unbound) drug concentrations (93% protein bound) were used for analyses not containing protein. Daptomycin MICs in the presence of protein were significantly higher than those in the absence of protein. Despite MICs below or at the susceptible breakpoint, all daptomycin regimens demonstrated limited kill in both pharmacodynamic models. A reduction of approximately 1 to 2 log10 CFU was seen for all isolates and dosages except daptomycin at 6 mg/kg, which achieved a reduction of 2.7 log10 CFU/g against one strain (Streptococcus gordonii 1649) in the endocardial model. Activity was similar in both pharmacodynamic models in the presence or absence of protein. Similar activity was noted in the kill curves over all multiples of the MIC. Regrowth by 24 h was seen even at 8× MIC. Postexposure daptomycin MICs for both pharmacodynamic models increased to >256 μg/ml for all isolates by 24 and 72 h. Despite susceptibility to daptomycin by standard MIC methods, these VGS developed high-level daptomycin resistance (HLDR) after a short duration following drug exposure not attributed to modification or inactivation of daptomycin. Further evaluation is warranted to determine the mechanism of resistance and clinical implications.
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