Daptomycin: A novel cyclic lipopeptide antimicrobial

Schriever, Christopher A.; Fernández, Cristina; Rodvold, Keith A.; Danziger, Larry H.

doi:10.1093/ajhp/62.11.1145

Cited by 73 publications

(33 citation statements)

References 81 publications

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“…Daptomycin ( DAP ) is a calcium-dependent lipopeptide antibiotic with potent bactericidal effects against most Gram-positive pathogens [1], [2]. Since its release for use in 2003 for skin and soft tissue infections, followed by approval for Staphylococcus aureus bacteremia and right-sided endocarditis in 2006, DAP has become a key antibiotic for invasive staphylococcal infections.…”

Section: Introductionmentioning

confidence: 99%

“…Since its release for use in 2003 for skin and soft tissue infections, followed by approval for Staphylococcus aureus bacteremia and right-sided endocarditis in 2006, DAP has become a key antibiotic for invasive staphylococcal infections. This is especially relevant to methicillin-resistant S. aureus ( MRSA ) infections in the era of rising vancomycin MICs associated with clinical treatment failures [3]–[5], as well as vancomycin (VAN)-intermediate S. aureus (VISA)-related infections [2], [5], [6]. Recently, there have been an alarming number of reports of both S. aureus and enterococcal DAP-resistant ( DAP-R ) strains emerging during DAP treatment failures [7]–[12].…”

Section: Introductionmentioning

confidence: 99%

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Phenotypic and Genotypic Characterization of Daptomycin-Resistant Methicillin-Resistant Staphylococcus aureus Strains: Relative Roles of mprF and dlt Operons

et al. 2014

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Development of in vivo daptomycin resistance (DAP-R) among Staphylococcus aureus clinical isolates, in association with clinical treatment failures, has become a major therapeutic problem. This issue is especially relevant to methicillin-resistant S. aureus (MRSA) strains in the context of invasive endovascular infections. In the current study, we used three well-characterized and clinically-derived DAP-susceptible (DAP-S) vs. resistant (DAP-R) MRSA strain-pairs to elucidate potential genotypic mechanisms of the DAP-R phenotype. In comparison to the DAP-S parental strains, DAP-R isolates demonstrated (i) altered expression of two key determinants of net positive surface charge, either during exponential or stationary growth phases (i.e., dysregulation of dltA and mprF), (ii) a significant increase in the D-alanylated wall teichoic acid (WTA) content in DAP-R strains, reflecting DltA gain-in-function; (iii) heightened elaboration of lysinylated-phosphatidylglyderol (L-PG) in DAP-R strains, reflecting MprF gain-in-function; (iv) increased cell membrane (CM) fluidity, and (v) significantly reduced susceptibility to prototypic cationic host defense peptides of platelet and leukocyte origins. In the tested DAP-R strains, genes conferring positive surface charge were dysregulated, and their functionality altered. However, there were no correlations between relative surface positive charge or cell wall thickness and the observed DAP-R phenotype. Thus, charge repulsion mechanisms via altered surface charge may not be sufficient to explain the DAP-R outcome. Instead, changes in the compositional or biophysical order of the DAP CM target of such DAP-R strains (i.e., increased fluidity) may be essential to this phenotype. Taken together, DAP-R in S. aureus appears to involve multi-factorial and strain-specific adaptive mechanisms.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Phenotypic and Genotypic Characterization of Daptomycin-Resistant Methicillin-Resistant Staphylococcus aureus Strains: Relative Roles of mprF and dlt Operons

et al. 2014

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“…Metabolic drug interactions are unlikely, because in vitro studies have shown that daptomycin neither induces nor inhibits CYP isoforms 1A2, 2A6, 2C9, 2C19, 2D6, 2E1, and 3A4 [36]. In rats, daptomycin decreased aminoglycoside-induced nephrotoxicity when both agents were coadministered.…”

Section: Daptomycinmentioning

confidence: 99%

“…In rats, daptomycin decreased aminoglycoside-induced nephrotoxicity when both agents were coadministered. In healthy subjects, a single dose of daptomycin 2 mg/kg, tobramycin 1 mg/kg, or the combination was not associated with a significant change in pharmacokinetic parameters or nephrotoxicity [33,36]. Because both daptomycin and hydroxymethyglutaryl-coenzyme A (HMG-CoA) reductase inhibitors may increase creatinine phosphokinase concentrations or cause rhabdomyolysis, the manufacturer recommends that HMG-CoA reductase inhibitors and other drugs associated with rhabdomyolysis be temporarily discontinued during daptomycin therapy [36].…”

Section: Daptomycinmentioning

confidence: 99%

Antibiotic Drug Interactions

Pai

Momary

Rodvold

2006

Medical Clinics of North America

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“…Daptomycin has a different mechanism of action from other antibacterial agents, such as vancomycin, against Gram-positive bacteria, acting through disruption and depolarisation of the cell membrane with subsequent inhibition of protein, DNA and RNA synthesis [4]. It has a concentrationdependent bactericidal action through cell membrane lysis against not only growing but also stationary phases of multidrug-resistant (MDR) Gram-positive organisms such as methicillin-resistant Staphylococcus aureus (MRSA), methicillin-resistant Staphylococcus epidermidis (MRSE), vancomycin-intermediate S. aureus, vancomycin-resistant S. aureus and vancomycin-resistant enterococci (VRE) [5].…”

Section: Introductionmentioning

confidence: 99%