Vancomycin-resistant Staphylococcus aureus

Lessing, M.P.A.; Mj, Raftery

doi:10.1016/s0140-6736(05)78597-4

Cited by 125 publications

(74 citation statements)

References 6 publications

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“…Early after the emergence of hVISA and VISA, it became clear that automated susceptibility testing methods and standard disc diffusion were inadequate for the detection of VISA let alone the low-level-resistant subpopulations present in hVISA strains (91,127,347). A number of screening tests for hVISA and VISA have since been developed and assessed, although the sensitivity has been generally low for the detection of hVISA (Table 5).…”

Section: Hvisamentioning

confidence: 99%

Reduced Vancomycin Susceptibility inStaphylococcus aureus, Including Vancomycin-Intermediate and Heterogeneous Vancomycin-Intermediate Strains: Resistance Mechanisms, Laboratory Detection, and Clinical Implications

et al. 2010

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SUMMARY The emergence of vancomycin-intermediate Staphylococcus aureus (VISA) and heterogeneous vancomycin-intermediate Staphylococcus aureus (hVISA) over the past decade has provided a challenge to diagnostic microbiologists to detect these strains, clinicians treating patients with infections due to these strains, and researchers attempting to understand the resistance mechanisms. Recent data show that these strains have been detected globally and in many cases are associated with glycopeptide treatment failure; however, more rigorous clinical studies are required to clearly define the contribution of hVISA to glycopeptide treatment outcomes. It is now becoming clear that sequential point mutations in key global regulatory genes contribute to the hVISA and VISA phenotypes, which are associated predominately with cell wall thickening and restricted vancomycin access to its site of activity in the division septum; however, the phenotypic features of these strains can vary because the mutations leading to resistance can vary. Interestingly, changes in the staphylococcal surface and expression of agr are likely to impact host-pathogen interactions in hVISA and VISA infections. Given the subtleties of vancomycin susceptibility testing against S. aureus, it is imperative that diagnostic laboratories use well-standardized methods and have a framework for detecting reduced vancomycin susceptibility in S. aureus.

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Section: Hvisamentioning

confidence: 99%

Reduced Vancomycin Susceptibility inStaphylococcus aureus, Including Vancomycin-Intermediate and Heterogeneous Vancomycin-Intermediate Strains: Resistance Mechanisms, Laboratory Detection, and Clinical Implications

et al. 2010

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“…2 These cases underscore the fact that limited numbers of drugs are available to prevent a simple Staph infections from becoming deadly. 3 At least four other strains of common bacterial species capable of causing life-threatening illnesses (Enterococcus faecalis, Mycobacterium tuberculosis, Escherichia coli O157:H7, and Pseudomonas aeruginosa) are already resistant to nearly all drugs in clinicians arsenal comprised of more than 100 drugs. 4,5 Thus, the search for new antibiotics that target enzymes in unexplored bacterial biosynthetic pathways is critically important, as confirmed in Supuran's excellent review of bacterial protease inhibitors.…”

mentioning

confidence: 99%

Inhibitors of bacterial N-succinyl-l,l-diaminopimelic acid desuccinylase (DapE) and demonstration of in vitro antimicrobial activity

Gillner

Armoush

Holz

et al. 2009

Bioorganic & Medicinal Chemistry Letters

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“…The spread of MRSA in hospitals and in the community resulted in widespread vancomycin use in S. aureus infections (10,11). With the widespread use of vancomycin, the first clinical isolate of S. aureus with intermediate resistance to vancomycin (VISA) was reported from Japan in 1996 and multiple strains of S. aureus with reduced susceptibilities to vancomycin have been reported in other countries (12)(13)(14)(15)(16)(17). The emergence of reduced vancomycin susceptibility in S. aureus made many clinicians concerned about the possibility that some strains would become fully resistant, and actually vancomycin-resistant S. aureus (VRSA) strains have been isolated from Michigan and Pennsylvania in 2002 (18,19).…”

Section: Resultsmentioning

confidence: 99%

Efficacy of Vancomycin-beta-lactam Combinations Against Heterogeneously Vancomycin-Resistant Staphylococcus aureus (hetero-VRSA)

et al. 2003

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There have been conflicting data about the interactions between vancomycin and -lactam agents against Staphylococcus aureus strains with heterogeneous resistance to vancomycin. We evaluated the efficacy of these combinations against Mu 3 and heterogeneously vancomycin-resistant S. aureus (hetero-VRSA) strains which were isolated from Korean patients using a population analysis method. Antagonistic effects were observed when less than 1 g/mL of -lactam antibiotics was combined with vancomycin, whereas synergistic effects were noticed with more than 4 g/mL of -lactam antibiotics. The antagonistic effects at low concentrations of -lactams were most prominent at 2 g/mL of vancomycin, which were the vancomycin MICs of tested hetero-VRSA strains. This study showed the variable effects of vancomycin--lactam combinations depending on the concentrations of -lactam antibiotics and this property could be used to develop screening methods for hetero-VRSA strains.

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Vancomycin-resistant Staphylococcus aureus

Cited by 125 publications

References 6 publications

Reduced Vancomycin Susceptibility inStaphylococcus aureus, Including Vancomycin-Intermediate and Heterogeneous Vancomycin-Intermediate Strains: Resistance Mechanisms, Laboratory Detection, and Clinical Implications

Reduced Vancomycin Susceptibility inStaphylococcus aureus, Including Vancomycin-Intermediate and Heterogeneous Vancomycin-Intermediate Strains: Resistance Mechanisms, Laboratory Detection, and Clinical Implications

Inhibitors of bacterial N-succinyl-l,l-diaminopimelic acid desuccinylase (DapE) and demonstration of in vitro antimicrobial activity

Efficacy of Vancomycin-beta-lactam Combinations Against Heterogeneously Vancomycin-Resistant Staphylococcus aureus (hetero-VRSA)

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