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Review
. 2017 Jun 23;90(2):269-281.
eCollection 2017 Jun.

Vancomycin Resistance in Staphylococcus aureus

Will A McGuinness  1 , Natalia Malachowa  1 , Frank R DeLeo  1
Affiliations
Review

Vancomycin Resistance in Staphylococcus aureus

Will A McGuinness et al. Yale J Biol Med. .

Abstract

The evolution of Staphylococcus aureus during the modern antibiotic era has been delineated by distinct strain emergence events, many of which include acquisition of antibiotic resistance. The relative high burden of methicillin-resistant S. aureus (MRSA) in healthcare and community settings is a major concern worldwide. Vancomycin, a glycopeptide antibiotic that inhibits cell wall biosynthesis, remains a drug of choice for treatment of severe MRSA infections. S. aureus strains exhibiting increased resistance to vancomycin, known as vancomycin intermediate-resistant S. aureus (VISA) (MIC = 4-8 µg/mL), were discovered in the 1990s. The molecular basis of resistance in VISA is polygenic and involves stepwise mutations in genes encoding molecules predominantly involved in cell envelope biosynthesis. S. aureus isolates with complete resistance to vancomycin (MIC ≥ 16 µg/mL) are termed vancomycin-resistant S. aureus (VRSA)-they were first reported in the U.S. in 2002. Resistance in VRSA is conferred by the vanA gene and operon, which is present on a plasmid. Although treatment of VRSA infections is challenging, the total number of human VRSA infections to date is limited (14 in the U.S.). By comparison, the burden of VISA is relatively high and the molecular mechanisms of resistance are less well-defined. VISA are associated with persistent infections, vancomycin treatment failure, and poor clinical outcomes. Here, we review in brief progress made toward understanding the acquisition of antibiotic resistance in S. aureus, with an emphasis on the molecular mechanisms underlying vancomycin resistance.

Keywords: Staphylococcus aureus; VISA; VRSA; antibiotic resistance; vancomycin.

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Figures

Figure 1
Figure 1
Timeline delineating the advent of antibiotic therapies and subsequent emergence of antibiotic-resistant S. aureus.
Figure 2
Figure 2
Schematic model illustrating the acquisition and molecular mechanism of vanA-type vancomycin resistance in S. aureus.
See this image and copyright information in PMC

References

    1. Classics in infectious diseases: “on abscesses”: Alexander Ogston (1844-1929). Rev Infect Dis. 1984;6(1):122–128. - PubMed
    1. Roberts S, Chambers S. Diagnosis and management of Staphylococcus aureus infections of the skin and soft tissue. Intern Med J. 2005;35(s2):S97–S105. - PubMed
    1. Mitchell DH, Howden BP. Diagnosis and management of Staphylococcus aureus bacteraemia. Intern Med J. 2005;35:S17–S24. - PubMed
    1. Murdoch DR, Corey GR, Hoen B. et al. Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis–Prospective Cohort Study. Arch Intern Med. 2009;169(5):463–473. - PMC - PubMed
    1. Murray R. Staphylococcus aureus infective endocarditis: diagnosis and management guidelines. Intern Med J. 2005;35(s2):S25–S44. - PubMed

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