Vancomycin-resistant Staphylococcus aureus
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Vancomycin-resistant Staphylococcus aureus refers to strains of Staphylococcus aureus that have become resistant to the glycopeptide antibiotic vancomycin. With the increase of staphylococcal resistance to methicillin, vancomycin (or another glycopeptide antibiotic, teicoplanin) is often a treatment of choice in infections with methicillin-resistant S. aureus (MRSA).
Three classes of vancomycin-resistant S. aureus have emerged that differ in vancomycin susceptibilities: vancomycin-intermediate S. aureus (VISA), heterogenous vancomycin-intermediate S. aureus (hVISA), and high-level vancomycin-resistant S. aureus (VRSA).
Vancomycin-intermediate S. aureus (VISA)
VISA was first identified in Japan in 1997 and has since been found in hospitals elsewhere in Asia, as well as in the United Kingdom, France, the U.S., and Brazil. It is also termed GISA (glycopeptide-intermediate Staphylococcus aureus), indicating resistance to all glycopeptide antibiotics. These bacterial strains present a thickening of the cell wall, which is believed to reduce the ability of vancomycin to diffuse into the division septum of the cell required for effective vancomycin treatment.
Even with the absence of high-level resistance to vancomycin, another concern posed by the presence of VISA is the increased difficulty in prescribing treatments, especially in situations where an effective treatment for an infection is needed urgently, before detailed resistance profiles can be obtained. In hospitals already endemic with multiresistant MRSA, the appearance of VRSA would make the treatment of infected patients much more difficult.
Vancomycin-resistant S. aureus (VRSA)
High-level vancomycin resistance in S. aureus has been rarely reported. In vitro and in vivo experiments reported in 1992 demonstrated that vancomycin resistance genes from Enterococcus faecalis could be transferred by horizontal gene transfer to S. aureus, conferring high-level vancomycin resistance to S. aureus. Until 2002 such a genetic transfer was not reported for wild S. aureus strains. In 2002, a VRSA strain was isolated from the catheter tip of a diabetic, renal dialysis patient in Michigan. The isolate contained the mecA gene for methicillin resistance. Vancomycin MICs of the VRSA isolate were consistent with the VanA phenotype of Enterococcus species, and the presence of the vanA gene was confirmed by polymerase chain reaction. The DNA sequence of the VRSA vanA gene was identical to that of a vancomycin-resistant strain of Enterococcus faecalis recovered from the same catheter tip. The vanA gene was later found to be encoded within a transposon located on a plasmid carried by the VRSA isolate. This transposon, Tn1546, confers vanA-type vancomycin resistance in enterococci.
From 2002 to 2010, ten additional VRSA isolates were reported, eight from the United States, one from Iran, and one from India. By the end of June 2013, VRSA isolates have been reported for the first time in Europe and in Latin America.
Trimethoprim/sulfamethoxazole was shown to have efficacy in treating the first known US case of VRSA. Linezolid, quinupristin/dalfopristin and daptomycin are treatments of consideration.
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