Epidemiology and clinical impact of glycopeptide resistance in Staphylococcus aureus

Abstract

Staphylococcus aureus with resistance to glycopeptide antibiotics has been considered to be a rare cause of clinically relevant infections. A review of the current literature shows that this is indeed the case for infections caused by S. aureus with high-level resistance to vancomycin (VRSA), as only isolated cases have been reported. VRSA develops following the insertion of the vanA gene, which is transferred from enterococci with vancomycin resistance. On the other hand, infections caused by S. aureus with intermediate resistance to glycopeptides (VISA), or heterogeneously expressed intermediate level glycopeptide resistance (hVISA), are more common. These infections are associated with clinical failure of glycopeptide therapy. While the biochemical and phenotypic features including a thickened cell wall of hVISA and VISA are well known, the genetic basis of these phenotypes remains unknown. Certain genetic regulatory elements such as agr II are associated with reduced susceptibility of S. aureus to glycopeptides. Available data suggest that certain infections might be successfully treated using higher doses of vancomycin. However, as treatment failure is particularly common in infections with a high bacterial load, it may be necessary to resort to other antibiotics such as linezolid, often combined with surgical intervention, in order to successfully treat these infections. Open questions regarding diagnosis, pathogenesis, epidemiology, and treatment of glycopeptide resistance in S. aureus are addressed in this review. Clinicians should be aware of these aspects, since S. aureus remains one of the most important bacteria in modern medicine.