Insensitivity of Staphylococcus aureus to glycopeptides became known at the end of the 1990s. To distinguish intermediate (VISA and GISA) and full resistance (vancomycin-resistant Staphylococcus aureus, VRSA) is of both epidemiological and clinical importance. The VISA (GISA) phenotype is obviously selected by glycopeptide usage in individual patients and can be disseminated by clonal spread of particularly affected staphylococcal isolates, preferentially methicillin-resistant S. aureus (MRSA). In the meantime emergence of VISA became known worldwide. VRSA evolve by acquisition of the vanA gene from enterococci, which are of significance as reservoir of resistance genes among gram-positive bacterial pathogens. Until now three independent single cases of emergence of VRSA became known from the USA, in two of them an association with vanA containing Enterococcus spp. at the same site of the affected patients could be established. The frequency of VISA (GISA) among MRSA in Central Europe is still low (<0.1%); no VRSA have been detected until now.