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Abstract
Serious infections caused by Staphylococcus aureus are a worldwide phenomenon and occur in both the hospital and community settings. Initially, penicillins G was an effective therapy option for S. aureus infections. However, the emergence of penicillin resistance in S. aureus isolates over the past 50 years has had an impact on how such infections are treated (CDC 2004).
By the 1970s, almost all hospital strains and a large number of community strains of S aureus were resistant to penicillin. The development of the semisynthetic penicillinase- resistant agents, methicillin and the isoxazolyl penicillins in 1960 was followed by the report of methicillin- resistant S aureus (MRSA) in 1961. The development of methicillin resistance, in particular, has been a cause for concern among physicians and microbiologists and effective treatment options are diminishing. In the USA, most clinical S. aureus isolates are resistant to penicillin (95%) and over half are resistant to methicillin; the prevalence of MRSA in Europe is also a problem (Tiemersma et al., 2004) and (Appelbaum, 2006).
The glycopeptide vancomycin represented a uniquely effective solution for treating infections caused by methicillin-resistant pathogens, including S. aureus. With the increasing prevalence of MRSA worldwide and the consequent increased use of vancomycin, it was inevitable that infections with vancomycin-resistant S aureus (VRSA) would be reported. The first clinical isolate of S aureus with reduced susceptibility to vancomycin was reported from Japan by hiramatsu et al., in 1997. Few years later vancomycin resistant S. aureus (VRSA) was reported. VRSA strains are more alarming, as these isolates demonstrate complete vancomycin resistance (Kacica et al., 2004).