title: Treatment of infections caused by resistant Staphylococcus aureus.
abstract: We review data on the treatment of infections caused by drug-resistant Staphylococcus aureus, particularly methicillin-resistant S. aureus (MRSA). In this review, we cover findings reported in the English language medical literature up to February 2006. Despite the emergence of resistant and multidrug resistant S. aureus, five effective drugs for which little resistance has been observed are in clinical use: vancomycin, quinupristin-dalfopristin, linezolid, tigecycline, and daptomycin. However, vancomycin is less effective for infections with MRSA isolates that have a high minimum inhibitory concentration in the susceptible range. Linezolid looks promising in the treatment of MRSA pneumonia and skin and soft-tissue infections (SSTIs). Daptomycin displays rapid bactericidal activity in vitro, and it has been shown to be noninferior to comparator agents in the treatment of SSTIs and bacteremia. Tigecycline was also noninferior to comparator drugs in the treatment of SSTIs. Clindamycin, trimethoprim-sulfamethoxazole, doxycycline, and minocycline are oral antistaphylococcal agents that may have utility in the treatment of SSTIs and osteomyelitis, but the clinical data for their efficacy is limited. There are four drugs with broad-spectrum activity against Gram-positive organisms at an advanced stage of clinical testing: ceptobiprole and three new glycopeptides with potent bactericidal activity, oritavancin, dalbavancin, and telavancin. Thus, there are currently many effective drugs to treat resistant S. aureus infections and many promising agents in the pipeline. Nevertheless, S. aureus remains a formidable adversary against which there are frequent treatment failures. The next goals are to determine the most appropriate indications and cost-effectiveness of each of these drugs in the treatment strategy against S. aureus.
authors.affiliation: Division of Infectious Diseases, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
authors.forename: Gregory M
authors.initials: GM
authors.lastname: Anstead
authors.forename: Gabriel
authors.initials: G
authors.lastname: Quinones-Nazario
authors.forename: James S
authors.initials: JS
authors.lastname: Lewis
mesh_terms: D000081:Acetamides / Q000627:therapeutic use; D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D017576:Daptomycin / Q000627:therapeutic use; D024881:Drug Resistance, Bacterial; D006801:Humans; D000069349:Linezolid; D016106:Methicillin Resistance; D008911:Minocycline / Q000031:analogs & derivatives / Q000627:therapeutic use; D023303:Oxazolidinones / Q000627:therapeutic use; D013203:Staphylococcal Infections / Q000188:drug therapy* / Q000382:microbiology; D013211:Staphylococcus aureus / Q000187:drug effects*; D000078304:Tigecycline; D014640:Vancomycin / Q000627:therapeutic use; D014769:Virginiamycin / Q000627:therapeutic use
chemical_list: D000081:Acetamides; D000900:Anti-Bacterial Agents; D023303:Oxazolidinones; D014769:Virginiamycin; C062940:quinupristin-dalfopristin; D014640:Vancomycin; D000078304:Tigecycline; D008911:Minocycline; D000069349:Linezolid; D017576:Daptomycin