Abstract
The clinical relevance of resistance to fusidic acid in Staphylococcus aureus is reviewed. Resistance due to a one-step chromosomal mutation emerges readily in vitro . These variants appear defective and are not encountered clinically as frequently as would be expected. The majority of strains isolated from patients probably have plasmid-mediated resistance. The plasmid may be unstable both in vitro and in vivo . There appears to be a low incidence of resistance emerging when fusidic acid is used alone to treat acute infections; however, there is a higher incidence in chronic infections. When fusidic acid is given concurrently with another antibacterial agent to treat severe infection, resistance may be acquired in up to 1% of cases. The use of fusidic acid topically to treat acute skin infection in domiciliary practice does not appear to be epidemiologically hazardous. Over the last 20 years, during which fusidic acid has been used widely in the management of staphylococcal infection, the general level of resistance has remained low at 1–2%.

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