These two isolates lacked cadDX gene and were found to belong to two unrelated clusters and spa types. The second resistance determinant was fusB found in two isolates. These isolates also possessed the staphylococcal enterotoxin H gene. Molecular typing showed that 14 of them harboured an agr group III and belonged to the same clonal complex (CC) spa type 127 and identical clonotype (cluster labelled A). The most common resistance determinant was fusC, found in 16 isolates. aureus isolates collected in 20, 18 (∼13%) exhibited resistance to fusidic acid. The agr group and the presence of toxin genes were monitored to characterize all FAR-SA isolates which were typed by pulsed-field gel electrophoresis (PFGE) and spa typing. fusB-positive strains were tested for a cadDX operon, encoding cadmium resistance. aureus (FAR-SA) isolates were tested for fusB and fusC genes and were evaluated for the detection of mutations in fusA and fusE ( rplF). aureus in Casablanca (Morocco) and to define the phenotypic and genotypic traits of these isolates and their clonal relationship. The aim of this study was to determine the prevalence and mechanisms of resistance to fusidic acid in clinical isolates of S.
Other mechanisms involved in this resistance are mutations in the riboprotein L6 operon within rplF. Resistance to fusidic acid in Staphylococcus aureus is caused by mutation of the elongation factor G (EF-G) encoded by fusA or by expression of a protein, encoded by fusB or fusC, that protects the drug target.