A previous study showed a similar result that a laboratory strain containing both fusA resistance mutation and fusB failed to increase the level of fusidic acid resistance [17]. The chromosomal gene fusC confer resistance to fusidic acid on S. aureus or S. intermedius is identified with 45% amino acid similarity to FusB, protect EF-G from the antibiotic [18]. Genes for FusB-type resistance (fusB and fusC) are thought to act by the same mechanism of protection the drug target [18]. It remains unclear whether these resistance
mechanisms of a strain do act in combination or not. The precise action mode of FusB-type resistance awaits further investigation. The level of fusidic acid resistance in isolate 32 did not decrease after curing the pUB101 plasmid. The Staurosporine in vivo result may indicate that the resistance mechanisms do not act synergistically or additively. In this website this study, all MRSA isolates met the criteria of being health-care associated. PFGE patterns revealed that there was greater than 80% similarity among the isolates. MLST and SCCmec typing showed that all isolates belonged to ST239 and carried SCCmec III elements, which is the most prevalent health care-associated strain of MRSA in Taiwan [31].
A previous study conducted in 2002-2007 in northern Taiwan also revealed that most of fusidic acid-resistant MRSA isolates carried SCCmec type III [27]. The two studies results suggest that a clonal strain had disseminated in Taiwan during the period of the study. In contrast to our findings, a previous
European study finding indicated that the majority of fusidic acid-resistant MRSA isolates belonged to CC80-MRSA-IV clone carrying fusB and CC5 clone harbouring fusC [30]. Conclusion In conclusion, we hypothesize that the prevalence of fusidic acid-resistance in S. aureus was commonly associated with the fusC determinant in our isolates. It is interesting to note that some studied isolates possessed more than one fusidic acid-resistance mechanism in our collection. The fusC and acquired FusB-family determinants in a single isolate were first detected and one isolate with fusC also carried a fusA mutation in H457Y. Phylogenetic Sclareol analysis clearly demonstrated the spread of a major clonal strain of fusidic acid-resistant MRSA in our institution. Due to the concern of clonal spread and growing expansion of fusidic acid-resistant determinants, particularly FusC in MRSA, large-scale, prospective surveillance monitoring for fusidic acid-resistance in S. aureus and MRSA is now ongoing in Taiwan. Acknowledgements We wish to thank Chien-Shun Chiou of the third branch office of Centers for Diseases Control of Taiwan for his assistance in PFGE analysis. This work was supported in part by research grant CMU97-104 from the China Medical University. References 1.