Fusidic Acid Resistance Rates and Prevalence of Resistance Mechanisms among Staphylococcus spp. Isolated in North America and Australia, 2007-2008

Abstract

ABSTRACT Among 4,167 Staphylococcus aureus and 790 coagulase-negative Staphylococcus (CoNS; not S. saprophyticus ) isolates collected consecutively from North American and Australian hospitals, only 87 (1.7% overall) isolates displayed a fusidic acid (FA; also known as CEM-102) MIC of ≥2 μg/ml (FA resistance). These strains were further evaluated with a multiplex PCR to amplify the acquired resistance genes fusB , fusC , and fusD. Mutations in fusA and fusE were evaluated in all isolates showing an absence of acquired resistance genes and/or showing FA MIC values of ≥64 μg/ml. S. aureus resistance rates were very low in the United States (0.3%) and were higher in Canada and Australia (7.0% for both countries). Among CoNS isolates, FA resistance rates were significantly more elevated than that for S. aureus (7.2 to 20.0%; the highest rates were in Canada). All 52 (41 CoNS) FA-resistant isolates from the United States showed FA MIC results of ≤64 μg/ml, and 7 of 11 S. aureus isolates carried fusC . CoNS strains from the United States carried fusB or fusC . In Canada, fusB and fusC occurrences were similar among S. aureus and CoNS isolates, and modestly elevated FA MIC values were observed (all MIC results were ≤32 μg/ml). Isolates from Australia showed MIC values ranging from 2 to 32 μg/ml, and S. aureus isolates were predominantly fusC positive. fusA mutations were detected in only three S. aureus isolates, conferring FA MIC values of 2 to 8 μg/ml. Target mutations have been considered the primary FA resistance mechanism among Staphylococcus spp.; however, acquired resistance genes appear to have a dominant role in resistance against this older antimicrobial agent. In summary, this study shows that acquired genes are highly prevalent among FA-resistant strains (>90%) in three nations with distinct or absence (United States) of fusidic acid clinical use.