Journal Article

Characterization of Global Patterns and the Genetics of Fusidic Acid Resistance

David J. Farrell, Mariana Castanheira and Ian Chopra

in Clinical Infectious Diseases

Published on behalf of Infectious Diseases Society of America

Volume 52, issue suppl_7, pages S487-S492
Published in print June 2011 | ISSN: 1058-4838
Published online June 2011 | e-ISSN: 1537-6591 | DOI: https://dx.doi.org/10.1093/cid/cir164
Characterization of Global Patterns and the Genetics of Fusidic Acid Resistance

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Fusidic acid binds to elongation factor G (EF-G), preventing its release from the ribosome, thus stalling bacterial protein synthesis. In staphylococci, high-level fusidic acid resistance is usually caused by mutations in the gene encoding EF-G, fusA, and low-level resistance is generally caused by the horizontally transferable mechanisms fusB and fusC that have a putative protective role on EF-G. In addition, fusD is responsible for intrinsic resistance in Staphylococcus saprophyticus, and alterations in the L6 portion of rplF (fusE) have a role in fusidic acid resistance. Fusidic acid has been used in Europe and Australia for decades. More recently, it has also been used in other countries and regions, but not in the United States. Worldwide fusidic acid resistance has been slow to develop, and the level of resistance and genetic mechanisms responsible generally reflect the time since introduction, indications for treatment, route of administration, and prescribing practices.

Journal Article.  3221 words.  Illustrated.

Subjects: Infectious Diseases ; Immunology ; Public Health and Epidemiology ; Microbiology

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