| Characterization of global patterns and the genetics of fusidic Acid resistance. | |
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MedLine Citation:
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PMID: 21546625 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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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. |
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Authors:
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David J Farrell; Mariana Castanheira; Ian Chopra |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Clinical infectious diseases : an official publication of the Infectious Diseases Society of America Volume: 52 Suppl 7 ISSN: 1537-6591 ISO Abbreviation: Clin. Infect. Dis. Publication Date: 2011 Jun |
Date Detail:
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Created Date: 2011-05-06 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9203213 Medline TA: Clin Infect Dis Country: United States |
Other Details:
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Languages: eng Pagination: S487-92 Citation Subset: IM |
Affiliation:
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JMI Laboratories, North Liberty, Iowa. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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