title: Mutations in fusA associated with posttherapy fusidic acid resistance in Clostridium difficile.
abstract: In silico, we identified fusA (2,067 bp) in Clostridium difficile 630. Sequencing of fusA in posttherapy fusidic acid-resistant C. difficile isolates from 12 patients with C. difficile-associated diarrhea (CDAD) identified fusA mutations, one or two nonsynonymous substitutions, or in one case a deletion of one codon associated with resistance. Five of these mutations have previously been described in fusA of fusidic acid-resistant Staphylococcus aureus, but seven were novel fusA mutations. Fusidic acid monotherapy for CDAD seemed to rapidly select conserved resistant mutants.
authors.affiliation: Department of Infectious Diseases, Orebro University Hospital, SE-701 85 Orebro, Sweden. torbjorn.noren@orebroll.se
authors.forename: T
authors.initials: T
authors.lastname: Norén
authors.forename: T
authors.initials: T
authors.lastname: Akerlund
authors.forename: M
authors.initials: M
authors.lastname: Wullt
authors.forename: L G
authors.initials: LG
authors.lastname: Burman
authors.forename: M
authors.initials: M
authors.lastname: Unemo
mesh_terms: D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D016360:Clostridioides difficile / Q000187:drug effects* / Q000235:genetics / Q000254:growth & development; D003967:Diarrhea / Q000188:drug therapy; D005672:Fusidic Acid / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D008826:Microbial Sensitivity Tests; D009154:Mutation; D020653:Peptide Elongation Factor G / Q000235:genetics*
chemical_list: D000900:Anti-Bacterial Agents; D020653:Peptide Elongation Factor G; D005672:Fusidic Acid