Resistance of to structurally diverse hydrophobic agents (HAs) has been associated with missense or deletion mutations in the ( ultiple transferable esistance egulator) gene of laboratory-derived strains but their prevalence in clinical isolates was heretofore unknown. Since faecal lipids provide strong selective pressure for the emergence of variants resistant to HAs (HA), the nucleotide sequence of the gene from rectal isolates of , which displayed different levels of HA, was determined. Compared to the gene possessed by the HA-sensitive strain FA19, each clinical isolate contained mutations in the coding and/or promoter regions of their gene. A missense mutation in codon 45 (Gly-45 to Asp) was the most common mutation found in the strains studied and impacted the structure of the helix-turn-helix domain of the MtrR protein thought to be important in DNA-binding activity. Two clinical isolates bearing a missense mutation in codon 45 also contained a single basepair deletion in a 13 bp inverted sequence positioned within the promoter region. Introduction of sequences amplified from the clinical isolates into strain FA19 revealed that acquisition of the single basepair deletion was correlated with high level HA while mutations in the -coding region provided for an intermediate level of HA.


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