Induction of vancomycin resistance in Enterococcus faecium by inhibition of transglycosylation

Vancomycin resistance has recently been recognized among clinical isolates of enterococci. Resistance is inducible, and associated with production of a novel 39 kDa membrane protein. The mechanism by which exposure to vancomycin, which does not penetrate the cell membrane, induces resistance is unkn...

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Bibliographic Details
Published in:FEMS microbiology letters 1990-07, Vol.70 (2), p.167-170
Main Authors: Handwerger, Sandra, Kolokathis, Antonia
Format: Article
Language:English
Subjects:
Cytoplasm - drug effects
Cytoplasm - metabolism
Drug Resistance, Microbial
Enterococcus faecium 228
Glycosylation - drug effects
Membrane Proteins - biosynthesis
Microbial Sensitivity Tests
Peptidoglycan - biosynthesis
Protein Precursors - biosynthesis
Streptococcus - drug effects
Streptococcus - metabolism
Vancomycin - pharmacology
Vancomycin resistance
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Summary:Vancomycin resistance has recently been recognized among clinical isolates of enterococci. Resistance is inducible, and associated with production of a novel 39 kDa membrane protein. The mechanism by which exposure to vancomycin, which does not penetrate the cell membrane, induces resistance is unknown. In the vancomycin resistant strain Enterococcus faecium 228, resistance was also inducible by moenomycin, suggesting that inhibition of the transglycosylation step in peptidoglycan synthesis may be required for induction of resistance. Cytoplasmic pools of peptidoglycan precursors were increased after exposure to vancomycin or moenomycin, representing a potential means for regulation of induction.
ISSN:0378-1097
1574-6968
DOI:10.1016/S0378-1097(05)80033-3