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 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.
Handwerger
S
S
Department of Medicine, Beth Israel Medical Center, New York, NY 10003.
Kolokathis
A
A
D003593:Cytoplasm / Q000187:drug effects / Q000378:metabolism; D004352:Drug Resistance, Microbial; D006031:Glycosylation / Q000187:drug effects; D008565:Membrane Proteins / Q000096:biosynthesis*; D008826:Microbial Sensitivity Tests; D010457:Peptidoglycan / Q000096:biosynthesis*; D011498:Protein Precursors / Q000096:biosynthesis*; D013291:Streptococcus / Q000187:drug effects* / Q000378:metabolism; D014640:Vancomycin / Q000494:pharmacology*
D008565:Membrane Proteins; D010457:Peptidoglycan; D011498:Protein Precursors; D014640:Vancomycin