Acquired and intrinsic glycopeptide resistance in enterococci.
Enterococci are Gram-positive cocci responsible for severe human infections, such as endocarditis, meningitis, and septicemia and constitute an increasingly frequent cause of nosocomial infections. Enterococci are resistant to nearly all classes of drugs including, since 1986, glycopeptides. Vancomycin and teicoplanin act by blocking cell wall formation and resistance is due to synthesis of modified late peptidoglycan precursors. Glycopeptide resistance can be intrinsic or acquired and strains may be resistant to vancomycin and teicoplanin, or to vancomycin only. Five types of glycopeptide resistance and their biochemical mechanisms have been described in enterococci. Clinical isolates that are dependent on vancomycin for growth have been isolated. Data suggest a dual origin for resistance: glycopeptide-producing organisms or enterococcal species intrinsically resistant to these drugs.
Gholizadeh
Y
Y
Unité des Agents Antibactériens, Institut Pasteur, 25, rue du Docteur Roux, 75724 Paris Cedex 15, France.
Courvalin
P
P
D000900:Anti-Bacterial Agents / Q000494:pharmacology; D016983:Enterococcus / Q000187:drug effects / Q000201:enzymology / Q000235:genetics*; D006801:Humans; D008826:Microbial Sensitivity Tests; D010453:Peptide Synthases / Q000145:classification / Q000378:metabolism; D010802:Phylogeny; D017334:Teicoplanin / Q000494:pharmacology; D014640:Vancomycin / Q000494:pharmacology; D020713:Vancomycin Resistance / Q000235:genetics* / Q000502:physiology
D000900:Anti-Bacterial Agents; D017334:Teicoplanin; D014640:Vancomycin; D010453:Peptide Synthases; C019638:D-alanylalanine synthetase