Gentamicin resistance in Staphylococcus aureus--a new mechanism?
Six multiply-resistant strains of Staphylococcus aureus were cured of their gentamicin resistance. For three strains, the loss or reduction of aminoglycoside-modifying enzymes in the sensitive variants was accompanied by an increase in intracellular gentamicin accumulation, confirming that modification of the antibiotic was associated with its impaired uptake. Resistance in the other three strains, however, did not show this association. For one strain the loss of gentamicin resistance was associated with a loss of enzyme production, but both resistant and sensitive variants accumulated [3H] gentamicin at the same rate. The sensitive variants of the two remaining strains showed no increase in [3H] gentamicin accumulation but still produced aminoglycoside-modifying enzymes, and it is suggested that the broad-spectrum aminoglycoside resistance of these two strains is due to some hitherto undescribed mechanisms of resistance rather than an alteration of the ribosomal target.
D000617:Aminoglycosides / Q000494:pharmacology; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D004352:Drug Resistance, Microbial; D005839:Gentamicins / Q000494:pharmacology*; D013211:Staphylococcus aureus / Q000187:drug effects* / Q000201:enzymology; D013997:Time Factors
D000617:Aminoglycosides; D000900:Anti-Bacterial Agents; D005839:Gentamicins