Cutler R R
J Antimicrob Chemother. 1983 Mar;11(3):263-9. doi: 10.1093/jac/11.3.263.
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.
六种耐多药金黄色葡萄球菌菌株的庆大霉素耐药性被消除。对于其中三株菌株,敏感变体中氨基糖苷修饰酶的丧失或减少伴随着细胞内庆大霉素积累的增加,证实抗生素的修饰与其摄取受损有关。然而,另外三株菌株的耐药性并未表现出这种关联。对于一株菌株,庆大霉素耐药性的丧失与酶产生的丧失有关,但耐药和敏感变体以相同速率积累[3H]庆大霉素。其余两株菌株的敏感变体[3H]庆大霉素积累未增加,但仍产生氨基糖苷修饰酶,提示这两株菌株的广谱氨基糖苷耐药性是由于一些迄今未描述的耐药机制,而非核糖体靶点的改变。