Several different biochemical mechanisms of resistance to aminoglycoside antibiotics have been identified in clinical bacterial isolates. The most significant and widespread mechanism is modification by R plasmid-encoded enzymes. In a general sense, the distribution of this form of resistance occurs by the dissemination of R plasmids through various mechanisms of intergeneric transfer; more specifically, this occurs by transposition. Transposable resistance elements encoding resistance to aminoglycoside antibiotics have been identified in most bacterial genera. The development of new aminoglycosides refractory to enzymatic modification and the use of inhibitors of aminoglycoside-modifying enzymes are two approaches to overcome bacterial resistance to the conventional aminoglycosides.
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Julian Davies (1983) studied this question.
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