Abstract
Epidemic aminoglycoside resistance may be caused by the spread of a species with distinctive chromosomal genes (e.g., Pseudomonas aeruginosa), or it may be due to the dissemination of plasmids or transposons between genera. Although strains of P. aeruginosa resistant to aminoglycosides because of impermeability may cause nosocomial outbreaks, most of the acute increases in aminoglycoside resistance are due to the spread of inactivating enzymes by plasmids. The index species for intergeneric outbreaks is usually Klebsiella pneumoniae carrying the ANT(2″) or AAC(3) gene; however, the distribution of resistance varies greatly by location and species. The AAC(6′)-I gene is most common in Serratia marcescens and in East Asian isolates of other species, whereas the AAC(3) gene is common in Chile. In the United States, the ANT(2″) and AAC(3) genes are particularly common among Enterobacteriaceae, except for Proteus and Providencia, which often carry the AAC(2′) gene. The most common patterns of epidemic resistance lead to the inactivation of gentamicin and, less frequently, tobramycin, but only rarely affect amikacin.
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