Prevalence and mechanisms of aminoglycoside resistance. A ten-year study.
Aminoglycoside resistance was monitored at St. Thomas' Hospital from 1975 to 1984. Gentamicin resistance had appeared in a number of species by 1975, but remained rare (less than 1 percent of isolates) in Escherichia coli throughout the study period. Gentamicin-resistant Klebsielleae had become fairly common (8 percent of isolates) by 1977, but little change has subsequently occurred in their frequency of isolation. Serratia species are not frequently isolated; gentamicin resistance in these organisms was not observed until 1979. Since then, 10 to 20 percent of isolates have been found to be resistant. Except for Providencia, most isolates of which were gentamicin-resistant, less than 5 percent of the Enterobacteriaceae isolated were found to be resistant to gentamicin during the 10-year period. Throughout the study, approximately 5 percent of the Pseudomonas aeruginosa isolates were resistant to gentamicin. Less than 5 percent of the isolates of Acinetobacter were resistant to gentamicin before 1979, at which time 40 percent were found to be resistant; subsequently, gentamicin resistance among these organisms has become somewhat less common. On the whole, tobramycin resistance has mirrored gentamicin resistance. However, before 1979, most gentamicin-resistant Klebsielleae isolates had retained susceptibility to tobramycin, as had most gentamicin-resistant isolates of Acinetobacter and P. aeruginosa. Amikacin resistance has remained very unusual in all organisms, apart from non-aeruginosa Pseudomonas species. Until 1977, nearly all the resistance among Enterobacteriaceae was attributable to AAC(3)-I, except for that caused by AAC(2') production in Providencia and the non-enzymatic resistance observed in E. coli. However, more recently, AAC(3)-II and AAD(2'') have become the most common mechanisms of resistance. The resistance of most gentamicin-resistant isolates of P. aeruginosa from 1974 to 1977 was attributable to non-enzymatic mechanisms; subsequently, such resistance was more often caused by AAC(3)-I, AAC(6'), or AAD(2''). Gentamicin resistance first appeared in Staphylococcus aureus in 1976, after which about 1 to 2 percent of the isolates from hospitalized patients were found to be resistant, mostly because of production of AAC(6') and APH(2'').
D000150:Acinetobacter / Q000187:drug effects; D000583:Amikacin / Q000494:pharmacology; D000617:Aminoglycosides / Q000494:pharmacology; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D003428:Cross Infection / Q000188:drug therapy; D004352:Drug Resistance, Microbial; D004755:Enterobacteriaceae / Q000187:drug effects* / Q000201:enzymology; D004756:Enterobacteriaceae Infections / Q000188:drug therapy; D005839:Gentamicins / Q000494:pharmacology; D006801:Humans; D008826:Microbial Sensitivity Tests; D011549:Pseudomonas / Q000187:drug effects; D013211:Staphylococcus aureus / Q000187:drug effects; D014031:Tobramycin / Q000494:pharmacology
D000617:Aminoglycosides; D000900:Anti-Bacterial Agents; D005839:Gentamicins; D000583:Amikacin; D014031:Tobramycin