Characterization of aminoglycoside-modifying enzymes in enterobacteriaceae clinical strains and characterization of the plasmids implicated in their diffusion

Elisenda Miró, Federico Grünbaum, Laura Gómez, Alba Rivera, Beatriz Mirelis, Pere Coll, Ferran Navarro

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Abstract

A total of 788 clinical Enterobacteriaceae were collected to describe the aminoglycoside-modifying genes (AME genes) and to characterize the plasmids that carry these genes. Among the 788 strains collected, 330 (41.8%) were aminoglycoside-resistant: 264 Escherichia coli (80%), 33 Proteus mirabilis (10%), 10 Klebsiella pneumoniae (3%), six K. oxytoca (1.8%), five Enterobacter cloacae (1.5%), three Morganella morganii (0.9%), three Providencia stuartii (0.9%), two Salmonella enterica (0.6%), and one each Citrobacter freundii, C. koseri, Proteus vulgaris, and Shigella sonnei. The most affected aminoglycoside was streptomycin (92.7%), followed by kanamycin (26.3%), gentamicin (18%), tobramycin (16.9%), netilmicin (3.6%), and amikacin (1.5%). The AME genes found were aph(3″)-Ib (65.4%), ant(3″)-Ia (37.5%), aph(3′)-Ia (13.9%), aac(3)-IIa (12.4%), aac(6′)-Ib (4.2%), ant(2″)-Ia (3.6%), and aph(3′)-IIa (1.2%). Thirty-four percent of the strains showed more than one enzyme. The most frequent association was ant(3″)-Ia plus aph(3″)-Ib (35 strains). From 66 selected AME genes, 24 were plasmid located: 12 aac(3)-IIa, six aph(3′)-Ia, three ant(3″)-Ia, two ant(2″)-Ia, and one aac(6′)-Ib. These genes were located in plasmids belonging to incompatibility groups F, FIA, FIB, or HI2. In conclusion, the AME genes involved in aminoglycoside-clinical resistance were aac(3)-IIa, aac(6′)-Ib, and ant(2″)-Ia, genes that confer resistance to tobramycin, gentamicin, and amikacin. © Copyright 2013, Mary Ann Liebert, Inc. 2013.
Original languageEnglish
Pages (from-to)94-99
JournalMicrobial Drug Resistance
Volume19
Issue number2
DOIs
Publication statusPublished - 1 Apr 2013

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