Article ID Journal Published Year Pages File Type
3359800 International Journal of Antimicrobial Agents 2010 5 Pages PDF
Abstract

A total of 81 clinical isolates of the three clinically important Acinetobacter spp., namely Acinetobacterbaumannii, Acinetobacter genospecies 3 and Acinetobacter genospecies 13TU, were analysed for differences in carbapenem resistance genes. Of the 81 isolates, 40 (49%) were resistant to carbapenems. Most A. baumannii isolates (47/53, 88.7%) contained the ISAba1–blaOXA-51-like gene and exhibited a higher minimum inhibitory concentration to imipenem than A. baumannii without the ISAba1 element. All four carbapenem-resistant A. genospecies 3 isolates contained blaIMP-1 and an ISAba3–blaOXA-58-like gene. Three A. genospecies 13TU isolates contained an ISAba3–blaOXA-58-like and either a blaIMP-1 or a blaVIM-11 gene. The five blaIMP-1-containing strains were resistant to imipenem and were positive for metallo-β-lactamase (MBL) activity by the Etest, and the two blaVIM-11-containing strains were susceptible to imipenem and were MBL-negative by Etest. Imipenem hydrolysis tests showed that the blaIMP-1-containing strains exhibited much higher imipenem-hydrolysing activity than the two blaVIM-11-containing strains. No transcripts of blaVIM-11 or blaOXA-58-like genes were detected. Analysis of outer membrane proteins showed that OprD was absent in the only blaIMP-1-containing A. genospecies 13TU strain owing to the presence of a premature stop codon in the oprD gene. In summary, several differences were detected between the carbapenem resistance genes of clinical Acinetobacter spp. in Taiwan, and loss of OprD may be associated with imipenem resistance in A. genospecies 13TU.

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