Abstract

A total of 81 clinical isolates of the three clinically important Acinetobacter spp., namely Acinetobacter baumannii, 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 ISA ba1– bla OXA-51-like gene and exhibited a higher minimum inhibitory concentration to imipenem than A. baumannii without the ISA ba1 element. All four carbapenem-resistant A. genospecies 3 isolates contained bla IMP-1 and an IS Aba3–bla OXA-58-like gene. Three A. genospecies 13TU isolates contained an IS Aba3–bla OXA-58-like and either a bla IMP-1 or a bla VIM-11 gene. The five bla IMP-1-containing strains were resistant to imipenem and were positive for metallo-β-lactamase (MBL) activity by the Etest, and the two bla VIM-11-containing strains were susceptible to imipenem and were MBL-negative by Etest. Imipenem hydrolysis tests showed that the bla IMP-1-containing strains exhibited much higher imipenem-hydrolysing activity than the two bla VIM-11-containing strains. No transcripts of bla VIM-11 or bla OXA-58-like genes were detected. Analysis of outer membrane proteins showed that OprD was absent in the only bla IMP-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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