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Published online ahead of print on 15 June 2009 as doi:10.1099/jmm.0.008524-0
Journal of Medical Microbiology 2009;58:1086.

J Med Microbiol (2009), DOI: 10.1099/jmm.0.008524-0
© 2009 Society for General Microbiology
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Triclosan resistance in clinical isolates of Acinetobacter baumannii

Yagang Chen, Borui Pi, Hua Zhou, Yun-Song Yu1 and Lanjuan Li

State Key Laboratory of Diagnosis and treatment for Infectious Disease, First Affiliated Hospital

1 E-mail: yvys119{at}163.com

Received December 4, 2008
Accepted May 5, 2009

The susceptibility of 732 clinical Acinetobacter baumannii isolates obtained from 25 hospitals in 16 cities in China through December 2004 to December 2005 to triclosan were screened by using agar dilution method. Triclosan MICs ranged between 0.015 and 16 mg/L and MIC90 was 0.5 mg/L, lower than the actual in-use concentration of triclosan. Twenty triclosan-resistant isolates (MICs ≥1 mg/L) were characterized by antibiotic susceptibility, clonal relatedness, fabI mutation, fabI expression, efflux pump phenotype and expression, to elucidate the resistance mechanism of A. baumannii to triclosan. The resistance rates of triclosan-resistant isolates to imipenem, levofloxacin, amikacin and tetracycline were higher than those of triclosan-sensitive isolates. Triclosan resistance was classified as low-level (MICs 1-2 mg/L) and high-levels (MICs ≥4 mg/L) artificially. High-level triclosan resistance was accounted for by Gly95Ser mutation of FabI. Wild-type fabI was observed overexpressed in low-level resistant isolates. Active efflux did not appear to be a major reason for acquired triclosan resistance, but acquisition of resistance appeared to be dependent upon a background of intrinsic triclosan efflux.






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