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J Med Microbiol 58 (2009), 1086-1091; DOI: 10.1099/jmm.0.008524-0
© 2009 Society for General Microbiology
ISSN 0022-2615

Triclosan resistance in clinical isolates of Acinetobacter baumannii

Yagang Chen, Borui Pi, Hua Zhou, Yunsong Yu and Lanjuan Li

State Key Laboratory for Diagnosis and Treatment of Infectious Disease, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, PR China

Correspondence
Yunsong Yu
yvys119{at}163.com

Received December 4, 2008
Accepted May 5, 2009

The susceptibility to triclosan of 732 clinical Acinetobacter baumannii isolates obtained from 25 hospitals in 16 cities in China from December 2004 to December 2005 was screened by using an agar dilution method. Triclosan MICs ranged between 0.015 and 16 mg l–1, and the MIC90 was 0.5 mg l–1, lower than the actual in-use concentration of triclosan. Twenty triclosan-resistant isolates (MICs ≥1 mg l–1) were characterized by antibiotic susceptibility, clonal relatedness, fabI mutation, fabI expression, and 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 artificially classified as low level (MICs 1–2 mg l–1) or high level (MICs ≥4 mg l–1). High-level triclosan resistance could be explained by a Gly95Ser mutation of FabI, whilst wild-type fabI was observed to be 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 on a background of intrinsic triclosan efflux.






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