Changes in antimicrobial susceptibility and major clones of acinetobacter calcoaceticus-baumannii complex isolates from a single hospital in Korea over 7 years

Acinetobacter species have emerged as opportunistic nosocomial pathogens in intensive care units. Epidemic spread and outbreaks of multidrug-resistant or carbapenem-resistant Acinetobacter baumannii infections have been described worldwide. Species distribution, antimicrobial resistance and genotypes were investigated for Acinetobacter species isolates collected from a single institution in Korea over 7 years. Two hundred and eighty-seven Acinetobacter species isolates were collected from patients with bloodstream infections in one Korean hospital from 2003 to 2010. Most of them belonged to the Acinetobacter calcoaceticus- baumannii complex (94.4%). The most frequently isolated species was A. baumannii (44.2%), followed by Acinetobacter nosocomialis (formerly Acinetobacter genomic species 13TU) (34.1%). The proportion of A. baumannii increased significantly from 2008 to 2010 (40.4 to 50.0%). From 2008, imipenem and meropenem resistance rates increased significantly compared with 2003-2007 (12.9% and 20.5%, respectively, to 41.4% and 41.5%, respectively). An increased carbapenem resistance rate between the two periods was identified more clearly amongst A. baumannii isolates. Polymyxin-resistant A. baumannii isolates emerged in 2008-2010, despite the availability of few isolates. The increase of carbapenem resistance in A. baumannii might be due to the substitution of main clones. Although ST92 and ST69 were the most prevalent clones amongst A. baumannii in 2003-2007 (47.8% and 15.9%, respectively), ST75 and ST138 had increased in 2008-2010 (39.7% and 25.9%, respectively). Although ST92 showed moderate resistance to carbapenems, most ST75 and ST138 isolates were resistant to carbapenems. All ST75 and ST138 isolates, but only one ST92 isolate, contained the bla _OXA-23-like gene. Increased carbapenem resistance in Acinetobacter species and A. baumannii isolates might be due to the expansion of specific carbapenem-resistant clones.