Molecular characterization and antimicrobial susceptibility of Acinetobacter baumannii isolates obtained from two hospital outbreaks in Los Angeles County, California, USA. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Warner, Wayne; Kuang, Shan; Hernandez, Rina; Chong, Melissa; Ewing, Peter; Fleischer, Jen; Meng, Jia; Chu, Sheena; Terashita, Dawn; English, L'Tanya; Chen, Wangxue; Xu, H.
• Is Part Of: BMC infectious diseases. Volume 16:Issue 1(2016)
• Page Start: 1
• Page End: 13
• Publication Date: 2016-12
• Subjects: Acinetobacter baumannii -- Nosocomial outbreak -- Epidemiology -- Antimicrobial susceptibility -- Mechanism of resistance; Communicable diseases -- Periodicals; Sexually Transmitted Diseases -- Periodicals; 616.905
• DOI: 10.1186/s12879-016-1526-y
• Languages: English
• ISSNs: 1471-2334

Abstract

Abstract Background Antibiotic resistant strains ofAcinetobacter baumannii have been responsible for an increasing number of nosocomial infections including bacteremia and ventilator-associated pneumonia. In this study, we analyzed 38 isolates ofA. baumannii obtained from two hospital outbreaks in Los Angeles County for the molecular epidemiology, antimicrobial susceptibility and resistance determinants. Methods Pulsed field gel electrophoresis, tri-locus multiplex PCR and multi-locus sequence typing (Pasteur scheme) were used to examine clonal relationships of the outbreak isolates. Broth microdilution method was used to determine antimicrobial susceptibility of these isolates. PCR and subsequent DNA sequencing were employed to characterize antibiotic resistance genetic determinants. Results Trilocus multiplex PCR showed these isolates belong to Global Clones I and II, which were confirmed to ST1 and ST2, respectively, by multi-locus sequence typing. Pulsed field gel electrophoresis analysis identified two clonal clusters, one with 20 isolates (Global Clone I) and the other with nine (Global Clone II), which dominated the two outbreaks. Antimicrobial susceptibility testing using 14 antibiotics indicated that all isolates were resistant to antibiotics belonging to four or more categories of antimicrobial agents. In particular, over three fourth of 38 isolates were found to be resistant to both imipenem and meropenem. Additionally, all isolates were found to be resistant to piperacillin, four cephalosporin antibiotics, ciprofloxacin and levofloxacin. Resistance phenotypes of these strains to fluoroquinolones were correlated with point mutations ingyrA andparC genes that render reduced affinity to target proteins. ISAba1 was detected immediately upstream of thebla OXA–23 gene present in those isolates that were found to be resistant to both carbapenems. Class 1 integron-associated resistance gene cassettes appear to contribute to resistance to aminoglycoside antibiotics. Conclusion The two outbreaks were found to be dominated by two clonal clusters ofA. baumannii belonging to MLST ST1 and ST2. All isolates were resistant to antibiotics of at least four categories of antimicrobial agents, and their antimicrobial susceptibility profiles correlate well with genetic determinants. The results of this study will facilitate our understanding of the molecular epidemiology, antimicrobial susceptibility and mechanisms of resistance ofA. baumannii obtained from Los Angeles hospitals.