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J Microbiol Immunol Infect. 2015 Feb;48(1):57-64. doi: 10.1016/j.jmii.2013.07.005. Epub 2013 Sep 21.

Evolution of carbapenem resistance in Acinetobacter baumannii: an 18-year longitudinal study from a medical center in northern Taiwan.

Author information

1
Division of Infectious Diseases, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
2
Division of Infectious Diseases, Department of Medicine, Cheng Hsin General Hospital, Taipei, Taiwan.
3
National Institute of Infectious Diseases and Vaccinology, National Health Research Institute, Maoli County, Taiwan; School of Medicine, National Yang Ming University, Taipei, Taiwan.
4
School of Medicine, National Yang Ming University, Taipei, Taiwan.
5
School of Medicine, National Yang Ming University, Taipei, Taiwan; Department of Emergency Medicine, Taipei Veterans General Hospital, Taipei, Taiwan. Electronic address: yitzulee@gmail.com.
6
Division of Infectious Diseases, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan; School of Medicine, National Yang Ming University, Taipei, Taiwan.

Abstract

BACKGROUND:

Carbapenem-resistant Acinetobacter baumannii has emerged as an important cause of nosocomial infections with high morbidity and mortality. The carbapenemases, especially class D carbapenem-hydrolyzing oxacillinases (CHDLs), play an important role, but the relationship between their prevalence trend and carbapenem resistance remains unclear.

MATERIALS AND METHODS:

Between 1995 and 2012, we collected 667 isolates of A. baumannii from a single medical center in northern Taiwan. Pulsed-field gel electrophoresis (PFGE) was used to determine clonality. Antimicrobial susceptibility was determined. Carbapenemase genes and associated genetic structures were detected by polymerase chain reaction.

RESULTS:

Isolates were heterogeneous on PFGE. Susceptibility to carbapenem decreased steadily over the study period from 88.1% (2001-2003) to <25% (2010-2012), whereas the isolates remained susceptible to colistin (nearly 100%) and partially susceptible to tigecycline (80%). Starting in 2001, isolates carrying the ISAba1-blaOXA-51-like allele were consistently identified. Isolates containing the transposons Tn2006 or Tn2008 first appeared in 2007 with increasing carriage rates from 17.5% (2007-2009) to 50.0% (2010-2012). The IS1008-ΔISAba3-blaOXA-58-like, blaOXA-72 and metallo-β-lactamase genes were detected only sporadically. Isolates carrying CHDL genes were resistant to multiple drugs, including carbapenem, but remained susceptible to colistin (100.0%).

CONCLUSION:

Increased carbapenem resistance in A. baumannii may be caused by the increased prevalence of isolates containing the ISAba1-blaOXA-51-like allele and the transposons Tn2006 and Tn2008.

KEYWORDS:

ISAba1-bla(OXA-23-like); ISAba1-bla(OXA-51-like); Tn2006; Tn2008

PMID:
24064289
DOI:
10.1016/j.jmii.2013.07.005
[Indexed for MEDLINE]
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