Wen-Wei Ku1, Che-Hsuang Kung1, Chi-Hung Lee1, Chih-Peng Tseng2, Ping-Feng Wu1, Shu-Chen Kuo3, Te-Li Chen4, Yi-Tzu Lee5, Fu-Der Wang6, Chang-Phone Fung6. 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.
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.
Authors: András Fodor; Birhan Addisie Abate; Péter Deák; László Fodor; Ervin Gyenge; Michael G Klein; Zsuzsanna Koncz; Josephat Muvevi; László Ötvös; Gyöngyi Székely; Dávid Vozik; László Makrai Journal: Pathogens Date: 2020-06-29