ABSTRACT
The aim of the current study was to describe the occurrence of the blaOXA-23 gene and the ISAba1 element in imipenem-susceptible Acinetobacter baumannii strains. By performing the polymerase chain reaction mapping using combinations of ISAba1 forward primers and the blaOXA-23-like gene reverse primers, we demonstrated that the ISAba1 element did not occur upstream of the blaOXA-23 gene in five of 31 isolates, which explained the lack of resistance to imipenem despite the presence of the blaOXA-23 gene. All of the blaOXA-23-positive isolates were susceptible to imipenem and meropenem with minimal inhibitory concentration ≤ 4 µg/mL. Pulsed-field gel electrophoresis analysis revealed four genotypes among the five blaOXA-23-positive isolates. The current report of the blaOXA-23 gene in imipenem-susceptible isolates provided evidence that this gene may be silently spread in a hospital environment and highlighted the threat of undetected reservoirs of carbapenemase genes.
Subject(s)
Acinetobacter baumannii/drug effects , Anti-Bacterial Agents/pharmacology , Drug Resistance, Bacterial/genetics , Imipenem/pharmacology , beta-Lactamases/genetics , Acinetobacter baumannii/enzymology , Acinetobacter baumannii/genetics , Disk Diffusion Antimicrobial Tests , Electrophoresis, Gel, Pulsed-Field , Humans , Polymerase Chain ReactionABSTRACT
The aim of the current study was to describe the occurrence of the blaOXA-23 gene and the ISAba1 element in imipenem-susceptible Acinetobacter baumannii strains. By performing the polymerase chain reaction mapping using combinations of ISAba1 forward primers and the blaOXA-23-like gene reverse primers, we demonstrated that the ISAba1 element did not occur upstream of the blaOXA-23 gene in five of 31 isolates, which explained the lack of resistance to imipenem despite the presence of the blaOXA-23 gene. All of the blaOXA-23-positive isolates were susceptible to imipenem and meropenem with minimal inhibitory concentration < 4 µg/mL. Pulsed-field gel electrophoresis analysis revealed four genotypes among the five blaOXA-23-positive isolates. The current report of the blaOXA-23 gene in imipenem-susceptible isolates provided evidence that this gene may be silently spread in a hospital environment and highlighted the threat of undetected reservoirs of carbapenemase genes.
Subject(s)
Humans , Acinetobacter baumannii , Anti-Bacterial Agents , Drug Resistance, Bacterial , Imipenem , beta-Lactamases , Acinetobacter baumannii/enzymology , Acinetobacter baumannii , Disk Diffusion Antimicrobial Tests , Electrophoresis, Gel, Pulsed-Field , Polymerase Chain ReactionABSTRACT
The present study reports the dissemination of multidrug-resistant (MDR) OXA-23-producing Acinetobacter baumannii clones throughout hospitals in Rio de Janeiro, Brazil. A total of 110 imipenem-resistant A. baumannii isolates were obtained from January 2006 to September 2007 in eight hospitals. The modified Hodge test was performed to screen for carbapenemase production. Polymerase chain reaction (PCR) and DNA sequencing were performed for the detection of bla(IMP), bla(VIM), bla(OXA-23-like), bla(OXA-24-like), bla(OXA-58) and the class 1 integron. Isolates were typed by pulsed-field gel electrophoresis (PFGE) following digestion with ApaI. All the isolates were MDR and 96 (87.3%) produced the carbapenemase OXA-23. No isolates produced OXA-24, OXA-58 or the metallo-beta-lactamases IMP and VIM. The class 1 integron was absent in all isolates. The A. baumannii isolates were separated into five genotypes, with the highest prevalence of genotype A (71.8%) followed by genotype B (22.7%). Genotype A was present in seven hospitals, whilst genotype B had spread in five hospitals. The OXA-23-producing isolates belonged to all genotypes. The presence of MDR OXA-23-producing A. baumannii in different hospitals in Rio de Janeiro emphasises the need to control the use of carbapenems and to prevent the spread of these organisms in Rio de Janeiro.
