Clonal spread of carbapenem-resistant Acinetobacter baumannii possessing blaOXA-23 in a Bulgarian hospital
Abstract number: P1503
Stoeva T., Higgins P.G., Bojkova K., Seifert H.
Objectives: To investigate the mechanism of carbapenem resistance (CR) in clinical isolates of Acinetobacter baumannii, collected during the period 19992006 from the University Hospital in Pleven, Bulgaria and to evaluate the clonal relationship between the isolates.
Methods: From October 1999 to September 2006, 29 CR and 15 carbapenem susceptible (CS) A. baumannii isolates, collected from different wards, were studied. Identification was confirmed by gyrB multiplex PCR and ARDRA. Antimicrobial susceptibility was tested by VITEK 2 and agar dilution method and the results were interpreted according to the current CLSI guidelines. Electrotransformation experiments were performed to determine carbapenem resistance as chromosomal- or plasmid-mediated. Detection of the carbapenemase encoding genes and the associated insertion sequences was performed by PCR, followed by sequence analysis. Isolates were genotyped by PFGE.
Results: All studied isolates revealed a multidrug resistance phenotype and possessed blaOXA-51-like and blaAmpC genes. In addition, a blaOXA-23-like gene was detected in all CR isolates. ISAba1 was located upstream of the blaOXA-23-like gene. Sequence analysis confirmed the presence of blaOXA-23. The unsuccessful electrotransformation experiments suggested chromosomal location of the blaOXA-23 gene. The CR isolates exhibited 2 PFGE pulsotypes. Pulsotype B dominated in the ICU between 1999 and 2000 and was also detected in three CS strains isolated from ICU patients during this period. Pulsotype A accounted for 24 CR strains and was spread among several wards during the period 20032006, but dominated in the ICU. However, one pulsotype A strain was already recovered in 1999.
Conclusions: The blaOXA-23 gene and ISAba1 were associated with carbapenem resistance. The increased rate of isolation of CR A. baumannii in the hospital during the period 19992006 was due to intrahospital dissemination of epidemic strains belonging to 2 clonal groups, A and B. These data demonstrate both the epidemic spread of CR A. baumannii and its longevity in the hospital environment.
|Session name:||18th European Congress of Clinical Microbiology and Infectious Diseases|
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