Presence of the carbapenem-hydrolyzing oxacillinase Oxa-58 in an Acinetobacter phenon 6/ct13TU clinical isolate
Abstract number: P1512
Marti S., Sanchez-Cespedes J., Blasco M.D., Alba V., Vila J.
Objectives: The main nosocomial pathogen within the Acinetobacter genus is Acinetobacter baumannii. Carbapenems usually retain good activity against these microorganisms. In spite of this, carbapenem resistance in A. baumannii has been reported worldwide. The main aim of our study was to investigate the mechanism of resistance to imipenem (IP) in an Acinetobacter phenon 6/ct13TU clinical isolate.
Methods: The study was performed in two Acinetobacter spp. (Ac054 and Ac058) isolates collected from two Spanish hospital during the same period of time. The characterisation of these strains was done by ARDRA and the MICs of IP were determined by Etest. The detection of OXA-58 was done by PCR and sequencing with specific primers from A. baumannii. Expression of the OXA-58 gene was determined by RT-PCR using the specific primers for this gene and the 16S as internal control. The genetic location of the gene was investigated by using the genomic mapping with I-CeuI followed by Southern blot and double hybridisation with probes for the blaOXA-58 gene and for the 23S gene.
Results: One isolate was identified as A. baumannii (Ac058) and the other as Acinetobacter phenon 6/ct13TU (Ac054). Both isolates, as expected, were different by Pulse-Field Gel Electrophoresis. Presence of the OXA-58 gene was determined by PCR with specific primers. The OXA-58 genes were sequenced and presented 100% homology. Analysis of gene expression by RT-PCR also revealed that OXA-58 was expressed in both isolates. However, A. baumannii strain Ac058 had a MIC of IP >32 mg/L while Acinetobacter phenon 6/ct13TU strain Ac054 had a MIC of IP = 6 mg/L which implies the presence in A. baumannii of an additional mechanism of resistance to imipenem.
Conclusion: The OXA-58 gene, with 100% homology to the same gene found in A. baumannii, has been detected for the first time in an Acinetobacter phenon 6/ct13TU clinical isolate. Its location in a plasmid suggests that these resistance genes may be transferred from one species to another.
|Session name:||18th European Congress of Clinical Microbiology and Infectious Diseases|
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