P 2029. Emergence of carbapenem resistant Acinetobacter baumannii producing OXA-23 gene in a major Saudi Arabian hospitals Abdulrahman . A. Alsultan King Faisal University, College of Medicine, Department of Biomedical Sciences Alahsa 31982, Alhafouf P.O. Box 400 Kingdome of Saudi Arabia.
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Emergence of carbapenem resistant Acinetobacterbaumannii producing OXA-23 gene in a major Saudi Arabian hospitalsAbdulrahman. A. AlsultanKing Faisal University, College of Medicine, Department of Biomedical SciencesAlahsa 31982, Alhafouf P.O. Box 400 Kingdome of Saudi Arabia
Materials and Methods
Acinetobacter baumannii is an important and opportunisticpathogen associated with immuno-compromised patients in intensive care units (ICUs) worldwide. The increase of carbapenem resistance in Acinetobacter baumannii is a global concern since it limits the range of therapeutic alternatives. Carbapenem resistance in Acinetobacter baumannii is largely manifested by class D β-lactamases,comprising OXA-23-like, OXA-40-like, OXA-51-likeand OXA-58-like β-lactamases. Some of these enzymes are able to hydrolyze carbapenems and responsible in multi-drug resistance. OXA-51-like β-lactamases are present in all isolates of A. baumanniiand carbapenem resistance has sometimes been associated with this gene. The emergence of MDR A. baumannii has been reported in several hospitals in Kingdom of Saudi Arabia, the aim of this work is to investigate the disseminations of carbapenem resistance in A. baumannii in a major Saudi Arabian hospital.
Materials and Methods:
A total of 29 non-repetitive, strains collected between January 2011 and April 2011 from different specimens from King Faisal Specialist Hospital and Research Centre (KFSHRC) in Riyadh. All isolates were identified presumptively by the Vitek compact II system. PCR was used to identify not only the intrinsic blaOXA-51-like gene but also the genes encoding the blaOXA-23. The MIC of antibiotics was determined by dilution test according to BSAC guidelines.
Twenty-nine clinical isolates were identified as A. baumannii by having the intrinsic of blaOXA-51-like gene. All isolates except one were resistant to imipenem (MIC > 16), three of which were highly resistant (MIC > 32mg/L). The sensitive strain had an MIC ≤ 1mg/L. All isolates were also resistant to meropenem, 25 of which had MICs > 32mg/L, two isolates had MICs = 16 mg/L. One strain was intermediate (MIC > 4 mg/L) and another sensitive (MIC MIC ≤ 0.5 mg/L). The OXA-23 β‑lactamase was the cause of imipenem and meropenem-resistance in 14 strains, which were resistant to carbapenems because they carried this gene of β-lactamase and no other; there was one strain harbouring the OXA-23 β‑lactamase which was sensitive to both carbapenems.
The high level of multi-resistance in carbapenems in A. baumannii responsible for infection in those patients due to the dissimination of the OXA-23 β‑lactamases in this Saudi Arabian hospital.
Acinetobacter baumannii has become an important pathogen emerged in the recent years associated with a range of infections causing a significant health problems particularly in immunocompromised patients (1). Carbapenems are often used as the last drugs for treating sever A. baumannii infections but are being compromised due to the emergence of β-lactamase and carbapenemase of molecular class B and D (2). OXA carbapenemases are more reported in Europe (3). Moreover the genes encoding OXA-23-like and OXA-51-like enzymes (4) have been found to be linked with the mobile element ISAba1, while the OXA-58-like encoding gene adjacent to ISAba2, ISAba3 and IS18 (3).
The purpose of this study is to investigate the prevalence of carbapenem resistant in A. baumannii in Saudi Arabian hospital
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