Epidemiology and mechanism of resistance of an outbreak of multidrug-resistant Acinetobacter baumannii at in a Lebanese hospital
Abstract number: 1733_506
Di Popolo A., Khan A.U., Daoud Z., Bagattini M., Afif C., Triassi M., Hakimé N.I., Zarrilli R.
An epidemiological study to investigate an outbreak of multidrug-resistant Acinetobacter baumannii conducted at the Saint George University Hospital, Beirut, Lebanon. The first cases were observed in November 2004, when A. baumannii was isolated from 17 patients, 11 from medical-surgical intensive care unit (ICU), 6 from other wards. Since then, more than 30 cases were identified and the strain of Acinetobacter baumannii became a frequent isolate in our lab.
Genotype analysis of all A. baumannii strains isolated during the outbreak identified one major PFGE type B, that differed in more than 6 bands from one additional strain isolated from ICU of the hospital six months before (PFGE type A). All A. baumannii strains of PFGE type B showed an identical multi-resistant antibiotype, being susceptible to colistin and trimetropim-sulphomethoxazole, of intermediate susceptibility to ampicillin-sulbactam and meropenem, while resistant to all other antimicrobial tested. In these isolates, inhibition of OXA enzymes by 200 mM of NaCl reduced imipenem MIC by up to 8-fold. Molecular analysis of antimicrobial resistance genes showed that all epidemic A. baumannii strains harboured in their genomic DNA a class 1 integron containing the aacA4, orfX, and blaOXA-20 gene cassettes, an ampC gene and a blaoxa-51-like allele. Moreover, a blaoxa-58 gene surrounded by regulatory insertion sequence elements ISAba1 and ISAba3 was identified in a 21 kb plasmid DNA from A. baumannii strains of PFGE type B, but not PFGE type A. No amplification products were obtained from genomic DNA of epidemic strains of PFGE type B for blaIMP-type, blaVIM-type or blaSIM-type metallo-b-lactamase genes or blaoxa-23 or blaoxa-24 carbapenem-hydrolysing oxacillinases. Also, both carbapenem-susceptible A. baumannii strains of PFGE type A and carbapenem-resistant strains of PFGE type B expressed 26-kDa outer membrane protein CarO. Conjugation experiments demonstrated that resistance to imipenem, along with the blaoxa-58 gene, was transferred from A. baumannii strains of PFGE type B to those of PFGE type A.
The selection and the spread between different wards of a single A. baumannii clone producing OXA-58 carbapenem-hydrolysing oxacillinase were responsible for the increase of A. baumannii infections that occurred in Saint George University Hospital of Beirut, Lebanon. The epidemiologic pattern of the resistant organism vary from hospital to hospital, and control measures or therapeutic approaches should be customised to each institution.
|Session name:||European Society of Clinical Microbiology and Infectious Diseases|
|Location:||ICC, Munich, Germany|
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