Characterisation of carbapenem-resistant Acinetobacter baumannii carrying different OXA-type carbapenemases from two hospital outbreaks in Berlin, Germany
Abstract number: R2312
Higgins P.G., Kohlenberg A., Seifert H.
Methods: Non-duplicate A. baumannii isolates were collected between June, 2005 and November, 2006 from clinical specimens from patients hospitalised on different wards in hospital 1 and between March and June, 2007 from patients hospitalised in hospital 2, respectively. Species identification was confirmed by gyrB multiplex PCR and ARDRA. Antimicrobial susceptibility was determined by VITEK 2 and agar dilution methods. Detection of IMP-, VIM- and OXA-type carbapenemases was performed by PCR. Epidemiological typing of isolates was performed by RAPD and PFGE.
Results: Forty-nine and fourteen A. baumannii isolates were collected from hospitals 1 and 2, respectively. Data on the CR isolates is summarised in the table. Molecular typing revealed that isolates from hospital 1 had 6 PFGE patterns (A-D, G, H), of which pattern A was the most prevalent. Patterns A1-A4 (5 isolates) were closely related to pattern A. Isolates with patterns A2, A3, B and C were isolated once each and were carbapenem-sensitive. Hospital 2 yielded two PFGE patterns, I and J, of which I was the predominant strain. All but the 4 isolates from hospital 1 mentioned above were resistant to all penicillins, cephalosporins, ciprofloxacin, gentamicin, tobramycin, amikacin, imipenem, and meropenem, and remained susceptible only to colistin, i.e. isolates were pandrug-resistant. All A. baumannii isolates carried the intrinsic OXA-51-like gene. With the exception of PFGE type H, all CRAb isolates had either an OXA-23-like, OXA-58-like or OXA-24-like gene. One isolate with PFGE pattern G carried an OXA-58-like and an OXA-24-like gene. PFGE type H was negative for IMP- or VIM-type metallo carbapenemases.
Conclusion: Carbapenem resistance was associated with the spread of distinct clonal strains that carried an OXA-type carbapenemase. In hospital 1 the predominant strain had closely-related carbapenem-sensitive isolates. Resistance was associated with this strain acquiring an OXA-23-like or OXA-58-like gene while one isolate has acquired both of these genes. Molecular typing of all the CRAb isolates reveals that there was no inter-hospital spread of CRAb, but rather it is the dissemination in two different locations of strains that have acquired an OXA-carbapenemase.
|Session name:||18th European Congress of Clinical Microbiology and Infectious Diseases|
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