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Journal of Clinical Microbiology, February 2007, p. 453-460, Vol. 45, No. 2
0095-1137/07/$08.00+0     doi:10.1128/JCM.01971-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Horizontal Gene Transfer in a Polyclonal Outbreak of Carbapenem-Resistant Acinetobacter baumannii{triangledown}

Jubelle K. Valenzuela,1 Lee Thomas,1,2 Sally R. Partridge,1 Tanny van der Reijden,3 Lenie Dijkshoorn,3 and Jon Iredell1*

Centre for Infectious Diseases and Microbiology, University of Sydney,1 Institute for Clinical Pathology and Medical Research, Westmead Hospital, Sydney, New South Wales 2145, Australia,2 Department of Infectious Diseases, Leiden University Medical Center, Leiden, The Netherlands3

Received 22 September 2006/ Returned for modification 3 November 2006/ Accepted 6 November 2006

In the last few years, phenotypically carbapenem resistant Acinetobacter strains have been identified throughout the world, including in many of the hospitals and intensive care units (ICUs) of Australia. Genotyping of Australian ICU outbreak-associated isolates by pulsed-field gel electrophoresis of whole genomic DNA indicated that different strains were cocirculating within one hospital. The carbapenem-resistant phenotype of these and other Australian isolates was found to be due to carbapenem-hydrolyzing activity associated with the presence of the blaOXA-23 gene. In all resistant strains examined, the blaOXA-23 gene was adjacent to the insertion sequence ISAba1 in a structure that has been found in Acinetobacter baumannii strains of a similar phenotype from around the world; blaOXA-51-like genes were also found in all A. baumannii strains but were not consistently associated with ISAba1, which is believed to provide the promoter required for expression of linked antibiotic resistance genes. Most isolates were also found to contain additional antibiotic resistance genes within the cassette arrays of class 1 integrons. The same cassette arrays, in addition to the ISAba1-blaOXA-23 structure, were found within unrelated strains, but no common plasmid carrying these accessory genetic elements could be identified. It therefore appears that antibiotic resistance genes are readily exchanged between cocirculating strains in epidemics of phenotypically indistinguishable organisms. Epidemiological investigation of major outbreaks should include whole-genome typing as well as analysis of potentially transmissible resistance genes and their vehicles.

* Corresponding author. Mailing address: Centre for Infectious Diseases and Microbiology, Level 3, ICPMR Building, Westmead Hospital, Wentworthville, New South Wales 2145, Australia. Phone: (61-2) 9845 6255. Fax: (61-2) 9891 5317. E-mail: joni{at}icpmr.wsahs.nsw.gov.au.

{triangledown} Published ahead of print on 15 November 2006.

Journal of Clinical Microbiology, February 2007, p. 453-460, Vol. 45, No. 2
0095-1137/07/$08.00+0     doi:10.1128/JCM.01971-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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