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Infection and Immunity, September 2009, p. 4102-4110, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.00398-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Identification of Specific and Universal Virulence Factors in Burkholderia cenocepacia Strains by Using Multiple Infection Hosts{triangledown} ,{dagger}

Susanne Uehlinger,1 Stephan Schwager,1 Steve P. Bernier,2,{ddagger} Kathrin Riedel,1 David T. Nguyen,2 Pamela A. Sokol,2 and Leo Eberl1*

Department of Microbiology, Institute of Plant Biology, University of Zurich, Zurich, Switzerland,1 Department of Microbiology and Infectious Diseases, University of Calgary, Calgary, Alberta, Canada2

Received 9 April 2009/ Returned for modification 14 May 2009/ Accepted 4 June 2009

Over the past few decades, strains of the Burkholderia cepacia complex have emerged as important pathogens for patients suffering from cystic fibrosis. Identification of virulence factors and assessment of the pathogenic potential of Burkholderia strains have increased the need for appropriate infection models. In previous studies, different infection hosts, including mammals, nematodes, insects, and plants, have been used. At present, however, the extent to which the virulence factors required to infect different hosts overlap is not known. The aim of this study was to analyze the roles of various virulence factors of two closely related Burkholderia cenocepacia strains, H111 and the epidemic strain K56-2, in a multihost pathogenesis system using four different model organisms, namely, Caenorhabditis elegans, Galleria mellonella, the alfalfa plant, and mice or rats. We demonstrate that most of the identified virulence factors are specific for one of the infection models, and only three factors were found to be essential for full pathogenicity in several hosts: mutants defective in (i) quorum sensing, (ii) siderophore production, and (iii) lipopolysaccharide biosynthesis were attenuated in at least three of the infection models and thus may represent promising targets for the development of novel anti-infectives.

* Corresponding author. Mailing address: Department of Microbiology, Institute of Plant Biology, University of Zurich, Zurich, Switzerland. Phone: 41-44-634-8220. Fax: 41-44-634-8204. E-mail: leberl{at}botinst.uzh.ch

{triangledown} Published ahead of print on 15 June 2009.

{dagger} Supplemental material for this article may be found at http://iai.asm.org/.

Editor: B. A. McCormick

{ddagger} Present address: Department of Microbiology and Immunology, Dartmouth Medical School, Hanover, NH.

Infection and Immunity, September 2009, p. 4102-4110, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.00398-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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