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Journal of Bacteriology, March 2004, p. 1484-1492, Vol. 186, No. 5
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.5.1484-1492.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Bordetella Species Are Distinguished by Patterns of Substantial Gene Loss and Host Adaptation

C. A. Cummings,1,2,{dagger} M. M. Brinig,1,2,{dagger} P. W. Lepp,1,2 S. van de Pas,1,2,{ddagger} and D. A. Relman1,2,3*

Departments of Microbiology and Immunology,1 Medicine, Stanford University School of Medicine, Stanford, California 94305,2 VA Palo Alto Health Care System, Palo Alto, California 943043

Received 12 August 2003/ Accepted 10 November 2003

Pathogens of the bacterial genus Bordetella cause respiratory disease in humans and animals. Although virulence and host specificity vary across the genus, the genetic determinants of this diversity remain unidentified. To identify genes that may underlie key phenotypic differences between these species and clarify their evolutionary relationships, we performed a comparative analysis of genome content in 42 Bordetella strains by hybridization of genomic DNA to a microarray representing the genomes of three Bordetella species and by subtractive hybridization. Here we show that B. pertussis and B. parapertussis are predominantly differentiated from B. bronchiseptica by large, species-specific regions of difference, many of which encode or direct synthesis of surface structures, including lipopolysaccharide O antigen, which may be important determinants of host specificity. The species also exhibit sequence diversity at a number of surface protein-encoding loci, including the fimbrial major subunit gene, fim2. Gene loss, rather than gene acquisition, accompanied by the proliferation of transposons, has played a fundamental role in the evolution of the pathogenic bordetellae and may represent a conserved evolutionary mechanism among other groups of microbial pathogens.

* Corresponding author. Mailing address: VA Palo Alto Health Care System, 3801 Miranda Ave., 154T, Palo Alto, CA 94304. Phone: (650) 852-3308. Fax: (650) 852-3291. E-mail: relman{at}cmgm.stanford.edu.

{dagger} M.M.B. and C.A.C. contributed equally to this study.

{ddagger} Present address: Department of Clinical Oncology, Leiden University Medical Center, Leiden, The Netherlands.

Journal of Bacteriology, March 2004, p. 1484-1492, Vol. 186, No. 5
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.5.1484-1492.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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