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Journal of Bacteriology, December 2006, p. 8385-8394, Vol. 188, No. 24
0021-9193/06/$08.00+0 doi:10.1128/JB.01081-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
,
,
C. A. Cummings,3,4,
H. G. J. van der Heide,1
M. van Gent,1
S. Liew,3,4
D. A. Relman,3,4,5 and
F. R. Mooi1*
Laboratory for Vaccine Preventable Diseases, National Institute of Public Health and the Environment, Bilthoven, The Netherlands,1 Eijkman Winkler Institute, University Medical Center, Utrecht, The Netherlands,2 Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California,3 VA Palo Alto Health Care System, Palo Alto, California,4 Department of Medicine, Stanford University School of Medicine, Stanford, California5
Received 21 July 2006/ Accepted 2 October 2006
The recently discovered pathogen Bordetella holmesii has been isolated from the airways and blood of diseased humans. Genetic events contributing to the emergence of B. holmesii are not understood, and its phylogenetic position among the bordetellae remains unclear. To address these questions, B. holmesii strains were analyzed by comparative genomic hybridization (CGH) to a Bordetella pertussis microarray and by multilocus sequence typing. Both methods indicated substantial sequence divergence between B. pertussis and B. holmesii. However, CGH identified a putative pathogenicity island of 66 kb that is highly conserved between these species and contains several IS481 elements that may have been laterally transferred from B. pertussis to B. holmesii. This island contains, among other genes, a functional, iron-regulated locus encoding the biosynthesis, export, and uptake of the siderophore alcaligin. The acquisition of this genomic island by B. holmesii may have significantly contributed to its emergence as a human pathogen. Horizontal gene transfer between B. pertussis and B. holmesii may also explain the unusually high sequence identity of their 16S rRNA genes.
Published ahead of print on 13 October 2006.
Supplemental material for this article may be found at http://jb.asm.org/.
D.A.D. and C.A.C. contributed equally to this work.
Present address: Department of Microbiology and Immunology, University of Melbourne, Parkville, Victoria, Australia.
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