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Infection and Immunity, March 2007, p. 1463-1472, Vol. 75, No. 3
0019-9567/07/$08.00+0 doi:10.1128/IAI.00372-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Departments of Molecular Microbiology,1 Pediatrics, Washington University School of Medicine, St. Louis, Missouri 631102
Received 7 March 2006/ Returned for modification 10 May 2006/ Accepted 15 December 2006
Iron acquisition systems are essential for the in vivo growth of bacterial pathogens. Despite the epidemiological importance of Klebsiella pneumoniae, few experiments have examined the importance of siderophores in the pathogenesis of this species. A previously reported signature-tagged mutagenesis screen identified an attenuated strain that featured an insertional disruption in ybtQ, which encodes a transporter for the siderophore yersiniabactin. We used this finding as a starting point to evaluate the importance of siderophores in the physiology and pathogenesis of K. pneumoniae. Isogenic strains carrying in-frame deletions in genes required for the synthesis of either enterobactin or yersiniabactin were constructed, and the growth of these mutants was examined both in vitro and in vivo using an intranasal infection model. The results suggest divergent functions for each siderophore in different environments, with enterobactin being more important for growth in vitro under iron limitation than in vivo and the reverse being true for the yersiniabactin locus. These observations represent the first examination of isogenic mutants in iron acquisition systems for K. pneumoniae and may indicate that the acquisition of nonenterobactin siderophores is an important step in the evolution of virulent enterobacterial strains.
Published ahead of print on 12 January 2007.
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