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.