ABSTRACT
Included among the defined virulence properties of the human pathogenic Yersinia species are iron acquisition systems. The connection between iron metabolism and disease outcome was established by Jackson and Burrows (Jackson and Burrows, 1956) who observed that non-pigmented (Pgm-) mutants of Yersinia pestis were avirulent unless injected into mice with iron or hemin. These Pgm-isolates, which failed to bind large quantities of exogenous hemin and form greenish-brown colonies at 26°C, likely arose from deletion of a 102-kb chromosomal region now termed the pgm locus (Fetherston et al., 1992; Lucier and Brubaker, 1992). The pgm locus contains the heminstorage (hms) locus that is required for the characteristic hemin-adsorption and is essential for the blockage of the flea proventricular valve (Hinnebusch et al., 1996; see also Chapter 4 of this book). However, the Hms system is not involved in iron or heme acquisition or storage for nutritional use by the bacterium (Lillard et al., 1999). The loss of mammalian virulence results from the deletion of the yersiniabactin (Ybt) siderophoredependent iron transport system encoded by a high pathogenicity island (HPI; see Chapter 14 of this book) within the pgm locus. The Ybt system is critical for the pathogenesis of all three pathogenic Yersinia-Y. pestis, Yersinia enterocolitica, and Yersinia pseudotuberculosis. Extensive analysis of iron and heme transport systems has
been performed in the first two organisms. Y. pseudotuberculosis and Y. pestis are closely related, thus systems encoded by Y. pestis are most likely also present in Y. pseudotuberculosis but have not been experimentally examined. The genomes of Y. pestis KIM10+ (biotype mediaevalis) and CO92 (biotype orientalis) have been sequenced and analysis has revealed 12 potential inorganic iron or heme transport systems.
