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University of Kentucky, Department of Microbiology and Immunology, MS415 Medical Center, Lexington, Kentucky 40536-0084, USA
Author for correspondence: Robert D. Perry. Tel: +1 606 323 6341. Fax: +1 606 257 8994. e-mail: rperry@pop.uky.edu
ABSTRACT
Summary: The haemin storage (Hms+) phenotype of Yersinia pestis enables this bacillus to form greenish/brown or red colonies on haemin or Congo Red agar plates, respectively, at 26 but not 37 °C. Escherichia coli strains that contain mutations in genes essential for siderophore biosynthesis, porphyrin generation and/or haemin transport remain unable to utilize exogenous haemin as a nutritional iron or porphyrin source when transformed with the cloned Y. pestis hmsHFRS locus. Further physiological analysis of the Hms+phenotype of Y. pestis strain KIM6+ suggests that the haemin and inorganic iron stored by the Hms system was not used nutritionally under subsequent iron-deficient conditions. In vitro analysis of the bactericidal effects of hydrogen peroxide, superoxide and nitric oxide showed that Hms-Y. pestis cells, in certain cases, were more susceptible than the Hms+parent cells to these reactive oxygen species at 26 and/or 37 °C. In adherence assays, a higher percentage of Hms+cells were associated with HeLa cells and normal human neutrophils, compared to Hms-cells. However, the Hms+phenotype did not provide any additional protection against the killing effects of neutrophils. Finally, LD50 analysis in subcutaneously infected mice showed that an Hms-strain was slightly more virulent than Hms+, indicating that the Hms phenotype is not essential for the pathogenesis of bubonic plague in mammals.
Present address: University of Alabama at Birmingham, Immunobiology Vaccine Center, 770 BBRB, 845 19th St So., Birmingham, AL 35294-2170, USA.
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