Affiliation:
1. Department of Veterinary Pathobiology, University of Missouri, Columbia, Missouri
Abstract
ABSTRACT
Yersinia pestis
causes primary pneumonic plague in many mammalian species, including humans, mice, and rats. Virulent
Y. pestis
strains undergo frequent spontaneous deletion of a 102-kb chromosomal DNA fragment, known as the pigmentation (
pgm
) locus, when grown in laboratory media, yet this locus is present in every virulent isolate. The
pgm
locus encodes, within a high-pathogenicity island, siderophore biosynthesis genes that are required for growth in the mammalian host when inoculated by peripheral routes. Recently, higher challenge doses of nonpigmented
Y. pestis
were reported to cause fatal pneumonic plague in mice, suggesting a useful model for studies of virulence and immunity. In this work, we show that intranasal infection of BALB/c mice with nonpigmented
Yersinia pestis
does not result in pneumonic plague. Despite persistent bacterial colonization of the lungs and the eventual death of infected mice, pulmonary inflammation was generally absent, and there was no disease pathology characteristic of pneumonic plague. Iron given to mice at the time of challenge, previously shown to enhance the virulence of
pgm
-deficient strains, resulted in an accelerated disease course, with less time to bacteremia and lethality, but lung inflammation and pneumonia were still absent. We examined other rodent models and found differences in lung inflammatory responses, some of which led to clearance and survival even when high challenge doses were used. Together, the results suggest that the
Y. pestis pgm
locus encodes previously unappreciated virulence factors required for the induction of pneumonic plague that are independent of iron scavenging from the mammalian host.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
40 articles.
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