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Yersinia pestis (YP) causes plague, and its potential for aerosol dissemination and rapid disease progression are of particular
concern for defence against bioterrorism. The high morbidity and mortality rates associated with plague and the recent
emergence of multidrug resistance makes YP a potential threat to humans. Growth of YP at temperatures of the flea vector
C) and of the mammalian host are known to induce different proteins, contributing to different virulence. Here, a study
comparing the disease progression of YP in a primary pneumonic mouse plague model following pre-incubation at 28?
C and at
C was conducted. Mice were exposed to two inhalational (intranasal and aerosol) routes of infection and the LD50, bacterial
dissemination, cytokine/chemokine production, and tissue damage at different time points over the course of infection were
determined. Pre-incubation of YP strain NCTC144 at 37?
C increased tissue dissemination and disease progression between
48 and 72h compared to at 28?
C. In both intranasal and aerosol model of infection there was an increase in the severity of
tissue injury that correlated with increased cytokine/chemokine expression at 37?
C. In the intranasal route, there was a distinct
difference in infection pattern between the two temperatures, with virulence higher at 37?
C. This distinction was absent in the
aerosol model. The present study correlates well with earlier reports of YP disease pattern in mice. Our study further confirms
that the virulence and pathogenesis of YP are dependant on incubation conditions and route of infection
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