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Role of the Yersinia pestis plasminogen activator in the incidence of distinct septicemic and bubonic forms of flea-borne plague

2006/03/27 by Florent Sebbane, Clayton O. Jarrett, Donald J. Gardner +2 · 2 citations
Biochemistry, Genetics and Molecular Biology · Immunology and Microbiology · #Yersinia bacterium, plague, ectoparasites research #Vector-borne infectious diseases #Bacillus and Francisella bacterial research

paper · doi:10.1073/pnas.0509544103

openalex publication_date 2006/03/27 · openalex created_date 2016/06/24 · openalex updated_date 2026/07/22

Abstract

Yersinia pestis is transmitted by fleas and causes bubonic plague, characterized by severe local lymphadenitis that progresses rapidly to systemic infection and life-threatening septicemia. Here, we show that although flea-borne transmission usually leads to bubonic plague in mice, it can also lead to primary septicemic plague. However, intradermal injection of Y. pestis, commonly used to mimic transmission by fleabite, leads only to bubonic plague. A Y. pestis strain lacking the plasmid-encoded cell-surface plasminogen activator, which is avirulent by intradermal or s.c. injection, was able to cause fatal primary septicemic plague at low incidence, but not bubonic plague, when transmitted by fleas. The results clarify a long-standing uncertainty about the etiology of primary septicemic plague and support an evolutionary scenario in which plague first emerged as a flea-borne septicemic disease of limited transmissibility. Subsequent acquisition of the plasminogen activator gene by horizontal transfer enabled the bubonic form of disease and increased the potential for epidemic spread.

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