<i>Pasteurella pestis</i>
            : Role of Pesticin I and Iron in Experimental Plague

Brubaker, Robert R.; Beesley, Earl D.; Surgalla, Michael J.

doi:10.1126/science.149.3682.422

Cited by 141 publications

(122 citation statements)

References 17 publications

Supporting

Mentioning

119

Contrasting

Order By: Relevance

“…Key support for the model came from results with a Y. pestis Pla Ϫ mutant. Consistent with previous reports (12,13,19), the LD 50 of our Pla Ϫ Y. pestis strain was Ͻ10 after i.v. inoculation, but Ϸ10 6 when injected ID (Table 1).…”

Section: Bubonic or Primary Septicemic Plague Can Follow Transmission Bysupporting

confidence: 93%

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

Sebbane¹,

Jarrett²,

Gardner

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

208

240

View full text Add to dashboard Cite

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.vector-borne disease

show abstract

Section: Bubonic or Primary Septicemic Plague Can Follow Transmission Bysupporting

confidence: 93%

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

Sebbane¹,

Jarrett²,

Gardner

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

208

240

View full text Add to dashboard Cite

show abstract

“…The 9.5-kb pPla plasmid encodes the Y. pestis plasminogen activator (Pla) (McDonough and Falkow 1989;Sodeinde and Goguen 1988). Although Pla is not required to produce a transmissible infection in the flea or to cause the low-incidence primary septicemic form of plague following flea-bite transmission, it is required for systemic dissemination and the development of bubonic plague following intradermal injection of Y. pestis by fleabite or by needle (Brubaker et al 1965;Hinnebusch et al 1998;Sebbane et al 2006;Sodeinde et al 1992). …”

Section: Arthropod-borne Transmission Factors Of Y Pestismentioning

confidence: 99%

“…More recent work indicates that instead of a role in producing a transmissible infection in the flea vector, the true biological role of Pla occurs after transmission. Plasminogen activation and other proteolytic activities of Pla are required for the development of bubonic plague, because they facilitate dissemination of Y. pestis from the skin and lymphatic system (Brubaker et al 1965;Korhonen et al 2004;Sebbane et al 2006;Sodeinde et al 1992). …”

Section: The Coagulase Model Of Proventricular Infectionmentioning

confidence: 99%

Yersinia pestis Biofilm in the Flea Vector and Its Role in the Transmission of Plague

Hinnebusch¹,

Erickson²

2008

Current Topics in Microbiology and Immunology

View full text Add to dashboard Cite

Transmission by fleabite is a relatively recent evolutionary adaptation of Yersinia pestis, the bacterial agent of bubonic plague. To produce a transmissible infection, Y. pestis grows as an attached biofilm in the foregut of the flea vector. Biofilm formation both in the flea foregut and in vitro is dependent on an extracellular matrix (ECM) synthesized by the Yersinia hms gene products. The hms genes are similar to the pga and ica genes of Escherichia coli and Staphylococcus epidermidis, respectively, that act to synthesize a poly-β-1,6-N-acetyl-dglucosamine ECM required for biofilm formation. As with extracellular polysaccharide production in many other bacteria, synthesis of the Hms-dependent ECM is controlled by intracellular levels of cyclic-di-GMP. Yersinia pseudotuberculosis, the food-and water-borne enteric pathogen from which Y. pestis evolved recently, possesses identical hms genes and can form biofilm in vitro but not in the flea. The genetic changes in Y. pestis that resulted in adapting biofilm-forming capability to the flea gut environment, a critical step in the evolution of vector-borne transmission, have yet to be identified. During a flea bite, Y. pestis is regurgitated into the dermis in a unique biofilm phenotype, and this has implications for the initial interaction with the mammalian innate immune response.

show abstract

“…When contemplating the clinical use of bacteriocins, one important consideration is their possible pathological effects. In early studies with partially purified bacteriocins (Montgomerie et al, 1973;Tagg & McGiven, 1972;Turnowsky et al, 1973) or strain pairs differing in their expression (Brubaker et al, 1965;Burrows, 1965;Smith, 1974), the data showed their potential toxicity, and also a relationship between the carriage of bacteriocinogenic factors and the virulence of certain strains. However, studies with purified substances have in many cases failed to confirm toxicity (Braude & Siemienski, 1965;Tagg et al, 1976).…”

Section: Bacteriocin Therapymentioning

confidence: 99%