A Yersinia pestis‐specific DNA fragment encodes temperature‐dependent coagulase and fibrinolysin associated phenotypes

McDonough, Kathleen A.; Falkow, Stanley

doi:10.1111/j.1365-2958.1989.tb00225.x

Cited by 47 publications

(44 citation statements)

References 61 publications

(40 reference statements)

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“…The 100-kb pFra plasmid encodes Yersinia murine toxin (Ymt), a phospholipase D that greatly enhances survival of Y. pestis in the flea midgut (Hinnebusch et al 2002b). 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%

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

Hinnebusch¹,

Erickson²

2008

Current Topics in Microbiology and Immunology

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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.

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Section: Arthropod-borne Transmission Factors Of Y Pestismentioning

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

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“…These activities are encoded by the same gene, pla, which has been cloned and sequenced and is present in a 9.5-kb plasmid designated pPst, or pPCP1 [2,[4][5][6][7]. The modulation between coagulase and fibrinolytic activities is temperature-dependent.…”

Section: Introductionmentioning

confidence: 99%

Development, characterisation and diagnostic application of monoclonal antibodies against Yersinia pestis fibrinolysin and coagulase

Feodorova

Devdariani

2000

Journal of Medical Microbiology

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A library of monoclonal antibodies (MAbs) which recognised different epitopes of Yersinia pestis fibrinolysin (Fib) was developed. These MAbs were species-specific and demonstrated no cross-reaction in indirect immunofluorescence tests (IIFT) with other gram-negative bacteria possessing plasminogen activator activity. All the MAbs provided equally high levels of immunofluorescence with pPst þ Y. pestis strains cultivated at 378C and at 288C. In all cases, the MAbs inhibited both fibrinolytic and coagulase (Coag) activities of Y. pestis in Fib-activity inhibition and coagulase-activity inhibition reactions, and reacted with 35-and 37-kDa proteins of Y. pestis in immunoblotting, demonstrating bifunctional activity possibly similar to the properties of MAbs produced by hybrid hybridomas. On the basis of these and earlier studies, the immunochemical identity of Fib and Coag, two distinct subunits of a bifunctional fusion protein whose specific functional activity depends upon the temperature factor, was established. A new rapid, cheap, strictly specific and safe dot-ELISA based on the use of MAb against Y. pestis Fib (MAb-Fib) for reliable identification of Y. pestis strains was developed. This technique has great advantages over monoclonal diagnostic kits based on the use of MAb against Y. pestis fraction I (FI) because it allows detection of plague bacilli grown at 378C as well as at 288C. This dot-ELISA will be valuable as a clinical diagnostic tool and might be applicable to field studies and plague surveillance.

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“…Development of disease from peripheral injection routes depends on a plasminogen activator (Pla) encoded by the pla gene located on the 10-kb pPst plasmid that is unique to Y. pestis (10,11). Typical Pla Ϫ Y. pestis strains have greatly reduced virulence when inoculated s.c. but are fully virulent when inoculated directly into the blood stream (12,13).…”

mentioning

confidence: 99%

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.

213

243

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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

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A Yersinia pestis‐specific DNA fragment encodes temperature‐dependent coagulase and fibrinolysin associated phenotypes

Cited by 47 publications

References 61 publications

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

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

Development, characterisation and diagnostic application of monoclonal antibodies against Yersinia pestis fibrinolysin and coagulase

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

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