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Review
. 2012 Jun;15(3):239-46.
doi: 10.1016/j.mib.201202003. Epub 2012 Mar 7.

Yersinia--flea interactions and the evolution of the arthropod-borne transmission route of plague

Affiliations
Review

Yersinia--flea interactions and the evolution of the arthropod-borne transmission route of plague

Iman Chouikha et al. Curr Opin Microbiol. 2012 Jun.

Abstract

Yersinia pestis, the causative agent of plague, is unique among the enteric group of Gram-negative bacteria in relying on a blood-feeding insect for transmission. The Yersinia-flea interactions that enable plague transmission cycles have had profound historical consequences as manifested by human plague pandemics. The arthropod-borne transmission route was a radical ecologic change from the food-borne and water-borne transmission route of Yersinia pseudotuberculosis, from which Y. pestis diverged only within the last 20000 years. Thus, the interactions of Y. pestis with its flea vector that lead to colonization and successful transmission are the result of a recent evolutionary adaptation that required relatively few genetic changes. These changes from the Y. pseudotuberculosis progenitor included loss of insecticidal activity, increased resistance to antibacterial factors in the flea midgut, and extending Yersinia biofilm-forming ability to the flea host environment.

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Figures

Figure 1
Figure 1
The flea digestive tract. (A) Uninfected X. cheopis flea immediately after taking a blood meal, with the midgut filled with fresh blood. (B, C) Digestive tracts dissected from uninfected fleas showing the anatomy of the proventriculus and the simple midgut.
Figure 2
Figure 2
The Y. pestis life stage in the flea. (A) Digestive tract from an X. cheopis flea dissected two weeks after infection with wild-type Y. pestis. Arrows indicate large aggregates of bacteria, one of which fills the proventriculus. (B) Wild-type Y. pestis aggregate dissected from the midgut. The dense mass of bacteria is brown-pigmented due to hmsHFRS-dependent sequestration of hemin derived from the flea blood meal and is enveloped by a viscous layer (indicated by the bracket) composed of biofilm ECM and lipid components, also derived from the blood meal [16]. (C) Fluorescence micrograph of the digestive tract from a flea blocked with wild-type Y. pestis expressing green fluorescent protein (GFP). The PV is swollen due to the large bacterial mass that fills it. (D) Digestive tract from a flea dissected two weeks after infection with hmsHFRS Y. pestis. Multicellular aggregates of bacteria are present in the midgut but the proventriculus is uninfected. (E) Aggregate of hmsHFRS Y. pestis dissected from the midgut. The bacterial aggregate is not pigmented and not surrounded by ECM. (F) Fluorescence micrograph of the digestive tract from a flea infected with hmsHFRS Y. pestis expressing GFP. The infection is confined to the midgut and does not involve the proventriculus. Dissected digestive tracts in both Fig. 1 and Fig. 2 were mounted in H20, which clears red blood cell material from previous blood meals but not the bacterial aggregates. MG, midgut; PV, proventriculus; E, esophagus; ECM, extracellular matrix. Scale bars = 0.05 mm.

References

    1. Achtman M, Zurth K, Morelli G, Torrea G, Guiyoule A, Carniel E. Yersinia pestis, the cause of plague, is a recently emerged clone of Yersinia pseudotuberculosis. Proc. Natl. Acad. Sci. USA. 1999;96:14043–14048. - PMC - PubMed
    1. Achtman M, Morelli G, Zhu P, Wirth T, Diehl I, Kusecek B, Vogler AJ, Wagner DM, Allender CJ, Easterday WR, et al. Microevolution and history of the plague bacillus, Yersinia pestis. Proc Natl Acad Sci U S A. 2004;101:17837–17842. - PMC - PubMed
    1. Beard CB, Butler JF, Hall DW. Prevalence and biology of endosymbionts of fleas (Siphonaptera: Pulicidae) from dogs and cats in Alachua County. Florida. JMed Entomol. 1990;27:1050–1061. - PubMed
    1. Pornwiroon W, Kearney MT, Husseneder C, Foil LD, Macaluso KR. Comparative microbiota of Rickettsia felis-uninfected and -infected colonized cat fleas, Ctenocephalides felis. ISME J. 2007;1:394–402. - PubMed
    1. Jones RT, McCormick KF, Martin AP. Bacterial communitites of Bartonella-positive fleas: diversity and community assembly patterns. Appl. Environ. Microbiol. 2008;74:1667–1670. - PMC - PubMed

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