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Variation in lipid A structure in the pathogenic yersiniae
The results suggest that the production of a less immunostimulatory form of LPS upon entry into the mammalian host is a conserved pathogenesis mechanism in the genus Yersinia, and that species‐specific lipid A forms may be important for life cycle and pathogenicity differences. Expand
Role of the Yersinia pestis Hemin Storage (hms) Locus in the Transmission of Plague by Fleas
Yersinia pestis hms mutants established long-term infection of the flea's midgut but failed to colonize the proventriculus, the site in the foregut where blockage normally develops, leading to a change in blood-feeding behavior and to efficient transmission of plague. Expand
Poor vector competence of fleas and the evolution of hypervirulence in Yersinia pestis.
It is shown that the infectivity of Y. pestis to its most proficient vector, the rat flea Xenopsylla cheopis, and subsequent transmission efficiency are both low, suggesting that the rapidly fatal gram-negative sepsis that typifies plague is a consequence of the high threshold bacteremia level that must be attained to complete the transmission cycle. Expand
Resistance of Yersinia pestis to Complement-Dependent Killing Is Mediated by the Ail Outer Membrane Protein
The role of Ail in infection of mice, Caenorhabditis elegans, and fleas was investigated and high-level expression of the three other Y. pestis Ail/Lom family proteins provided no protection against complement-mediated bacterial killing. Expand
Transmission of Yersinia pestis from an infectious biofilm in the flea vector.
It is shown that the hms genes are also required to produce an extracellular matrix and a biofilm in vitro, supporting the hypothesis that a transmissible infection in the flea depends on the development of aBiofilm on the hydrophobic, acellular surface of spines that line the interior of the proventriculus. Expand
The evolution of flea-borne transmission in Yersinia pestis.
Transmission by fleabite is a recent evolutionary adaptation that distinguishes Yersinia pestis, the agent of plague, from Yersinia pseudotuberculosis and all other enteric bacteria. The very closeExpand
Kinetics of disease progression and host response in a rat model of bubonic plague.
A model of bubonic plague using the inbred Brown Norway strain of Rattus norvegicus is developed to characterize the progression and kinetics of infection and the host immune response after intradermal inoculation of Y. pestis. Expand
Role of the Yersinia pestis plasminogen activator in the incidence of distinct septicemic and bubonic forms of flea-borne plague.
An evolutionary scenario in which plague first emerged as a flea-borne septicemic disease of limited transmissibility is supported, in which subsequent acquisition of the plasminogen activator gene by horizontal transfer enabled the bubonic form of disease and increased the potential for epidemic spread. Expand
Depolymerization of β-1,6-N-Acetyl-d-Glucosamine Disrupts the Integrity of Diverse Bacterial Biofilms
Enzymatic hydrolysis of poly-beta-1,6-GlcNAc, demonstrated for the first time by chromatography and mass spectrometry, disrupts biofilm formation by Escherichia coli and Staphylococcus epidermidis and by Yersinia pestis and Pseudomonas fluorescens, which possess pgaABCD homologues. Expand
Structural insights into Ail-mediated adhesion in Yersinia pestis.
A structural description of how a bacterial outer membrane protein uses a multivalent approach to bind host cells is constituted, and it is shown that a 40 kDa domain of laminin called LG4-5 specifically binds to Ail. Expand