Exemplar Abstract for Yersinia pseudotuberculosis pestis Bercovier et al. 1981 and Yersinia pestis (Lehmann and Neumann 1896) van Loghem 1944 (Approved Lists 1980).

2003 ◽  
Author(s):  
Charles Thomas Parker ◽  
Dorothea Taylor ◽  
George M Garrity
Keyword(s):  
Yersinia Pestis ◽  
Yersinia Pseudotuberculosis

Effective discrimination of Yersinia pestis and Yersinia pseudotuberculosis by MALDI-TOF MS using multivariate analysis

Talanta ◽  
2021 ◽  
pp. 122640
Author(s):  
Bin Feng ◽  
Liyuan Shi ◽  
Haipeng Zhang ◽  
Haimei Shi ◽  
Chuanfan Ding ◽  
...  
Keyword(s):  
Multivariate Analysis ◽  
Yersinia Pestis ◽  
Yersinia Pseudotuberculosis ◽  
Maldi Tof Ms ◽  
Maldi Tof ◽  
Tof Ms

scholarly journals The Importance of the Small RNA Chaperone Hfq for Growth of Epidemic Yersinia pestis, but Not Yersinia pseudotuberculosis, with Implications for Plague Biology

2010 ◽  
Vol 192 (16) ◽  
pp. 4239-4245 ◽  
Author(s):  
Guangchun Bai ◽  
Andrey Golubov ◽  
Eric A. Smith ◽  
Kathleen A. McDonough
Keyword(s):  
Yersinia Pestis ◽  
Small Rna ◽  
Small Rnas ◽  
Yersinia Pseudotuberculosis ◽  
Etiologic Agent ◽  
Growth Restriction ◽  
Rna Chaperone ◽  
Unique Biology ◽  
Severe Growth

ABSTRACT Yersinia pestis, the etiologic agent of plague, has only recently evolved from Yersinia pseudotuberculosis. hfq deletion caused severe growth restriction at 37°C in Y. pestis but not in Y. pseudotuberculosis. Strains from all epidemic plague biovars were similarly affected, implicating Hfq, and likely small RNAs (sRNAs), in the unique biology of the plague bacillus.

scholarly journals A quadruplex real-time PCR assay for the detection of Yersinia pestis and its plasmids

2008 ◽  
Vol 57 (3) ◽  
pp. 324-331 ◽  
Author(s):  
Alvin Stewart ◽  
Benjamin Satterfield ◽  
Marissa Cohen ◽  
Kim O'Neill ◽  
Richard Robison
Keyword(s):  
Yersinia Pestis ◽  
Real Time ◽  
Real Time Pcr ◽  
Yersinia Pseudotuberculosis ◽  
Target Sequence ◽  
Health Departments ◽  
Pcr Assay ◽  
Virulence Plasmids ◽  
Taqman Probes ◽  
Sporadic Disease

Yersinia pestis, the aetiological agent of the plague, causes sporadic disease in endemic areas of the world and is classified as a National Institute of Allergy and Infectious Diseases Category A Priority Pathogen because of its potential to be used as a bioweapon. Health departments, hospitals and government agencies need the ability to rapidly identify and characterize cultured isolates of this bacterium. Assays have been developed to perform this function; however, they are limited in their ability to distinguish Y. pestis from Yersinia pseudotuberculosis. This report describes the creation of a real-time PCR assay using Taqman probes that exclusively identifies Y. pestis using a unique target sequence of the yihN gene on the chromosome. As with other Y. pestis PCR assays, three major genes located on each of the three virulence plasmids were included: lcrV on pCD1, caf1 on pMT1 and pla on pPCP1. The quadruplex assay was validated on a collection of 192 Y. pestis isolates and 52 near-neighbour isolates. It was discovered that only 72 % of natural plague isolates from the states of New Mexico and Utah harboured all three virulence plasmids. This quadruplex assay proved to be 100 % successful in differentiating Y. pestis from all near neighbours tested and was able to reveal which of the three virulence plasmids a particular isolate possessed.

scholarly journals Attenuated enzootic (pestoides) isolates of Yersinia pestis express active aspartase

Microbiology ◽  
2009 ◽  
Vol 155 (1) ◽  
pp. 198-209 ◽  
Author(s):  
Scott W. Bearden ◽  
Christopher Sexton ◽  
Joshua Pare ◽  
Janet M. Fowler ◽  
Cindy G. Arvidson ◽  
...  
Keyword(s):  
Yersinia Pestis ◽  
Yersinia Pseudotuberculosis ◽  
Amino Acid Position ◽  
Enzymic Activity ◽  
Broad Host Range ◽  
Missense Mutations ◽  
Tissue Invasion ◽  
Muroid Rodents ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Reduced Activity

It is established that Yersinia pestis, the causative agent of bubonic plague, recently evolved from enteropathogenic Yersinia pseudotuberculosis by undergoing chromosomal degeneration while acquiring two unique plasmids that facilitate tissue invasion (pPCP) and dissemination by fleabite (pMT). Thereafter, plague bacilli spread from central Asia to sylvatic foci throughout the world. These epidemic isolates exhibit a broad host range including man as opposed to enzootic (pestoides) variants that remain in ancient reservoirs where infection is limited to muroid rodents. Cells of Y. pseudotuberculosis are known to express glucose-6-phosphate dehydrogenase (Zwf) and aspartase (AspA); these activities are not detectable in epidemic Y. pestis due to missense mutations (substitution of proline for serine at amino position 155 of Zwf and leucine for valine at position 363 of AspA). In this study, functional Zwf was found in pestoides strains E, F and G but not seven other enzootic isolates; enzymic activity was associated with retention of serine at amino acid position 155. Essentially, full AspA activity occurred in pestoides isolates where valine (pestoides A, B, C and D) or serine (pestoides E, F, G and I) occupied position 363. Reduced activity occurred in strains Angola and A16, which contained phenylalanine at this position. The k cat but not K m of purified AspA from strain Angola was significantly reduced. In this context, aspA of the recently described attenuated enzootic microtus biovar encodes active valine at position 363, further indicating that functional AspA is a biomarker for avirulence of Y. pestis in man.

scholarly journals Identification of gmhA, a Yersinia pestis Gene Required for Flea Blockage, by Using a Caenorhabditis elegans Biofilm System

2005 ◽  
Vol 73 (11) ◽  
pp. 7236-7242 ◽  
Author(s):  
Creg Darby ◽  
Sandya L. Ananth ◽  
Li Tan ◽  
B. Joseph Hinnebusch
Keyword(s):  
Caenorhabditis Elegans ◽  
Yersinia Pestis ◽  
Biofilm Formation ◽  
Yersinia Pseudotuberculosis ◽  
C Elegans ◽  
Transposon Insertion ◽  
Insertion Mutants ◽  
Random Screening

ABSTRACT Yersinia pestis, the cause of bubonic plague, blocks feeding by its vector, the flea. Recent evidence indicates that blockage is mediated by an in vivo biofilm. Y. pestis and the closely related Yersinia pseudotuberculosis also make biofilms on the cuticle of the nematode Caenorhabditis elegans, which block this laboratory animal's feeding. Random screening of Y. pseudotuberculosis transposon insertion mutants with a C. elegans biofilm assay identified gmhA as a gene required for normal biofilms. gmhA encodes phosphoheptose isomerase, an enzyme required for synthesis of heptose, a conserved component of lipopolysaccharide and lipooligosaccharide. A Y. pestis gmhA mutant was constructed and was severely defective for C. elegans biofilm formation and for flea blockage but only moderately defective in an in vitro biofilm assay. These results validate use of the C. elegans biofilm system to identify genes and pathways involved in Y. pestis flea blockage.

scholarly journals Early evolutionary loss of the lipid A modifying enzyme PagP resulting in innate immune evasion in Yersinia pestis

2020 ◽  
Vol 117 (37) ◽  
pp. 22984-22991 ◽  
Author(s):  
Courtney E. Chandler ◽  
Erin M. Harberts ◽  
Mark R. Pelletier ◽  
Iyarit Thaipisuttikul ◽  
Jace W. Jones ◽  
...  
Keyword(s):  
Yersinia Pestis ◽  
Immune Evasion ◽  
Lipid A ◽  
Yersinia Pseudotuberculosis ◽  
Innate Immune ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Structural Modifications ◽  
Tlr4 Signaling Pathway ◽  
Innate Immune Evasion

Immune evasion through membrane remodeling is a hallmark of Yersinia pestis pathogenesis. Yersinia remodels its membrane during its life cycle as it alternates between mammalian hosts (37 °C) and ambient (21 °C to 26 °C) temperatures of the arthropod transmission vector or external environment. This shift in growth temperature induces changes in number and length of acyl groups on the lipid A portion of lipopolysaccharide (LPS) for the enteric pathogens Yersinia pseudotuberculosis (Ypt) and Yersinia enterocolitica (Ye), as well as the causative agent of plague, Yersinia pestis (Yp). Addition of a C16 fatty acid (palmitate) to lipid A by the outer membrane acyltransferase enzyme PagP occurs in immunostimulatory Ypt and Ye strains, but not in immune-evasive Yp. Analysis of Yp pagP gene sequences identified a single-nucleotide polymorphism that results in a premature stop in translation, yielding a truncated, nonfunctional enzyme. Upon repair of this polymorphism to the sequence present in Ypt and Ye, lipid A isolated from a Yp pagP+ strain synthesized two structures with the C16 fatty acids located in acyloxyacyl linkage at the 2′ and 3′ positions of the diglucosamine backbone. Structural modifications were confirmed by mass spectrometry and gas chromatography. With the genotypic restoration of PagP enzymatic activity in Yp, a significant increase in lipid A endotoxicity mediated through the MyD88 and TRIF/TRAM arms of the TLR4-signaling pathway was observed. Discovery and repair of an evolutionarily lost lipid A modifying enzyme provides evidence of lipid A as a crucial determinant in Yp infectivity, pathogenesis, and host innate immune evasion.

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