Yersinia pestis and plague

2003 ◽  
Vol 31 (1) ◽  
pp. 104-107 ◽  
Author(s):  
R.W. Titball ◽  
J. Hill ◽  
D.G. Lawton ◽  
K.A. Brown
Keyword(s):  
Host Cell ◽  
Yersinia Pestis ◽  
Genome Sequence ◽  
Yersinia Pseudotuberculosis ◽  
Cell Types ◽  
Mammalian Host ◽  
Aetiological Agent ◽  
Mild Disease ◽  
Regulatory Systems ◽  
Obligate Pathogen

Yersinia pestis is the aetiological agent of plague, a disease of humans that has potentially devastating consequences. Evidence indicates that Y. pestis evolved from Yersinia pseudotuberculosis, an enteric pathogen that normally causes a relatively mild disease. Although Y. pestis is considered to be an obligate pathogen, the lifestyle of this organism is surprisingly complex. The bacteria are normally transmitted to humans from a flea vector, and Y. pestis has a number of mechanisms which allow survival in the flea. Initially, the bacteria have an intracellular lifestyle in the mammalian host, surviving in macrophages. Later, the bacteria adopt an extracellular lifestyle. These different interactions with different host cell types are regulated by a number of systems, which are not well characterized. The availability of the genome sequence for this pathogen should now allow a systematic dissection of these regulatory systems.

scholarly journals Yersinia pestis--etiologic agent of plague.

1997 ◽  
Vol 10 (1) ◽  
pp. 35-66 ◽  
Author(s):  
R D Perry ◽  
J D Fetherston
Keyword(s):  
Yersinia Pestis ◽  
Etiologic Agent ◽  
Clinical Aspects ◽  
Virulence Determinants ◽  
Health Issues ◽  
Regulatory Systems ◽  
Wide Range ◽  
Parasite Relationship ◽  
Obligate Pathogen ◽  
Host Parasite

Plague is a widespread zoonotic disease that is caused by Yersinia pestis and has had devastating effects on the human population throughout history. Disappearance of the disease is unlikely due to the wide range of mammalian hosts and their attendant fleas. The flea/rodent life cycle of Y. pestis, a gram-negative obligate pathogen, exposes it to very different environmental conditions and has resulted in some novel traits facilitating transmission and infection. Studies characterizing virulence determinants of Y. pestis have identified novel mechanisms for overcoming host defenses. Regulatory systems controlling the expression of some of these virulence factors have proven quite complex. These areas of research have provide new insights into the host-parasite relationship. This review will update our present understanding of the history, etiology, epidemiology, clinical aspects, and public health issues of plague.

scholarly journals Expression of heterologous O-antigen in Yersinia pestis KIM does not affect virulence by the intravenous route

2003 ◽  
Vol 52 (4) ◽  
pp. 289-294 ◽  
Author(s):  
P.C. F. Oyston ◽  
J.L. Prior ◽  
S. Kiljunen ◽  
M. Skurnik ◽  
J. Hill ◽  
...  
Keyword(s):  
Antimicrobial Peptides ◽  
Yersinia Pestis ◽  
Yersinia Enterocolitica ◽  
Yersinia Pseudotuberculosis ◽  
Intravenous Route ◽  
Aetiological Agent ◽  
Wild Type ◽  
Bubonic Plague ◽  
Metabolic Burden ◽  
O Antigen

All strains of Yersinia pestis examined have been found to lack an O-antigen. In other members of the Enterobacteriaceae, the rough phenotype often results in attenuation. However, Y. pestis is the aetiological agent of bubonic plague. In evolving from the ancestral enteropathogenic Yersinia pseudotuberculosis, and with the development of an arthropod-vectored systemic pathogenesis, smooth LPS production is not necessary for Y. pestis virulence and the metabolic burden has been alleviated by inactivation of the O-antigen biosynthetic operon. To investigate this, Y. pestis strain KIM D27 was transformed with a plasmid carrying the operon encoding the O-antigen of Yersinia enterocolitica O : 3. Expression of the O-antigen could be detected in silver-stained gels. The receptor for bacteriophage ϕYeO3-12 has been shown to be O-antigen, and infection by this bacteriophage results in lysis of Y. enterocolitica O : 3. Expression of the O-antigen in Y. pestis conferred sensitivity to lysis by ϕYeO3-12. The O-antigen-expressing clone was shown to be as virulent in mice by the intravenous route of challenge as the rough wild-type. Assays showed no alteration in the ability of Y. pestis to resist lysis by cationic antimicrobial peptides, serum or polymyxin.

scholarly journals Expression of Anaplasma marginale Ankyrin Repeat-Containing Proteins during Infection of the Mammalian Host and Tick Vector

2011 ◽  
Vol 79 (7) ◽  
pp. 2847-2855 ◽  
Author(s):  
Solomon S. Ramabu ◽  
David A. Schneider ◽  
Kelly A. Brayton ◽  
Massaro W. Ueti ◽  
Telmo Graça ◽  
...  
Keyword(s):  
Host Cell ◽  
Nuclear Localization ◽  
Cell Nucleus ◽  
Anaplasma Marginale ◽  
Cell Types ◽  
Mammalian Host ◽  
Specific Cell ◽  
Content Type ◽  
Tick Vector ◽  
Host Cell Nucleus

ABSTRACTTransmission of tick-borne pathogens requires transition between distinct host environments with infection and replication in host-specific cell types.Anaplasma marginaleillustrates this transition: in the mammalian host, the bacterium infects and replicates in mature (nonnucleated) erythrocytes, while in the tick vector, replication occurs in nucleated epithelial cells. We hypothesized that proteins containing ankyrin motifs would be expressed byA. marginaleonly in tick cells and would traffic to the infected host cell nucleus.A. marginaleencodes three proteins containing ankyrin motifs, an AnkA orthologue (the AM705 protein), AnkB (the AM926 protein), and AnkC (the AM638 protein). All threeA. marginaleAnks were confirmed to be expressed during intracellular infection: AnkA is expressed at significantly higher levels in erythrocytes, AnkB is expressed equally by both infected erythrocytes and tick cells, and AnkC is expressed exclusively in tick cells. There was no evidence of any of the Ank proteins trafficking to the nucleus. Thus, the hypothesis that ankyrin-containing motifs were predictive of cell type expression and nuclear localization was rejected. In contrast, AnkA orthologues in the closely relatedA. phagocytophilumandEhrlichia chaffeensishave been shown to localize to the host cell nucleus. This difference, together with the lack of a nuclear localization signal in any of the AnkA orthologues, suggests that trafficking may be mediated by a separate transporter rather than by endogenous signals. Selection for divergence in Ank function amongAnaplasmaandEhrlichiaspp. is supported by both locus and allelic analyses of genes encoding orthologous proteins and their ankyrin motif compositions.

scholarly journals Evaluation of the Role of theopgGHOperon in Yersinia pseudotuberculosis and Its Deletion during the Emergence of Yersinia pestis

2015 ◽  
Vol 83 (9) ◽  
pp. 3638-3647 ◽  
Author(s):  
Kévin Quintard ◽  
Amélie Dewitte ◽  
Angéline Reboul ◽  
Edwige Madec ◽  
Sébastien Bontemps-Gallo ◽  
...  
Keyword(s):  
Yersinia Pestis ◽  
Cell Size ◽  
Biofilm Formation ◽  
Yersinia Pseudotuberculosis ◽  
Acyl Carrier Protein ◽  
Size Control ◽  
Growth Conditions ◽  
Mammalian Host ◽  
Dickeya Dadantii ◽  
Content Type

TheopgGHoperon encodes glucosyltransferases that synthesize osmoregulated periplasmic glucans (OPGs) from UDP-glucose, using acyl carrier protein (ACP) as a cofactor. OPGs are required for motility, biofilm formation, and virulence in various bacteria. OpgH also sequesters FtsZ in order to regulate cell size according to nutrient availability.Yersinia pestis(the agent of flea-borne plague) lost theopgGHoperon during its emergence from the enteropathogenYersinia pseudotuberculosis. When expressed in OPG-negative strains ofEscherichia coliandDickeya dadantii,opgGHfromY. pseudotuberculosisrestored OPGs synthesis, motility, and virulence. However,Y. pseudotuberculosisdid not produce OPGs (i) under various growth conditions or (ii) when overexpressing itsopgGHoperon, itsgalUFoperon (governing UDP-glucose), or theopgGHoperon or Acp fromE. coli. A ΔopgGHY. pseudotuberculosisstrain showed normal motility, biofilm formation, resistance to polymyxin and macrophages, and virulence but was smaller. Consistently,Y. pestiswas smaller thanY. pseudotuberculosiswhen cultured at ≥37°C, except when the plague bacillus expressedopgGH.Y. pestisexpressingopgGHgrew normally in serum and within macrophages and was fully virulent in mice, suggesting that small cell size was not advantageous in the mammalian host. Lastly,Y. pestisexpressingopgGHwas able to infectXenopsylla cheopisfleas normally. Our results suggest an evolutionary scenario whereby an ancestralYersiniastrain lost a factor required for OPG biosynthesis but keptopgGH(to regulate cell size). TheopgGHoperon was presumably then lost because OpgH-dependent cell size control became unnecessary.

scholarly journals Evaluation of the Role of Constitutive Isocitrate Lyase Activity in Yersinia pestis Infection of the Flea Vector and Mammalian Host

2004 ◽  
Vol 72 (12) ◽  
pp. 7334-7337 ◽  
Author(s):  
Florent Sebbane ◽  
Clayton O. Jarrett ◽  
Jan R. Linkenhoker ◽  
B. Joseph Hinnebusch
Keyword(s):  
Yersinia Pestis ◽  
Yersinia Pseudotuberculosis ◽  
Isocitrate Lyase ◽  
Mammalian Host ◽  
Lyase Activity ◽  
Glyoxylate Pathway

ABSTRACT Yersinia pestis, unlike the closely related Yersinia pseudotuberculosis, constitutively produces isocitrate lyase (ICL). Here we show that the Y. pestis aceA homologue encodes ICL and is required for growth on acetate but not for flea infection or virulence in mice. Thus, deregulation of the glyoxylate pathway does not underlie the recent adaptation of Y. pestis to arthropod-borne transmission.

scholarly journals Review onTrypanosoma cruzi: Host Cell Interaction

2010 ◽  
Vol 2010 ◽  
pp. 1-18 ◽  
Author(s):  
Wanderley de Souza ◽  
Tecia Maria Ulisses de Carvalho ◽  
Emile Santos Barrias
Keyword(s):  
Trypanosoma Cruzi ◽  
Host Cell ◽  
Mammalian Cells ◽  
Cell Types ◽  
Cell Interaction ◽  
Host Cells ◽  
Mammalian Host ◽  
Blood Sucking ◽  
Number Of Individuals ◽  
Host Cell Interaction

Trypanosoma cruzi, the causative agent of Chagas' disease, which affects a large number of individuals in Central and South America, is transmitted to vertebrate hosts by blood-sucking insects. This protozoan is an obligate intracellular parasite. The infective forms of the parasite are metacyclic and bloodstream trypomastigote and amastigote. Metacyclic trypomastigotes are released with the feces of the insect while amastigotes and bloodstream trypomastigotes are released from the infected host cells of the vertebrate host after a complex intracellular life cycle. The recognition between parasite and mammalian host cell involves numerous molecules present in both cell types. Here, we present a brief review of the interaction betweenTrypanosoma cruziand its host cells, mainly emphasizing the mechanisms and molecules that participate in theT. cruziinvasion process of the mammalian cells.

scholarly journals Plasmodium yoelii Sporozoites with Simultaneous Deletion of P52 and P36 Are Completely Attenuated and Confer Sterile Immunity against Infection

2007 ◽  
Vol 75 (8) ◽  
pp. 3758-3768 ◽  
Author(s):  
Mehdi Labaied ◽  
Anke Harupa ◽  
Ronald F. Dumpit ◽  
Isabelle Coppens ◽  
Sebastian A. Mikolajczak ◽  
...  
Keyword(s):  
Host Cell ◽  
Genetic Manipulation ◽  
Parasitophorous Vacuole ◽  
Plasmodium Yoelii ◽  
Blood Stage ◽  
Mammalian Host ◽  
Electron Microscopic ◽  
Rodent Host ◽  
Blood Stage Infection ◽  
Stage Infection

ABSTRACT Malaria infection starts when sporozoites are transmitted to the mammalian host during a mosquito bite. Sporozoites enter the blood circulation, reach the liver, and infect hepatocytes. The formation of a parasitophorous vacuole (PV) establishes their intracellular niche. Recently, two members of the 6-Cys domain protein family, P52 and P36, were each shown to play an important albeit nonessential role in Plasmodium berghei sporozoite infectivity for the rodent host. Here, we generated p52/p36-deficient Plasmodium yoelii parasites by the simultaneous deletion of both genes using a single genetic manipulation. p52/p36-deficient parasites exhibited normal progression through the life cycle during blood-stage infection, transmission to mosquitoes, mosquito-stage development, and sporozoite infection of the salivary glands. p52/p36-deficient sporozoites also showed normal motility and cell traversal activity. However, immunofluorescence analysis and electron microscopic observations revealed that p52/p36-deficient parasites did not form a PV within hepatocytes in vitro and in vivo. The p52/p36-deficient parasites localized as free entities in the host cell cytoplasm or the host cell nucleoplasm and did not develop as liver stages. Consequently, they did not cause blood-stage infections even at high sporozoite inoculation doses. Mice immunized with p52/p36-deficient sporozoites were completely protected against infectious sporozoite challenge. Our results demonstrate for the first time the generation of two-locus gene deletion-attenuated parasites that infect the liver but do not progress to blood-stage infection. The study will critically guide the design of Plasmodium falciparum live attenuated malaria vaccines.

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