Journal articles: 'Yersinia pestis – Transmission'

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Brubaker, R. R. "Factors promoting acute and chronic diseases caused by yersiniae." Clinical Microbiology Reviews 4, no. 3 (July 1991): 309–24. http://dx.doi.org/10.1128/cmr.4.3.309.

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The experimental system constructed with the medically significant yersiniae provides a powerful basic model for comparative study of factors required for expression of acute versus chronic disease. The system exploits the close genetic similarity between Yersinia pestis, the etiological agent of bubonic plague, and enteropathogenic Yersinia pseudotuberculosis and Yersinia enterocolitica. Y. pestis possesses three plasmids, of which one, shared by the enteropathogenic species, mediates a number of virulence factors that directly or indirectly promote survival within macrophages and immunosuppression. The two remaining plasmids are unique and encode functions that promote acute disease by enhancing bacterial dissemination in tissues and resistance to phagocytosis by neutrophils and monocytes. These properties are replaced in the enteropathogenic yersiniae by host cell invasins and an adhesin which promote chronic disease; the latter are cryptic in Y. pestis. Additional distinctions include specific mutational losses in Y. pestis which result in loss of fitness in natural environments plus gain of properties that facilitate transmission and infection via fleabite.

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Sebbane, Florent, Vladimir N. Uversky, and Andrey P. Anisimov. "Yersinia pestis Plasminogen Activator." Biomolecules 10, no. 11 (November 14, 2020): 1554. http://dx.doi.org/10.3390/biom10111554.

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The Gram-negative bacterium Yersinia pestis causes plague, a fatal flea-borne anthropozoonosis, which can progress to aerosol-transmitted pneumonia. Y. pestis overcomes the innate immunity of its host thanks to many pathogenicity factors, including plasminogen activator, Pla. This factor is a broad-spectrum outer membrane protease also acting as adhesin and invasin. Y. pestis uses Pla adhesion and proteolytic capacity to manipulate the fibrinolytic cascade and immune system to produce bacteremia necessary for pathogen transmission via fleabite or aerosols. Because of microevolution, Y. pestis invasiveness has increased significantly after a single amino-acid substitution (I259T) in Pla of one of the oldest Y. pestis phylogenetic groups. This mutation caused a better ability to activate plasminogen. In paradox with its fibrinolytic activity, Pla cleaves and inactivates the tissue factor pathway inhibitor (TFPI), a key inhibitor of the coagulation cascade. This function in the plague remains enigmatic. Pla (or pla) had been used as a specific marker of Y. pestis, but its solitary detection is no longer valid as this gene is present in other species of Enterobacteriaceae. Though recovering hosts generate anti-Pla antibodies, Pla is not a good subunit vaccine. However, its deletion increases the safety of attenuated Y. pestis strains, providing a means to generate a safe live plague vaccine.

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Sebbane, Florent, Clayton O. Jarrett, Jan R. Linkenhoker, and B. Joseph Hinnebusch. "Evaluation of the Role of Constitutive Isocitrate Lyase Activity in Yersinia pestis Infection of the Flea Vector and Mammalian Host." Infection and Immunity 72, no. 12 (December 2004): 7334–37. http://dx.doi.org/10.1128/iai.72.12.7334-7337.2004.

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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.

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Perry, R. D., and J. D. Fetherston. "Yersinia pestis--etiologic agent of plague." Clinical Microbiology Reviews 10, no. 1 (January 1997): 35–66. http://dx.doi.org/10.1128/cmr.10.1.35.

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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.

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Easterday, W. Ryan, Kyrre L. Kausrud, Bastiaan Star, Lise Heier, Bradd J. Haley, Vladimir Ageyev, Rita R. Colwell, and Nils Chr Stenseth. "An additional step in the transmission of Yersinia pestis?" ISME Journal 6, no. 2 (August 11, 2011): 231–36. http://dx.doi.org/10.1038/ismej.2011.105.

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Green, Monica. "Editor's Introduction to Pandemic Disease in the Medieval World: Rethinking the Black Death." Medieval Globe 1, no. 1 (2015): 9–26. http://dx.doi.org/10.17302/tmg.1-1.2.

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Extraction of the genetic material of the causative organism of plague, Yersinia pestis, from the remains of persons who died during the Black Death has confirmed that pathogen’s role in one of the largest pandemics of human history. This then opens up historical research to investigations based on modern science, which has studied Yersinia pestis from a variety of perspectives, most importantly its evolutionary history and its complex ecology of transmission. The contributors to this special issue argue for the benefits of a multidisciplinary and collaborative approach to the many remaining mysteries associated with the plague’s geographical extent, rapid transmission, deadly outcomes, and persistence.

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Erickson, David L., Clayton O. Jarrett, Julie A. Callison, Elizabeth R. Fischer, and B. Joseph Hinnebusch. "Loss of a Biofilm-Inhibiting Glycosyl Hydrolase during the Emergence of Yersinia pestis." Journal of Bacteriology 190, no. 24 (October 17, 2008): 8163–70. http://dx.doi.org/10.1128/jb.01181-08.

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ABSTRACT Yersinia pestis, the bacterial agent of plague, forms a biofilm in the foregut of its flea vector to produce a transmissible infection. The closely related Yersinia pseudotuberculosis, from which Y. pestis recently evolved, can colonize the flea midgut but does not form a biofilm in the foregut. Y. pestis biofilm in the flea and in vitro is dependent on an extracellular matrix synthesized by products of the hms genes; identical genes are present in Y. pseudotuberculosis. The Yersinia Hms proteins contain functional domains present in Escherichia coli and Staphylococcus proteins known to synthesize a poly-β-1,6-N-acetyl-d-glucosamine biofilm matrix. In this study, we show that the extracellular matrices (ECM) of Y. pestis and staphylococcal biofilms are antigenically related, indicating a similar biochemical structure. We also characterized a glycosyl hydrolase (NghA) of Y. pseudotuberculosis that cleaved β-linked N-acetylglucosamine residues and reduced biofilm formation by staphylococci and Y. pestis in vitro. The Y. pestis nghA ortholog is a pseudogene, and overexpression of functional nghA reduced ECM surface accumulation and inhibited the ability of Y. pestis to produce biofilm in the flea foregut. Mutational loss of this glycosidase activity in Y. pestis may have contributed to the recent evolution of flea-borne transmission.

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Hinnebusch, B. Joseph, Clayton O. Jarrett, and David M. Bland. "Molecular and Genetic Mechanisms That Mediate Transmission of Yersinia pestis by Fleas." Biomolecules 11, no. 2 (February 3, 2021): 210. http://dx.doi.org/10.3390/biom11020210.

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The ability to cause plague in mammals represents only half of the life history of Yersinia pestis. It is also able to colonize and produce a transmissible infection in the digestive tract of the flea, its insect host. Parallel to studies of the molecular mechanisms by which Y. pestis is able to overcome the immune response of its mammalian hosts, disseminate, and produce septicemia, studies of Y. pestis–flea interactions have led to the identification and characterization of important factors that lead to transmission by flea bite. Y. pestis adapts to the unique conditions in the flea gut by altering its metabolic physiology in ways that promote biofilm development, a common strategy by which bacteria cope with a nutrient-limited environment. Biofilm localization to the flea foregut disrupts normal fluid dynamics of blood feeding, resulting in regurgitative transmission. Many of the important genes, regulatory pathways, and molecules required for this process have been identified and are reviewed here.

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Skurnik, Mikael, Salla Jaakkola, Laura Mattinen, Lotta von Ossowski, Ayesha Nawaz, Maria I. Pajunen, and Lotta J. Happonen. "Bacteriophages fEV-1 and fD1 Infect Yersinia pestis." Viruses 13, no. 7 (July 16, 2021): 1384. http://dx.doi.org/10.3390/v13071384.

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Bacteriophages vB_YpeM_fEV-1 (fEV-1) and vB_YpeM_fD1 (fD1) were isolated from incoming sewage water samples in Turku, Finland, using Yersinia pestis strains EV76 and KIM D27 as enrichment hosts, respectively. Genomic analysis and transmission electron microscopy established that fEV-1 is a novel type of dwarf myovirus, while fD1 is a T4-like myovirus. The genome sizes are 38 and 167 kb, respectively. To date, the morphology and genome sequences of some dwarf myoviruses have been described; however, a proteome characterization such as the one presented here, has currently been lacking for this group of viruses. Notably, fEV-1 is the first dwarf myovirus described for Y. pestis. The host range of fEV-1 was restricted strictly to Y. pestis strains, while that of fD1 also included other members of Enterobacterales such as Escherichia coli and Yersinia pseudotuberculosis. In this study, we present the life cycles, genomes, and proteomes of two Yersinia myoviruses, fEV-1 and fD1.

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Uittenbogaard, Annette M., Tanya Myers-Morales, Amanda A. Gorman, Erin Welsh, Christine Wulff, B. Joseph Hinnebusch, Timo K. Korhonen, and Susan C. Straley. "Temperature-dependence of yadBC phenotypes in Yersinia pestis." Microbiology 160, no. 2 (February 1, 2014): 396–405. http://dx.doi.org/10.1099/mic.0.073205-0.

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YadB and YadC are putative trimeric autotransporters present only in the plague bacterium Yersinia pestis and its evolutionary predecessor, Yersinia pseudotuberculosis. Previously, yadBC was found to promote invasion of epithelioid cells by Y. pestis grown at 37 °C. In this study, we found that yadBC also promotes uptake of 37 °C-grown Y. pestis by mouse monocyte/macrophage cells. We tested whether yadBC might be required for lethality of the systemic stage of plague in which the bacteria would be pre-adapted to mammalian body temperature before colonizing internal organs and found no requirement for early colonization or growth over 3 days. We tested the hypothesis that YadB and YadC function on ambient temperature-grown Y. pestis in the flea vector or soon after infection of the dermis in bubonic plague. We found that yadBC did not promote uptake by monocyte/macrophage cells if the bacteria were grown at 28 °C, nor was there a role of yadBC in colonization of fleas by Y. pestis grown at 21 °C. However, the presence of yadBC did promote recoverability of the bacteria from infected skin for 28 °C-grown Y. pestis. Furthermore, the gene for the proinflammatory chemokine CXCL1 was upregulated in expression if the infecting Y. pestis lacked yadBC but not if yadBC was present. Also, yadBC was not required for recoverability if the bacteria were grown at 37 °C. These findings imply that thermally induced virulence properties dominate over effects of yadBC during plague but that yadBC has a unique function early after transmission of Y. pestis to skin.

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Erickson, David L., Clayton O. Jarrett, Brendan W. Wren, and B. Joseph Hinnebusch. "Serotype Differences and Lack of Biofilm Formation Characterize Yersinia pseudotuberculosis Infection of the Xenopsylla cheopis Flea Vector of Yersinia pestis." Journal of Bacteriology 188, no. 3 (February 1, 2006): 1113–19. http://dx.doi.org/10.1128/jb.188.3.1113-1119.2006.

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ABSTRACT Yersinia pestis, the agent of plague, is usually transmitted by fleas. To produce a transmissible infection, Y. pestis colonizes the flea midgut and forms a biofilm in the proventricular valve, which blocks normal blood feeding. The enteropathogen Yersinia pseudotuberculosis, from which Y. pestis recently evolved, is not transmitted by fleas. However, both Y. pestis and Y. pseudotuberculosis form biofilms that adhere to the external mouthparts and block feeding of Caenorhabditis elegans nematodes, which has been proposed as a model of Y. pestis-flea interactions. We compared the ability of Y. pestis and Y. pseudotuberculosis to infect the rat flea Xenopsylla cheopis and to produce biofilms in the flea and in vitro. Five of 18 Y. pseudotuberculosis strains, encompassing seven serotypes, including all three serotype O3 strains tested, were unable to stably colonize the flea midgut. The other strains persisted in the flea midgut for 4 weeks but did not increase in numbers, and none of the 18 strains colonized the proventriculus or produced a biofilm in the flea. Y. pseudotuberculosis strains also varied greatly in their ability to produce biofilms in vitro, but there was no correlation between biofilm phenotype in vitro or on the surface of C. elegans and the ability to colonize or block fleas. Our results support a model in which a genetic change in the Y. pseudotuberculosis progenitor of Y. pestis extended its pre-existing ex vivo biofilm-forming ability to the flea gut environment, thus enabling proventricular blockage and efficient flea-borne transmission.

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Buhnerkempe, Michael G., Rebecca J. Eisen, Brandon Goodell, Kenneth L. Gage, Michael F. Antolin, and Colleen T. Webb. "Transmission Shifts Underlie Variability in Population Responses to Yersinia pestis Infection." PLoS ONE 6, no. 7 (July 25, 2011): e22498. http://dx.doi.org/10.1371/journal.pone.0022498.

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Salkeld, D. J., and P. Stapp. "Seroprevalence Rates and Transmission of Plague (Yersinia pestis) in Mammalian Carnivores." Vector-Borne and Zoonotic Diseases 6, no. 3 (September 2006): 231–39. http://dx.doi.org/10.1089/vbz.2006.6.231.

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Johnson, Tammi L., B. Joseph Hinnebusch, Karen A. Boegler, Christine B. Graham, Katherine MacMillan, John A. Montenieri, Scott W. Bearden, Kenneth L. Gage, and Rebecca J. Eisen. "Yersinia murine toxin is not required for early-phase transmission of Yersinia pestis by Oropsylla montana (Siphonaptera: Ceratophyllidae) or Xenopsylla cheopis (Siphonaptera: Pulicidae)." Microbiology 160, no. 11 (November 1, 2014): 2517–25. http://dx.doi.org/10.1099/mic.0.082123-0.

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Plague, caused by Yersinia pestis, is characterized by quiescent periods punctuated by rapidly spreading epizootics. The classical ‘blocked flea’ paradigm, by which a blockage forms in the flea’s proventriculus on average 1–2 weeks post-infection (p.i.), forces starving fleas to take multiple blood meals, thus increasing opportunities for transmission. Recently, the importance of early-phase transmission (EPT), which occurs prior to blockage formation, has been emphasized during epizootics. Whilst the physiological and molecular mechanisms of blocked flea transmission are well characterized, the pathogen–vector interactions have not been elucidated for EPT. Within the blocked flea model, Yersinia murine toxin (Ymt) has been shown to be important for facilitating colonization of the midgut within the flea. One proposed mechanism of EPT is the regurgitation of infectious material from the flea midgut during feeding. Such a mechanism would require bacteria to colonize and survive for at least brief periods in the midgut, a process that is mediated by Ymt. Two key bridging vectors of Y. pestis to humans, Oropsylla montana (Siphonaptera: Ceratophyllidae) or Xenopsylla cheopis (Siphonaptera: Pulicidae), were used in our study to test this hypothesis. Fleas were infected with a mutant strain of Y. pestis containing a non-functional ymt that was shown previously to be incapable of colonizing the midgut and were then allowed to feed on SKH-1 mice 3 days p.i. Our results show that Ymt was not required for EPT by either flea species.

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Lane, M. Chelsea, Jonathan D. Lenz, and Virginia L. Miller. "Proteolytic processing of the Yersinia pestis YapG autotransporter by the omptin protease Pla and the contribution of YapG to murine plague pathogenesis." Journal of Medical Microbiology 62, no. 8 (August 1, 2013): 1124–34. http://dx.doi.org/10.1099/jmm.0.056275-0.

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Autotransporter protein secretion represents one of the simplest forms of secretion across Gram-negative bacterial membranes. Once secreted, autotransporter proteins either remain tethered to the bacterial surface or are released following proteolytic cleavage. Autotransporters possess a diverse array of virulence-associated functions such as motility, cytotoxicity, adherence and autoaggregation. To better understand the role of autotransporters in disease, our research focused on the autotransporters of Yersinia pestis, the aetiological agent of plague. Y. pestis strain CO92 has nine functional conventional autotransporters, referred to as Yaps for Yersinia autotransporter proteins. Three Yaps have been directly implicated in virulence using established mouse models of plague infection (YapE, YapJ and YapK). Whilst previous studies from our laboratory have shown that most of the CO92 Yaps are cell associated, YapE and YapG are processed and released by the omptin protease Pla. In this study, we identified the Pla cleavage sites in YapG that result in many released forms of YapG in Y. pestis, but not in the evolutionarily related gastrointestinal pathogen, Yersinia pseudotuberculosis, which lacks Pla. Furthermore, we showed that YapG does not contribute to Y. pestis virulence in established mouse models of bubonic and pneumonic infection. As Y. pestis has a complex life cycle involving a wide range of mammalian hosts and a flea vector for transmission, it remains to be elucidated whether YapG has a measurable role in any other stage of plague disease.

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Vetter, Sara M., Rebecca J. Eisen, Anna M. Schotthoefer, John A. Montenieri, Jennifer L. Holmes, Alexander G. Bobrov, Scott W. Bearden, Robert D. Perry, and Kenneth L. Gage. "Biofilm formation is not required for early-phase transmission of Yersinia pestis." Microbiology 156, no. 7 (July 1, 2010): 2216–25. http://dx.doi.org/10.1099/mic.0.037952-0.

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Early-phase transmission (EPT) is a recently described model of plague transmission that explains the rapid spread of disease from flea to mammal host during an epizootic. Unlike the traditional blockage-dependent model of plague transmission, EPT can occur when a flea takes its first blood meal after initially becoming infected by feeding on a bacteraemic host. Blockage of the flea gut results from biofilm formation in the proventriculus, mediated by the gene products found in the haemin storage (hms) locus of the Yersinia pestis chromosome. Although biofilms are required for blockage-dependent transmission, the role of biofilms in EPT has yet to be determined. An artificial feeding system was used to feed Xenopsylla cheopis and Oropsylla montana rat blood spiked with the parental Y. pestis strain KIM5(pCD1)+, two different biofilm-deficient mutants (ΔhmsT, ΔhmsR), or a biofilm-overproducer mutant (ΔhmsP). Infected fleas were then allowed to feed on naïve Swiss Webster mice for 1–4 days after infection, and the mice were monitored for signs of infection. We also determined the bacterial loads of each flea that fed upon naïve mice. Biofilm-defective mutants transmitted from X. cheopis and O. montana as efficiently as the parent strain, whereas the EPT efficiency of fleas fed the biofilm-overproducing strain was significantly less than that of fleas fed either the parent or a biofilm-deficient strain. Fleas infected with a biofilm-deficient strain harboured lower bacterial loads 4 days post-infection than fleas infected with the parent strain. Thus, defects in biofilm formation did not prevent flea-borne transmission of Y. pestis in our EPT model, although biofilm overproduction inhibited efficient EPT. Our results also indicate, however, that biofilms may play a role in infection persistence in the flea.

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Bosio, Christopher F., Clayton O. Jarrett, Dana P. Scott, Jonathan Fintzi, and B. Joseph Hinnebusch. "Comparison of the transmission efficiency and plague progression dynamics associated with two mechanisms by which fleas transmit Yersinia pestis." PLOS Pathogens 16, no. 12 (December 7, 2020): e1009092. http://dx.doi.org/10.1371/journal.ppat.1009092.

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Yersinia pestis can be transmitted by fleas during the first week after an infectious blood meal, termed early-phase or mass transmission, and again after Y. pestis forms a cohesive biofilm in the flea foregut that blocks normal blood feeding. We compared the transmission efficiency and the progression of infection after transmission by Oropsylla montana fleas at both stages. Fleas were allowed to feed on mice three days after an infectious blood meal to evaluate early-phase transmission, or after they had developed complete proventricular blockage. Transmission was variable and rather inefficient by both modes, and the odds of early-phase transmission was positively associated with the number of infected fleas that fed. Disease progression in individual mice bitten by fleas infected with a bioluminescent strain of Y. pestis was tracked. An early prominent focus of infection at the intradermal flea bite site and dissemination to the draining lymph node(s) soon thereafter were common features, but unlike what has been observed in intradermal injection models, this did not invariably lead to further systemic spread and terminal disease. Several of these mice resolved the infection without progression to terminal sepsis and developed an immune response to Y. pestis, particularly those that received an intermediate number of early-phase flea bites. Furthermore, two distinct types of terminal disease were noted: the stereotypical rapid onset terminal disease within four days, or a prolonged onset preceded by an extended, fluctuating infection of the lymph nodes before eventual systemic dissemination. For both modes of transmission, bubonic plague rather than primary septicemic plague was the predominant disease outcome. The results will help to inform mathematical models of flea-borne plague dynamics used to predict the relative contribution of the two transmission modes to epizootic outbreaks that erupt periodically from the normal enzootic background state.

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Bouvenot, Typhanie, Amélie Dewitte, Nadia Bennaceur, Elizabeth Pradel, François Pierre, Sébastien Bontemps-Gallo, and Florent Sebbane. "Interplay between Yersinia pestis and its flea vector in lipoate metabolism." ISME Journal 15, no. 4 (January 21, 2021): 1136–49. http://dx.doi.org/10.1038/s41396-020-00839-0.

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AbstractTo thrive, vector-borne pathogens must survive in the vector’s gut. How these pathogens successfully exploit this environment in time and space has not been extensively characterized. Using Yersinia pestis (the plague bacillus) and its flea vector, we developed a bioluminescence-based approach and employed it to investigate the mechanisms of pathogenesis at an unprecedented level of detail. Remarkably, lipoylation of metabolic enzymes, via the biosynthesis and salvage of lipoate, increases the Y. pestis transmission rate by fleas. Interestingly, the salvage pathway’s lipoate/octanoate ligase LplA enhances the first step in lipoate biosynthesis during foregut colonization but not during midgut colonization. Lastly, Y. pestis primarily uses lipoate provided by digestive proteolysis (presumably as lipoyl peptides) rather than free lipoate in blood, which is quickly depleted by the vector. Thus, spatial and temporal factors dictate the bacterium’s lipoylation strategies during an infection, and replenishment of lipoate by digestive proteolysis in the vector might constitute an Achilles’ heel that is exploited by pathogens.

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Suntsov, V. V. "Genesis of Flea-Born Transmission of Plague Microbe, Yersinia pestis: Two Approachs – Molecular-Genetic and Ecological Ones." Problems of Particularly Dangerous Infections, no. 2 (July 4, 2018): 37–44. http://dx.doi.org/10.21055/0370-1069-2018-2-37-44.

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Two approaches to studying the origin and transmission mechanism of the flea-borne plague pathogen, Yersinia pestis: molecular-genetic and ecological ones – are considered in this review. The molecular genetic approach is based on saltation evolutionary ideology and relies upon the phenomenon of horizontal gene transfer of pla and ymt as critical evolutionary events. Further deletion of some structural and regulatory genes optimized “blockage” mechanism of transmission. The Ecological approach is based on the modern synthetic theory of evolution. It posits a gradual population-genetic transformation in the Marmot – Flea (Marmota sibirica – Oropsylla silantiewi) transitional (heterothermal, heteroimmune) host-parasite system in Late Pleistocene – Holocene epochs. The best prospects for disclosing the mechanisms of evolutionary formation of flea-borne Y. pestis transmission consist in the synthesis of molecular-genetic and ecological approaches.

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Zhou, Dongsheng, Yanping Han, Yajun Song, Zongzhong Tong, Jin Wang, Zhaobiao Guo, Decui Pei, et al. "DNA Microarray Analysis of Genome Dynamics in Yersinia pestis: Insights into Bacterial Genome Microevolution and Niche Adaptation." Journal of Bacteriology 186, no. 15 (August 1, 2004): 5138–46. http://dx.doi.org/10.1128/jb.186.15.5138-5146.2004.

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ABSTRACT Genomics research provides an unprecedented opportunity for us to probe into the pathogenicity and evolution of the world's most deadly pathogenic bacterium, Yersinia pestis, in minute detail. In our present work, extensive microarray analysis in conjunction with PCR validation revealed that there are considerable genome dynamics, due to gene acquisition and loss, in natural populations of Y. pestis. We established a genomotyping system to group homologous isolates of Y. pestis, based on profiling or gene acquisition and loss in their genomes, and then drew an outline of parallel microevolution of the Y. pestis genome. The acquisition of a number of genomic islands and plasmids most likely induced Y. pestis to evolve rapidly from Yersinia pseudotuberculosis to a new, deadly pathogen. Horizontal gene acquisition also plays a key role in the dramatic evolutionary segregation of Y. pestis lineages (biovars and genomovars). In contrast to selective genome expansion by gene acquisition, genome reduction occurs in Y. pestis through the loss of DNA regions. We also theorized about the links between niche adaptation and genome microevolution. The transmission, colonization, and expansion of Y. pestis in the natural foci of endemic plague are parallel and directional and involve gradual adaptation to the complex of interactions between the environment, the hosts, and the pathogen itself. These adaptations are based on the natural selections against the accumulation of genetic changes within genome. Our data strongly support that the modern plague originated from Yunnan Province in China, due to the arising of biovar orientalis from biovar antiqua rather than mediaevalis.

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Sebbane, Florent, Clayton Jarrett, Donald Gardner, Daniel Long, and B. Joseph Hinnebusch. "The Yersinia pestis caf1M1A1 Fimbrial Capsule Operon Promotes Transmission by Flea Bite in a Mouse Model of Bubonic Plague." Infection and Immunity 77, no. 3 (December 22, 2008): 1222–29. http://dx.doi.org/10.1128/iai.00950-08.

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ABSTRACT Plague is a zoonosis transmitted by fleas and caused by the gram-negative bacterium Yersinia pestis. During infection, the plasmidic caf1M1A1 operon that encodes the Y. pestis F1 protein capsule is highly expressed, and anti-F1 antibodies are protective. Surprisingly, the capsule is not required for virulence after injection of cultured bacteria, even though it is an antiphagocytic factor and capsule-deficient Y. pestis strains are rarely isolated. We found that a caf-negative Y. pestis mutant was not impaired in either flea colonization or virulence in mice after intradermal inoculation of cultured bacteria. In contrast, absence of the caf operon decreased bubonic plague incidence after a flea bite. Successful development of plague in mice infected by flea bite with the caf-negative mutant required a higher number of infective bites per challenge. In addition, the mutant displayed a highly autoaggregative phenotype in infected liver and spleen. The results suggest that acquisition of the caf locus via horizontal transfer by an ancestral Y. pestis strain increased transmissibility and the potential for epidemic spread. In addition, our data support a model in which atypical caf-negative strains could emerge during climatic conditions that favor a high flea burden. Human infection with such strains would not be diagnosed by the standard clinical tests that detect F1 antibody or antigen, suggesting that more comprehensive surveillance for atypical Y. pestis strains in plague foci may be necessary. The results also highlight the importance of studying Y. pestis pathogenesis in the natural context of arthropod-borne transmission.

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Morozova, Irina, Artem Kasianov, Sergey Bruskin, Judith Neukamm, Martyna Molak, Elena Batieva, Aleksandra Pudło, Frank J. Rühli, and Verena J. Schuenemann. "New ancient Eastern European Yersinia pestis genomes illuminate the dispersal of plague in Europe." Philosophical Transactions of the Royal Society B: Biological Sciences 375, no. 1812 (October 5, 2020): 20190569. http://dx.doi.org/10.1098/rstb.2019.0569.

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Yersinia pestis , the causative agent of plague, has been prevalent among humans for at least 5000 years, being accountable for several devastating epidemics in history, including the Black Death. Analyses of the genetic diversity of ancient strains of Y. pestis have shed light on the mechanisms of evolution and the spread of plague in Europe. However, many questions regarding the origins of the pathogen and its long persistence in Europe are still unresolved, especially during the late medieval time period. To address this, we present four newly assembled Y. pestis genomes from Eastern Europe (Poland and Southern Russia), dating from the fifteenth to eighteenth century AD. The analysis of polymorphisms in these genomes and their phylogenetic relationships with other ancient and modern Y. pestis strains may suggest several independent introductions of plague into Eastern Europe or its persistence in different reservoirs. Furthermore, with the reconstruction of a partial Y. pestis genome from rat skeletal remains found in a Polish ossuary, we were able to identify a potential animal reservoir in late medieval Europe. Overall, our results add new information concerning Y. pestis transmission and its evolutionary history in Eastern Europe. This article is part of the theme issue ‘Insights into health and disease from ancient biomolecules’.

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Jarrett, Clayton O., Florent Sebbane, Jeffrey J. Adamovicz, Gerard P. Andrews, and B. Joseph Hinnebusch. "Flea-Borne Transmission Model To Evaluate Vaccine Efficacy against Naturally Acquired Bubonic Plague." Infection and Immunity 72, no. 4 (April 2004): 2052–56. http://dx.doi.org/10.1128/iai.72.4.2052-2056.2004.

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ABSTRACT A flea-to-mouse transmission model was developed for use in testing new candidate vaccines for the ability to protect against flea-borne plague. The model was used to evaluate a recombinant fusion protein vaccine consisting of the Yersinia pestis F1 and V antigens. After one to three challenges with Y. pestis-infected fleas, 14 of 15 unvaccinated control mice developed plague, with an average septicemia level of 9.2 × 108 Y. pestis CFU/ml. None of 15 vaccinated mice developed the disease after similar challenges, and serological testing indicated that transmitted bacteria were eliminated by the immune system before extensive replication and systemic infection could occur. The transmission and development of disease in control mice correlated with the number of bites by blocked fleas but not with the total number of fleabites. The model provides a means to directly assess the efficacy of new vaccines to prevent naturally acquired bubonic plague and to study events at the vector-host interface that lead to dissemination and disease.

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Dudina, L. G., M. A. Malkova, A. V. Chernyad’ev, S. G. Litvinets, and A. A. Byvalov. "Effect of Bacteriophages and Gentamycine on Morphology and Vesicle Formation of Bacteria Yersinia pestis EV." Problems of Particularly Dangerous Infections, no. 2 (July 3, 2019): 50–54. http://dx.doi.org/10.21055/0370-1069-2019-2-50-54.

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Objective was to assess the effect of specific bacteriophages and gentamycine on the morphological-functional properties of bacteria in the vaccine strain Yersinia pestis EV.Materials and methods. The vaccine strain Y. pestis EV, Pokrovskaya bacteriophage and the pseudotuberculous diagnostic bacteriophage were used for the study. The microbial culture was grown on solid and in liquid growth media at 27 °C for 20–24 h. The co-incubation of bacteria and bacteriophage or gentamycine was carried out at 27 °C for 20 minutes or at 37 °C for 2 hours, respectively. Culture preparations were examined by transmission electron microscopy.Results and discussion. The influence of cultivation conditions and various stress factors on the vesicle production by the vaccine strain Y. pestis EV cells was evaluated. The nature and intensity of morphological-functional changes in Y. pestis EV cells in response to the effect of bacteriophages (plague Pokrovskaya and pseudotuberculous bacteriophages) or an antibiotic (gentamycine) were determined. It was established that co-incubation of Y. pestis EV with Pokrovskaya bacteriophage or gentamycine for 20 min leads to the increase in the production of extracellular vesicles and is accompanied by the development of degenerative changes in bacterial cells.

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Sun, Yi-Cheng, Clayton O. Jarrett, Christopher F. Bosio, and B. Joseph Hinnebusch. "Retracing the Evolutionary Path that Led to Flea-Borne Transmission of Yersinia pestis." Cell Host & Microbe 15, no. 5 (May 2014): 578–86. http://dx.doi.org/10.1016/j.chom.2014.04.003.

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Brown, Richard. "Is behavioural thermoregulation a factor in flea-to-human transmission of Yersinia pestis?" Lancet 345, no. 8954 (April 1995): 931. http://dx.doi.org/10.1016/s0140-6736(95)90050-0.

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Rempe, K. A., A. K. Hinz, and V. Vadyvaloo. "Hfq Regulates Biofilm Gut Blockage That Facilitates Flea-Borne Transmission of Yersinia pestis." Journal of Bacteriology 194, no. 8 (February 10, 2012): 2036–40. http://dx.doi.org/10.1128/jb.06568-11.

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Lemon, Athena, Nathan Cherzan, and Viveka Vadyvaloo. "Influence of Temperature on Development of Yersinia pestis Foregut Blockage in Xenopsylla cheopis (Siphonaptera: Pulicidae) and Oropsylla montana (Siphonaptera: Ceratophyllidae)." Journal of Medical Entomology 57, no. 6 (June 13, 2020): 1997–2001. http://dx.doi.org/10.1093/jme/tjaa113.

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Abstract Plague, caused by the flea-transmitted bacterial pathogen Yersinia pestis, is primarily a disease of wild rodents distributed in temperate and tropical zones worldwide. The ability of Y. pestis to develop a biofilm blockage that obstructs the flea foregut proventriculus facilitates its efficient transmission through regurgitation into the host bite site during flea blood sucking. While it is known that temperature influences transmission, it is not well-known if blockage dynamics are similarly in accord with temperature. Here, we determine the influence of the biologically relevant temperatures, 10 and 21°C, on blockage development in flea species, Xenopsylla cheopis (Rothschild) and Oropsylla montana (Baker), respectively, characterized by geographical distribution as cosmopolitan, tropical or endemic, temperate. We find that both species exhibit delayed development of blockage at 10°C. In Y. pestis infected X. cheopis, this is accompanied by significantly lower survival rates and slightly decreased blockage rates, even though these fleas maintain similar rates of persistent infection as at 21°C. Conversely, irrespective of infection status, O. montana withstand 21 and 10°C similarly well and show significant infection rate increases and slightly greater blocking rates at 10 versus 21°C, emphasizing that cooler temperatures are favorable for Y. pestis transmission from this species. These findings assert that temperature is a relevant parameter to consider in assessing flea transmission efficiency in distinct flea species residing in diverse geographical regions that host endemic plague foci. This is important to predict behavioral dynamics of plague regarding epizootic outbreaks and enzootic maintenance and improve timeous implementation of flea control programs.

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Chandler, Courtney E., Erin M. Harberts, Mark R. Pelletier, Iyarit Thaipisuttikul, Jace W. Jones, Adeline M. Hajjar, Jason W. Sahl, et al. "Early evolutionary loss of the lipid A modifying enzyme PagP resulting in innate immune evasion in Yersinia pestis." Proceedings of the National Academy of Sciences 117, no. 37 (August 31, 2020): 22984–91. http://dx.doi.org/10.1073/pnas.1917504117.

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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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Namouchi, Amine, Meriam Guellil, Oliver Kersten, Stephanie Hänsch, Claudio Ottoni, Boris V. Schmid, Elsa Pacciani, et al. "Integrative approach using Yersinia pestis genomes to revisit the historical landscape of plague during the Medieval Period." Proceedings of the National Academy of Sciences 115, no. 50 (November 26, 2018): E11790—E11797. http://dx.doi.org/10.1073/pnas.1812865115.

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Over the last few years, genomic studies on Yersinia pestis, the causative agent of all known plague epidemics, have considerably increased in numbers, spanning a period of about 5,000 y. Nonetheless, questions concerning historical reservoirs and routes of transmission remain open. Here, we present and describe five genomes from the second half of the 14th century and reconstruct the evolutionary history of Y. pestis by reanalyzing previously published genomes and by building a comprehensive phylogeny focused on strains attributed to the Second Plague Pandemic (14th to 18th century). Corroborated by historical and ecological evidence, the presented phylogeny, which includes our Y. pestis genomes, could support the hypothesis of an entry of plague into Western European ports through distinct waves of introduction during the Medieval Period, possibly by means of fur trade routes, as well as the recirculation of plague within the human population via trade routes and human movement.

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Bramanti, Barbara, Yarong Wu, Ruifu Yang, Yujun Cui, and Nils Chr Stenseth. "Assessing the origins of the European Plagues following the Black Death: A synthesis of genomic, historical, and ecological information." Proceedings of the National Academy of Sciences 118, no. 36 (August 31, 2021): e2101940118. http://dx.doi.org/10.1073/pnas.2101940118.

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The second plague pandemic started in Europe with the Black Death in 1346 and lasted until the 19th century. Based on ancient DNA studies, there is a scientific disagreement over whether the bacterium, Yersinia pestis, came into Europe once (Hypothesis 1) or repeatedly over the following four centuries (Hypothesis 2). Here, we synthesize the most updated phylogeny together with historical, archeological, evolutionary, and ecological information. On the basis of this holistic view, we conclude that Hypothesis 2 is the most plausible. We also suggest that Y. pestis lineages might have developed attenuated virulence during transmission, which can explain the convergent evolutionary signals, including pla decay, that appeared at the end of the pandemics.

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Zimbler, Daniel L., Justin L. Eddy, Jay A. Schroeder, and Wyndham W. Lathem. "Inactivation of Peroxiredoxin 6 by the Pla Protease of Yersinia pestis." Infection and Immunity 84, no. 1 (November 9, 2015): 365–74. http://dx.doi.org/10.1128/iai.01168-15.

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Pneumonic plague represents the most severe form of disease caused byYersinia pestisdue to its ease of transmission, rapid progression, and high mortality rate. TheY. pestisouter membrane Pla protease is essential for the development of pneumonic plague; however, the complete repertoire of substrates cleaved by Pla in the lungs is not known. In this study, we describe a proteomic screen to identify host proteins contained within the bronchoalveolar lavage fluid of mice that are cleaved and/or processed byY. pestisin a Pla-dependent manner. We identified peroxiredoxin 6 (Prdx6), a host factor that contributes to pulmonary surfactant metabolism and lung defense against oxidative stress, as a previously unknown substrate of Pla. Pla cleaves Prdx6 at three distinct sites, and these cleavages disrupt both the peroxidase and phospholipase A2activities of Prdx6. In addition, we found that infection with wild-typeY. pestisreduces the abundance of extracellular Prdx6 in the lungs compared to that after infection with ΔplaY. pestis, suggesting that Pla cleaves Prdx6 in the pulmonary compartment. However, following infection with either wild-type or Δpla Y. pestis, Prdx6-deficient mice exhibit no differences in bacterial burden, host immune response, or lung damage from wild-type mice. Thus, while Pla is able to disrupt Prdx6 functionin vitroand reduce Prdx6 levelsin vivo, the cleavage of Prdx6 has little detectable impact on the progression or outcome of pneumonic plague.

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Ginting, Nuraida Br, Garuda Ginting, and Natalia Silalahi. "Sistem Pakar Mendiagnosa Penyakit Sampar Menggunakan Metode Hybrid Case Based." JURNAL MEDIA INFORMATIKA BUDIDARMA 3, no. 1 (March 1, 2019): 65. http://dx.doi.org/10.30865/mib.v3i1.1062.

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Sampar, also known as a pest or black death or plague, is a bacterial infection of Yersinia pestis (Y.pestis), where the disease is actually a zoonotic disease, which is an animal disease transmitted by humans. This disease is caused by the bacterium yersinia pestis which lives on fleas, where these fleas live in rodents (especially mice). Fleas spread disease when sucking rat or human blood. This disease is also called plague due to black patches found in the skin of the patient at the beginning of the outbreak. This pestilence was once an epidemic in 1347-1351 in Europe and other regions and killed approximately 75 million people in the world. This disease in Indonesia is still under monitoring and is one of the infectious diseases in the outbreak law that must be reported to the health office. According to WHO this disease is one of the deadly infectious diseases after infection and patients can die within 24 hours. So that people are more careful with this disease so that they are not exposed to pestilence. Because many people do not recognize the transmission of Yersinia pestis bacterial infections and do not know the symptoms that arise from pestilence. then a system for pestilence is created which aims to better diagnose early onset of this pestilence. The method applied in expert systems and one of them is a case based hybrid. Hybrid case based is one of the mathematical theories for proof based on belief functions and plausible reasoning, which is used to combine separate pieces of information or evidence to calculate a probability of an event (Arthur P.Dempster and Glen Shafer)

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Nair, Manoj K. M., Leon De Masi, Min Yue, Estela M. Galván, Huaiqing Chen, Fang Wang, and Dieter M. Schifferli. "Adhesive Properties of YapV and Paralogous Autotransporter Proteins of Yersinia pestis." Infection and Immunity 83, no. 5 (February 17, 2015): 1809–19. http://dx.doi.org/10.1128/iai.00094-15.

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Yersinia pestisis the causative agent of plague. This bacterium evolved from an ancestral enteroinvasiveYersinia pseudotuberculosisstrain by gene loss and acquisition of new genes, allowing it to use fleas as transmission vectors. Infection frequently leads to a rapidly lethal outcome in humans, a variety of rodents, and cats. This study focuses on theY. pestisKIMyapVgene and its product, recognized as an autotransporter protein by its typical sequence, outer membrane localization, and amino-terminal surface exposure. Comparison ofYersiniagenomes revealed that DNA encoding YapV or each of three individual paralogous proteins (YapK, YapJ, and YapX) was present as a gene or pseudogene in a strain-specific manner and only inY. pestisandY. pseudotuberculosis. YapV acted as an adhesin for alveolar epithelial cells and specific extracellular matrix (ECM) proteins, as shown with recombinantEscherichia coli,Y. pestis, or purified passenger domains. Like YapV, YapK and YapJ demonstrated adhesive properties, suggesting that their previously relatedin vivoactivity is due to their capacity to modulate binding properties ofY. pestisin its hosts, in conjunction with other adhesins. A differential host-specific type of binding to ECM proteins by YapV, YapK, and YapJ suggested that these proteins participate in broadening the host range ofY. pestis. A phylogenic tree including 36Y. pestisstrains highlighted an association between the gene profile for the four paralogous proteins and the geographic location of the corresponding isolated strains, suggesting an evolutionary adaption ofY. pestisto specific local animal hosts or reservoirs.

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Spinner, Justin L., Aaron B. Carmody, Clayton O. Jarrett, and B. Joseph Hinnebusch. "Role of Yersinia pestis Toxin Complex Family Proteins in Resistance to Phagocytosis by Polymorphonuclear Leukocytes." Infection and Immunity 81, no. 11 (August 19, 2013): 4041–52. http://dx.doi.org/10.1128/iai.00648-13.

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ABSTRACTYersinia pestiscarries homologues of the toxin complex (Tc) family proteins, which were first identified in other Gram-negative bacteria as having potent insecticidal activity. TheY. pestisTc proteins are neither toxic to fleas nor essential for survival of the bacterium in the flea, even thoughtcgene expression is highly upregulated and much more of the Tc proteins YitA and YipA are produced in the flea than whenY. pestisis grownin vitro. We show that Tc+and Tc−Y. pestisstrains are transmitted equivalently from coinfected fleas, further demonstrating that the Tc proteins have no discernible role, either positive or negative, in transmission by the flea vector. Tc proteins did, however, conferY. pestiswith increased resistance to killing by polymorphonuclear leukocytes (PMNs). Resistance to killing was not the result of decreased PMN viability or increased intracellular survival but instead correlated with a Tc protein-dependent resistance to phagocytosis that was independent of the type III secretion system (T3SS). Correspondingly, we did not detect T3SS-dependent secretion of the native Tc proteins YitA and YipA or the translocation of YitA– or YipA–β-lactamase fusion proteins into CHO-K1 (CHO) cells or human PMNs. Thus, although highly produced byY. pestiswithin the flea and related to insecticidal toxins, the Tc proteins do not affect interaction with the flea or transmission. Rather, theY. pestisTc proteins inhibit phagocytosis by mouse PMNs, independent of the T3SS, and may be important for subverting the mammalian innate immune response immediately following transmission from the flea.

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Jones, Ryan T., Sara M. Vetter, and Kenneth L. Gage. "Exposing Laboratory-Reared Fleas to Soil and Wild Flea Feces Increases Transmission of Yersinia pestis." American Journal of Tropical Medicine and Hygiene 89, no. 4 (October 9, 2013): 784–87. http://dx.doi.org/10.4269/ajtmh.13-0138.

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Bland, David M., and B. Joseph Hinnebusch. "Feeding Behavior Modulates Biofilm-Mediated Transmission of Yersinia pestis by the Cat Flea, Ctenocephalides felis." PLOS Neglected Tropical Diseases 10, no. 2 (February 1, 2016): e0004413. http://dx.doi.org/10.1371/journal.pntd.0004413.

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de Almeida, A., L. Alves, R. Amaral, W. França, and N. Leal. "Transmission of Yersinia pestis cultures with different plasmid content from Xenopsylla cheopis to Calomys callosus." Parasitology Research 89, no. 3 (February 2003): 159–62. http://dx.doi.org/10.1007/s00436-002-0731-3.

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Benedictow, Ole J. "Epidemiology of Plague: Problems with the Use of Mathematical Epidemiological Models in Plague Research and the Question of Transmission by Human Fleas and Lice." Canadian Journal of Infectious Diseases and Medical Microbiology 2019 (August 18, 2019): 1–20. http://dx.doi.org/10.1155/2019/1542024.

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This article addresses the recent use of mathematical epidemiological SIR or SEIR models in plague research. This use of S(E)IR models is highly problematic, but the problems are not presented and considered. Serious problems show in that such models are used to “prove” that historical plague was a (1) Filoviridae disease and (2) a bacterial disease caused by Yersinia pestis which was transmitted by human fleas and lice. (3) They also support early-phase transmission (by fleas). They purportedly consistently disprove (4) the conventional view that plague is/was a rat-and-rat-flea-borne disease. For these reasons, the focus is on methodological problems and on empirical testing by modern medical, entomological, and historical epidemiological data. An important or predominant vectorial role in plague epidemics for human fleas and lice requires that several necessary conditions are satisfied, which are generally not considered by advocates of the human ectoparasite hypothesis of plague transmission: (1) the prevalence and levels of human plague bacteraemia (human plague cases as sources of infection of feeding human ectoparasites); (2) the general size of blood meals ingested by human fleas and lice; (3) the consequent number of ingested plague bacteria; (4) the lethal dose of bacteria for 50% of a normal sample of infected human beings, LD50; and (5) efficient mechanism of transmission by lice and by fleas. The factual answers to these crucial questions can be ascertained and shown to invalidate the human ectoparasite hypothesis. The view of the standard works on plague has been corroborated, that bubonic plague, historical and modern, is/was a rat-and-rat-flea-borne disease caused by Yersinia pestis. These conclusions are concordant with and corroborate recent studies which, by laboratory experiments, invalidated the early-transmission hypothesis as a mechanism of transmission of LDs to humans in plague epidemics and removed this solution to the problem of transmission by human fleas.

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Dean, Katharine R., Fabienne Krauer, and Boris V. Schmid. "Epidemiology of a bubonic plague outbreak in Glasgow, Scotland in 1900." Royal Society Open Science 6, no. 1 (January 2019): 181695. http://dx.doi.org/10.1098/rsos.181695.

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On 3 August 1900, bubonic plague ( Yersinia pestis ) broke out in Glasgow for the first time during the Third Pandemic. The local sanitary authorities rigorously tracked the spread of the disease and they found that nearly all of the 35 cases could be linked by contact with a previous case. Despite trapping hundreds of rats in the area, there was no evidence of a rat epizootic and the investigators speculated that the outbreak could be due to human-to-human transmission of bubonic plague. Here we use a likelihood-based method to reconstruct transmission trees for the outbreak. From the description of the outbreak and the reconstructed trees, we infer several epidemiological parameters. We found that the estimated mean serial interval was 7.4–9.2 days and the mean effective reproduction number dropped below 1 after implementation of control measures. We also found a high rate of secondary transmissions within households and observations of transmissions from individuals who were not terminally septicaemic. Our results provide important insights into the epidemiology of a bubonic plague outbreak during the Third Pandemic in Europe.

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Hinnebusch, B. J., R. D. Perry, and T. G. Schwan. "Role of the Yersinia pestis Hemin Storage (hms) Locus in the Transmission of Plague by Fleas." Science 273, no. 5273 (July 19, 1996): 367–70. http://dx.doi.org/10.1126/science.273.5273.367.

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Bland, David M., Clayton O. Jarrett, Christopher F. Bosio, and B. Joseph Hinnebusch. "Infectious blood source alters early foregut infection and regurgitative transmission of Yersinia pestis by rodent fleas." PLOS Pathogens 14, no. 1 (January 22, 2018): e1006859. http://dx.doi.org/10.1371/journal.ppat.1006859.

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Bazanova, L. P., and A. Ya Nikitin. "Plague Microbe Aggregation in the Organism of Fleas (Siphonaptera) with Different Vector Ability." Problems of Particularly Dangerous Infections, no. 4(114) (August 20, 2012): 15–17. http://dx.doi.org/10.21055/0370-1069-2012-4-15-17.

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The following factors have been used to characterize 12 species and subspecies of fleas (Siphonaptera) and plague microbe (Yersinia pestis subs. pestis): the proportion of fleas with “blocks”, “blockules” and their ratio, called the index of microbe aggregation. The block formation is registered in 10, whereas formation of blockules are registered in all of the studied species and subspecies of Siphonaptera , the difference between active and passive transmitters according to the last characteristics being unreliable. The fleas, among of which “blocked” ones are not revealed in the experiments, are capable to transmit the causative agent of plague, sometimes with generalization of infectious process in animals, that can provide for continuous transmission of microbe without formation of “blocks” in the proventriculus. Thus, the high value of “rate of block formation” does not reflect the existence of coevolution in the interactions between microbe and its transmitter.

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Achtman, Mark. "Insights from genomic comparisons of genetically monomorphic bacterial pathogens." Philosophical Transactions of the Royal Society B: Biological Sciences 367, no. 1590 (March 19, 2012): 860–67. http://dx.doi.org/10.1098/rstb.2011.0303.

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Some of the most deadly bacterial diseases, including leprosy, anthrax and plague, are caused by bacterial lineages with extremely low levels of genetic diversity, the so-called ‘genetically monomorphic bacteria’. It has only become possible to analyse the population genetics of such bacteria since the recent advent of high-throughput comparative genomics. The genomes of genetically monomorphic lineages contain very few polymorphic sites, which often reflect unambiguous clonal genealogies. Some genetically monomorphic lineages have evolved in the last decades, e.g. antibiotic-resistant Staphylococcus aureus , whereas others have evolved over several millennia, e.g. the cause of plague, Yersinia pestis . Based on recent results, it is now possible to reconstruct the sources and the history of pandemic waves of plague by a combined analysis of phylogeographic signals in Y. pestis plus polymorphisms found in ancient DNA. Different from historical accounts based exclusively on human disease, Y. pestis evolved in China, or the vicinity, and has spread globally on multiple occasions. These routes of transmission can be reconstructed from the genealogy, most precisely for the most recent pandemic that was spread from Hong Kong in multiple independent waves in 1894.

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Eisen, R. J., S. W. Bearden, A. P. Wilder, J. A. Montenieri, M. F. Antolin, and K. L. Gage. "Early-phase transmission of Yersinia pestis by unblocked fleas as a mechanism explaining rapidly spreading plague epizootics." Proceedings of the National Academy of Sciences 103, no. 42 (October 10, 2006): 15380–85. http://dx.doi.org/10.1073/pnas.0606831103.

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Bontemps‐Gallo, Sébastien, Marion Fernandez, Amélie Dewitte, Etienne Raphaël, Frank C. Gherardini, Pradel Elizabeth, Lionel Koch, Fabrice Biot, Angéline Reboul, and Florent Sebbane. "Nutrient depletion may trigger the Yersinia pestis OmpR‐EnvZ regulatory system to promote flea‐borne plague transmission." Molecular Microbiology 112, no. 5 (September 13, 2019): 1471–82. http://dx.doi.org/10.1111/mmi.14372.

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Richgels, Katherine L. D., Robin E. Russell, Gebbiena M. Bron, and Tonie E. Rocke. "Evaluation of Yersinia pestis Transmission Pathways for Sylvatic Plague in Prairie Dog Populations in the Western U.S." EcoHealth 13, no. 2 (May 27, 2016): 415–27. http://dx.doi.org/10.1007/s10393-016-1133-9.

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Forman, Stanislav, Alexander G. Bobrov, Olga Kirillina, Susannah K. Craig, Jennifer Abney, Jacqueline D. Fetherston, and Robert D. Perry. "Identification of critical amino acid residues in the plague biofilm Hms proteins." Microbiology 152, no. 11 (November 1, 2006): 3399–410. http://dx.doi.org/10.1099/mic.0.29224-0.

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Yersinia pestis biofilm formation causes massive adsorption of haemin or Congo red in vitro as well as colonization and eventual blockage of the flea proventriculus in vivo. This blockage allows effective transmission of plague from some fleas, like the oriental rat flea, to mammals. Four Hms proteins, HmsH, HmsF, HmsR and HmsS, are essential for biofilm formation, with HmsT and HmsP acting as positive and negative regulators, respectively. HmsH has a β-barrel structure with a large periplasmic domain while HmsF possesses polysaccharide deacetylase and COG1649 domains. HmsR is a putative glycosyltransferase while HmsS has no recognized domains. In this study, specific amino acids within conserved domains or within regions of high similarity in HmsH, HmsF, HmsR and HmsS proteins were selected for site-directed mutagenesis. Some but not all of the substitutions in HmsS and within the periplasmic domain of HmsH were critical for protein function. Substitutions within the glycosyltransferase domain of HmsR and the deacetylase domain of HmsF abolished biofilm formation in Y. pestis. Surprisingly, substitution of highly conserved residues within COG1649 did not affect HmsF function.

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Fleck-Derderian, Shannon, Christina A. Nelson, Katharine M. Cooley, Zachary Russell, Shana Godfred-Cato, Nadia L. Oussayef, Titilope Oduyebo, Sonja A. Rasmussen, Denise J. Jamieson, and Dana Meaney-Delman. "Plague During Pregnancy: A Systematic Review." Clinical Infectious Diseases 70, Supplement_1 (May 1, 2020): S30—S36. http://dx.doi.org/10.1093/cid/ciz1228.

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Abstract Background Yersinia pestis continues to cause sporadic cases and outbreaks of plague worldwide and is considered a tier 1 bioterrorism select agent due to its potential for intentional use. Knowledge about the clinical manifestations of plague during pregnancy, specifically the maternal, fetal, and neonatal risks, is very limited. Methods We searched 12 literature databases, performed hand searches, and consulted plague experts to identify publications on plague during pregnancy. Articles were included if they reported a case of plague during pregnancy and at least 1 maternal or fetal outcome. Results Our search identified 6425 articles, of which 59 were eligible for inclusion and described 160 cases of plague among pregnant women. Most published cases occurred during the preantibiotic era. Among those treated with antimicrobials, the most commonly used were sulfonamides (75%) and streptomycin (54%). Among cases treated with antimicrobials, maternal mortality and fetal fatality were 29% and 62%, respectively; for untreated cases, maternal mortality and fetal fatality were 67% and 74%, respectively. Five cases demonstrated evidence of Y. pestis in fetal or neonatal tissues. Conclusions Untreated Y. pestis infection during pregnancy is associated with a high risk of maternal mortality and pregnancy loss. Appropriate antimicrobial treatment can improve maternal survival, although even with antimicrobial treatment, there remains a high risk of pregnancy loss. Limited evidence suggests that maternal-fetal transmission of Y. pestis is possible, particularly in the absence of antimicrobial treatment. These results emphasize the need to treat or prophylax pregnant women with suspected plague with highly effective antimicrobials as quickly as possible.

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Dean, Katharine R., Fabienne Krauer, Lars Walløe, Ole Christian Lingjærde, Barbara Bramanti, Nils Chr Stenseth, and Boris V. Schmid. "Human ectoparasites and the spread of plague in Europe during the Second Pandemic." Proceedings of the National Academy of Sciences 115, no. 6 (January 16, 2018): 1304–9. http://dx.doi.org/10.1073/pnas.1715640115.

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Plague, caused by the bacterium Yersinia pestis, can spread through human populations by multiple transmission pathways. Today, most human plague cases are bubonic, caused by spillover of infected fleas from rodent epizootics, or pneumonic, caused by inhalation of infectious droplets. However, little is known about the historical spread of plague in Europe during the Second Pandemic (14–19th centuries), including the Black Death, which led to high mortality and recurrent epidemics for hundreds of years. Several studies have suggested that human ectoparasite vectors, such as human fleas (Pulex irritans) or body lice (Pediculus humanus humanus), caused the rapidly spreading epidemics. Here, we describe a compartmental model for plague transmission by a human ectoparasite vector. Using Bayesian inference, we found that this model fits mortality curves from nine outbreaks in Europe better than models for pneumonic or rodent transmission. Our results support that human ectoparasites were primary vectors for plague during the Second Pandemic, including the Black Death (1346–1353), ultimately challenging the assumption that plague in Europe was predominantly spread by rats.

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Journal articles on the topic 'Yersinia pestis – Transmission'

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