Thematische Bibliographien / Yersinia pestis – Transmission

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Auswahl der wissenschaftlichen Literatur zum Thema „Yersinia pestis – Transmission“

Autor: Grafiati

Veröffentlicht am 25. Juni 2021

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Zeitschriftenartikel zum Thema "Yersinia pestis – Transmission"

Brubaker, R. R. „Factors promoting acute and chronic diseases caused by yersiniae.“ Clinical Microbiology Reviews 4, Nr. 3 (Juli 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 und Andrey P. Anisimov. „Yersinia pestis Plasminogen Activator“. Biomolecules 10, Nr. 11 (14.11.2020): 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 und 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, Nr. 12 (Dezember 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., und J. D. Fetherston. „Yersinia pestis--etiologic agent of plague.“ Clinical Microbiology Reviews 10, Nr. 1 (Januar 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 und Nils Chr Stenseth. „An additional step in the transmission of Yersinia pestis?“ ISME Journal 6, Nr. 2 (11.08.2011): 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, Nr. 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 und B. Joseph Hinnebusch. „Loss of a Biofilm-Inhibiting Glycosyl Hydrolase during the Emergence of Yersinia pestis“. Journal of Bacteriology 190, Nr. 24 (17.10.2008): 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 und David M. Bland. „Molecular and Genetic Mechanisms That Mediate Transmission of Yersinia pestis by Fleas“. Biomolecules 11, Nr. 2 (03.02.2021): 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 und Lotta J. Happonen. „Bacteriophages fEV-1 and fD1 Infect Yersinia pestis“. Viruses 13, Nr. 7 (16.07.2021): 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 und Susan C. Straley. „Temperature-dependence of yadBC phenotypes in Yersinia pestis“. Microbiology 160, Nr. 2 (01.02.2014): 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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Dissertationen zum Thema "Yersinia pestis – Transmission"

Bouvenot, Typhanie. „Nouvelles perspectives sur les mécanismes génétiques impliqués dans la propagation de la peste par les puces grâce à l’utilisation de la bioluminescence“. Thesis, Lille 2, 2020. http://www.theses.fr/2020LIL2S020.

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L'agent de la peste, Yersinia pestis, obstrue le tube digestif de la puce pour augmenter seschances d'être transmise à un hôte mammifère. Ici, nous avons cherché à identifier et à étudier lerôle de nouveaux gènes de Y. pestis impliqués dans la production d'une infection transmissible parles puces. Pour cela, nous avons d'abord développé une méthode (fondée sur la bioluminescence)qui permet d’évaluer des mutants dans l’insecte à un rythme sans précédent. Puis, nous avonsappliqué notre méthode pour cribler une banque de mutants (chacun dépourvu d'un ou plusieursdes gènes précédemment identifiés comme étant surexprimés chez les puces) que nous avonsgénérée. Notre criblage a listé plusieurs nouveaux facteurs potentiellement importants dans latransmission de Y. pestis par les puces. Parmi eux figure LipB qui catalyse la première étape desynthèse du lipoate (un cofacteur greffé de manière covalente à au moins trois enzymes dumétabolisme central). Nos études ultérieures ont également révélé que la deuxième et dernièreenzyme de la voie biosynthèse du lipoate, LipA, mais aussi la lipoate ligase LplA (greffant sur lesapoenzymes le lipoate collecté depuis le milieu extérieur) sont également requis pour produire uneinfection transmissible par les puces. Grâce à des approches bactériologiques, microscopiques etbiochimiques réalisées in vitro, ex-vivo et in vivo, nous avons mis au jour que la voie debiosynthèse et de récupération du lipoate sont impliquées dans la colonisation du proventricule etde l'estomac de l'insecte. De manière intéressante, nous avons également révélé que LplAparticipe, grâce son activité octanoate ligase, à la première étape de la biosynthèse du lipoatependant la colonisation du proventricule, mais pas pendant la colonisation de l’estomac. Enfin,nous avons découvert que, dans la puce, Y. pestis utilise principalement le lipoate fourni par laprotéolyse digestive (vraisemblablement sous forme de peptides de lipoylés) plutôt que le lipoatelibre dans le sang car le lipoate est rapidement épuisé par le vecteur. Ainsi, des facteurs spatiauxet temporels dictent les stratégies de lipoylation de la bactérie lors d'une infection, et leréapprovisionnement en lipoate par protéolyse digestive dans le vecteur pourrait constituer untalon d'Achille exploité par les pathogènes
The agent of the plague, Yersinia pestis, obstructs the flea's digestive tract to be transmitted byfleas. Here, we sought to identify and study the role of new Y. pestis genes involved in theproduction of a transmissible infection in fleas. To this end, we developed a bioluminescencebasedapproach and employed it to investigate the mechanisms of pathogenesis at anunprecedented level of detail. Notably, we used our method to screen a library of mutants (eachlacking one or more of the genes previously identified as over-expressed in fleas) that wegenerated. Our screening listed several new and potentially important factors needed for fleabornetransmission of Y. pestis. Among them is LipB that catalyzes the first step of lipoatesynthesis (a cofactor covalently attached to at least three central metabolism enzymes). Oursubsequent studies have also revealed that the second and last enzyme of the lipoate biosynthesispathway, LipA, but also the lipoate ligase LplA (attaching lipoate scavenged from the environmentto apoenzymes) are also required to produce a transmissible infection in fleas. Thanks tobacteriological, microscopic and biochemical approaches carried out in vitro, ex-vivo and in vivo,we have revealed that bot the lipoate biosynthesis pathway and the lipoate scavenge pathway areinvolved in the colonization of the insect's proventriculus and midgut. Interestingly, we alsorevealed the salvage pathway’s enzyme LplA enhances the first step in lipoate biosynthesis duringforegut colonization but not during midgut colonization thanks to its octanoate activity. Lastly, wefound that Y. pestis primarily uses lipoate provided by digestive proteolysis (presumably as lipoylpeptides) rather than free lipoate in blood, which is quickly depleted by the vector. Thus, spatialand temporal factors dictate the bacterium’s lipoylation strategies during an infection, andreplenishment of lipoate by digestive proteolysis in the vector might constitute an Achilles’ heel thatis exploited by pathogens

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Malek, Maliya Alia. „Plague in Maghreb“. Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM5021/document.

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Yersinia pestis, agent causal de la peste, persiste dans la nature maintenu par un cycle enzootique dans des foyers conduisant à la réémergence de la maladie. En Afrique du Nord, où une réémergence a eu lieu après des années de ‘silence’, nous avons répertorié les différents épisodes ainsi que le nombre de cas en sur six pays à compter de 1940 en mettant en évidence l’importation de la maladie et un mode de contamination négligé, la transmission par voie orale. Une étude en Algérie sur 237 micromammifères confirme deux foyers et en revèle trois nouveaux porteurs d’un nouveau génotype (MST) de biotype Orientalis. Apodemus sylvaticus est par la même ajouté à la liste des rongeurs pestiférés. La projection des foyers de peste ainsi actualisés sur une carte géographique et écologique met en évidence la proximité des foyers de peste aux points d’eau saumâtre. Une étude statistique a confirmé une corrélation significative entre foyer de peste/eau salée à une proximité minimale <3 km en comparaison à des zones d’eau douce. Des échantillons environnementaux salés ont permis l’isolement d’une souche Y. pestis Algeria 3. Cette découverte confortée par l’observation expérimentale de la résistance de Y. pestis à un milieu hyper salé à 150g/L NaCl se traduisant par un protéome spécifique en réponse à ce stress avec une forme d’adaptation de type forme L de la bactérie dans ce type d’environnement. Notre travail éclaire de façon originale un facteur méconnu de persistance tellurique de Y. pestis, conditionnant la réémergence de la peste dans des foyers séculaires au Maghreb contrairement aux rivages Nord de la Méditerranée où la peste autochtone a disparu depuis un siècle
Yersinia pestis, the causal agent of plague, persists in nature maintained by an enzootic cycle in foci leading to the re-emergence of the disease. In North Africa, where re-emergence took place after years of 'silence', we have listed the various episodes and the number of cases in six countries from 1940 onwards, highlighting the importation of the disease and A method of neglected contamination, oral transmission. A study in Algeria on 237 micromammals confirms two foci and reveals three new carriers of a new genotype (MST) of orientalis biotype. Apodemus sylvaticus is by the same added to the list of plague rodents. The projection of the plague foci thus updated on a geographical and ecological map highlights the proximity of plague foci to brackish water points. A statistical study confirmed a significant correlation between plague / salt water at a minimal proximity <3 km compared to freshwater areas. Saline environmental samples allowed the isolation of a Y. pestis Algeria 3 strain. This discovery was confirmed by the experimental observation of the resistance of Y. pestis to a hyper-saline medium at 150 g / L NaCl resulting in a specific proteome In response to this stress with an adaptation form of form L of the bacterium in this type of environment. Our work illuminates in an original way an unknown factor of telluric persistence of Y. pestis, conditioning the re-emergence of the plague in secular centers in the Maghreb unlike the northern shores of the Mediterranean where the indigenous plague has disappeared for a century

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SILVEIRA, FILHO Vladimir da Mota. „Caracterização molecular dos fatores de transmissão/patogenicidade e tipagem de cepas de Yersinia pestis isoladas no foco do Nordeste do Brasil“. Universidade Federal de Pernambuco, 2012. https://repositorio.ufpe.br/handle/123456789/12477.

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Submitted by Luiz Felipe Barbosa (luiz.fbabreu2@ufpe.br) on 2015-03-13T14:43:13Z No. of bitstreams: 2 Vladimir da Mota Silveira Filho - Tese PPGG.pdf: 7570223 bytes, checksum: 939c1f76d28cf506a0b7eff7badba469 (MD5) license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5)
Made available in DSpace on 2015-03-13T14:43:13Z (GMT). No. of bitstreams: 2 Vladimir da Mota Silveira Filho - Tese PPGG.pdf: 7570223 bytes, checksum: 939c1f76d28cf506a0b7eff7badba469 (MD5) license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) Previous issue date: 2012-03-15
CPqAM CAPES CNPq Serviço de Referência em Peste
A peste, zoonose causada pela bactéria Yersinia pestis, continua sendo uma ameaça mundial. Como outras enfermidades relacionadas à pobreza, a peste é considerada uma doença negligenciada nos países tropicais, incluindo Brasil, onde ainda há detecção sorológica de atividade pestosa em animais-sentinela nos focos naturais. A ausência de uma vacina segura/efetiva, o surgimento de cepas multirresistentes e a possibilidade de seu uso como arma biológica aumentaram o interesse nos estudos genéticos/epidemiológicos do patógeno. Este trabalho teve como objetivos (1) comparar dois métodos moleculares de tipagem para identificar qual deles é capaz de estabelecer melhor correlação temporal e geográfica entre isolados brasileiros de Y. pestis; e (2) aprofundar os conhecimentos sobre os mecanismos de patogenicidade da bactéria. 25 cepas brasileiras de Y. pestis foram tipadas pela análise de múltiplos locos com número variável de repetições em tandem (MLVA) e pela eletroforese em gel de campo pulsado (PFGE). A associação entre essas técnicas demonstrou, pela primeira vez, diversidade genética entre cepas brasileiras de Y. pestis. Contudo, apenas MLVA permitiu estabelecer correlação entre os isolados de diferentes eventos epidemiológicos, mostrando-se mais eficiente para tipagem de Y. pestis, em relação ao PFGE. Quatro cepas avirulentas P.CE 882/1R e 32R, P.Exu 369 e 390, e uma cepa controle indiana altamente virulenta (195P) foram comparadas a nível fenotípico, genotípico, transcricional e proteômico, a fim de identificar possíveis causas da perda de virulência. Não foi encontrada diferença fenotípica e genotípica entre os cinco isolados, onde foi detectada a presença dos genes irp2, psn, ybtE (localizados na Ilha de Alta Patogenicidade - HPI), fur, hmsH, YPO2271, YPO2281, sodA, phoP, psaA (cromossomais) e pla, lcrV, ymt, caf1 (plasmidiais). Entretanto, a análise transcricional mostrou diferentes níveis de transcrição dos genes da HPI, apesar de nenhuma alteração estrutural de sequência ter sido detectada. Provavelmente a presença de ferro livre no meio de cultura utilizado ativou a proteína Fur, um regulador transcricional negativo da HPI. A análise quantitativa revelou níveis de transcrição dos genes da HPI acima do esperado nas cepas P.Exu 369 e 390, sugerindo possível disfunção no mecanismo regulatório da captura de ferro. A análise proteômica da subcultura P.CE 882/1R sugere que distúrbios metabólicos decorrentes do subcultivo e/ou estocagem podem estar associados ao fenótipo de avirulência. Estes achados sobre os mecanismos de virulência de Y. pestis poderão contribuir para identificação de alvos importantes para o desenvolvimento de novas vacinas e abordagens terapêuticas contra a peste.

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Pocock, Michael James Orlando. „The spatial population dynamics of house mice (Mus musculus domesticus) with reference to the potential transmission of zoonoses“. Thesis, University of York, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.369343.

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Bücher zum Thema "Yersinia pestis – Transmission"

Abbott, Rachel C. Plague. Reston, Va: U.S. Department of the Interior, U.S. Geological Survey, 2012.

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Buchteile zum Thema "Yersinia pestis – Transmission"

Hinnebusch, B. Joseph. „Biofilm-Dependent and Biofilm-Independent Mechanisms of Transmission of Yersinia pestis by Fleas“. In Advances in Yersinia Research, 237–43. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3561-7_30.

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Hinnebusch, B. Joseph. „Transmission Factors: Yersinia pestis Genes Required to Infect the Flea Vector of Plague“. In Advances in Experimental Medicine and Biology, 55–62. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/0-306-48416-1_11.

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Hinnebusch, B. J., und D. L. Erickson. „Yersinia pestis Biofilm in the Flea Vector and Its Role in the Transmission of Plague“. In Current Topics in Microbiology and Immunology, 229–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-75418-3_11.

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Mehlhorn, Heinz. „Yersina pestis: Discovery of transmission“. In Encyclopedia of Parasitology, 3073–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_3520.

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Mehlhorn, Heinz. „Yersina pestis: Discovery of transmission“. In Encyclopedia of Parasitology, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_3520-1.

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Prentice, Michael. „Plague: Yersinia pestis“. In Oxford Textbook of Medicine, herausgegeben von Christopher P. Conlon, 1081–85. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0121.

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Bubonic plague is a flea-borne zoonosis caused by the Gram-negative bacterium Yersinia pestis, which mainly affects small burrowing mammals including domestic rats. Human disease occurs in endemic countries—currently mainly in Africa (including Madagascar)—following bites from fleas recently hosted by a bacteraemic animal. Historical use of Y. pestis as a biological warfare agent has raised fears of its future use in bioterrorism. The commonest presentation is acute painful lymphadenitis (80–95% of suspected cases), with sudden onset of fever, chills, weakness, headache, and development of an intensely painful swollen lymph node (bubo). Primary septicaemia with no bubo occurs in 10% of cases. Spread to the lungs occurs in less than 10% of cases, resulting in pneumonia which can result in onward respiratory transmission by droplet infection. Overall mortality without treatment is 50–90%.

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„The Evolution of Flea-Borne Transmission in Yersinia pestis“. In Quality of Life in Aphasia, 72–101. Psychology Press, 2003. http://dx.doi.org/10.4324/9780203498040-10.

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Hinnebusch, B. Joseph. „Interactions of Yersinia pestis with its flea vector that lead to the transmission of plague“. In Microbe-vector Interactions in Vector-borne Diseases, 331–44. Cambridge University Press, 2001. http://dx.doi.org/10.1017/cbo9780511754845.015.

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