Virulence of pPst+ and pPst- strains of Yersinia pestis for guinea-pigs

Самойлова, С. В.; Самойлова, Л. В.; Yezhov, I. N.; Drozdov, I. G.; Anisimov, Andrey P.

doi:10.1099/00222615-45-6-440

Cited by 39 publications

(29 citation statements)

References 25 publications

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“…These data indicate that historical outbreaks of human pneumonic plague in the Caucasus region, where there are natural plague foci in common voles, may have been caused by pPst-negative Y. pestis strains. 59 Taken together, the data pertaining to Pla and virulence suggest this protein may be more important for virulence by the subcutaneous route of infection compared to the respiratory route. …”

Section: Role Of Plasmids In Y Pestis Virulencementioning

confidence: 99%

Current Trends in Plague Research: From Genomics to Virulence

Huang

Nikolich²,

Lindler³

2006

Clinical Medicine & Research

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Yersinia pestis is the causative agent of plague, which diverged from Yersinia pseudotuberculosis within the past 20,000 years. Although these two species share a high degree of homology at the DNA level (>90%), they differ radically in their pathogenicity and transmission. In this review, we briefly outline the known virulence factors that differentiate these two species and emphasize genetic studies that have been conducted comparing Y. pestis and Y. pseudotuberculosis.These comparisons have led to a better understanding of the genetic contributions to the differences in the virulence and pathogenicity between these two organisms and have generated information that can be applied in future diagnostic and vaccine development. Comparison of the genetic differences between Y. pestis and Y. pseudotuberculosis has also lent insight into the emergence of acute pathogens from organisms causing milder diseases.

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Section: Role Of Plasmids In Y Pestis Virulencementioning

confidence: 99%

Current Trends in Plague Research: From Genomics to Virulence

Huang

Nikolich²,

Lindler³

2006

Clinical Medicine & Research

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“…35 A likely explanation for this observation is the growth condition of cultures, as virulent Y. pestis strains grown at 37°C are more virulent for lung infections in guinea pigs than are the same strains propagated at 26°C. 44 We conclude that guinea pigs represent an excellent animal model for the study of pneumonic plague.…”

Section: Discussionmentioning

confidence: 80%

“…Growth of Y. pestis at 26°C is thought to mimic the ambient temperature in infected fleas before transmission of bubonic plague. 44 Plague bacilli were washed and diluted in sterile PBS to the required concentration. Guinea pigs were infected by s.c. injection with bacterial suspensions and were observed for morbidity, mortality, or recovery for 21 days.…”

Section: Plague Challenge Experimentsmentioning

confidence: 99%

“…For this experiment, Y. pestis CO92 was grown in heart infusion broth supplemented with 2.5 mmol/L calcium at 37°C overnight, conditions that mimic the temperature during man-to-man transmission of pneumonic plague. 44 Plague bacteria were washed and diluted in sterile PBS at the required concentration. Guinea pigs were observed for morbidity, mortality, or recovery for 14 days.…”

Section: Plague Challenge Experimentsmentioning

confidence: 99%

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Plague in Guinea Pigs and Its Prevention by Subunit Vaccines

Quenee

Ciletti

Berube

et al. 2011

The American Journal of Pathology

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Human pneumonic plague is a devastating and transmissible disease for which a Food and Drug Administration-approved vaccine is not available. Suitable animal models may be adopted as a surrogate for human plague to fulfill regulatory requirements for vaccine efficacy testing. To develop an alternative to pneumonic plague in nonhuman primates, we explored guinea pigs as a model system. On intranasal instillation of a fully virulent strain, Yersinia pestis CO92, guinea pigs developed lethal lung infections with hemorrhagic necrosis, massive bacterial replication in the respiratory system, and blood-borne dissemination to other organ systems. Expression of the Y. pestis F1 capsule was not required for the development of pulmonary infection; however, the capsule seemed to be important for the establishment of bubonic plague. The mean lethal dose (MLD) for pneumonic plague in guinea pigs was estimated to be 1000 colony-forming units. Immunization of guinea pigs with the recombinant forms of LcrV, a protein that resides at the tip of Yersinia type III secretion needles, or F1 capsule generated robust humoral immune responses. Whereas LcrV immunization resulted in partial protection against pneumonic plague challenge with 250 MLD Y. pestis CO92, immunization with recombinant F1 did not. rV10, a vaccine variant lacking LcrV residues 271-300, elicited protection against pneumonic plague, which seemed to be based on conformational antibodies directed against LcrV.

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“…Pla is considered to be an essential factor for the flea-borne route of transmission because it greatly enhances dissemination following subcutaneous injection, which is assumed to mimic transmission by fleas (Sodeinde et al, 1992). The requirement for Pla for dissemination from peripheral infection sites may not be universally true for all Y. pestis strains or for all animals, however (Samoilova et al, 1996;Welkos et al, 1997).…”

Section: The Hms Genes and The Biofilm Model Of Proventricular Blockagementioning

confidence: 99%

The Evolution of Flea-borne Transmission inYersinia pestis

Hinnebusch

2005

Current Issues in Molecular Biology

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Transmission by fleabite is a recent evolutionary adaptation that distinguishes Yersinia pestis, the agent of plague, from Yersinia pseudotuberculosis and all other enteric bacteria. The very close genetic relationship between Y. pestis and Y. pseudotuberculosis indicates that just a few discrete genetic changes were sufficient to give rise to fleaborne transmission. Y. pestis exhibits a distinct infection phenotype in its flea vector, and a transmissible infection depends on genes that are specifically required in the flea, but not the mammal. Transmission factors identified to date suggest that the rapid evolutionary transition of Y. pestis to flea-borne transmission within the last 1,500 to 20,000 years involved at least three steps: acquisition of the two Y. pestis-specific plasmids by horizontal gene transfer; and recruitment of endogenous chromosomal genes for new functions. Perhaps reflective of the recent adaptation, transmission of Y. pestis by fleas is inefficient, and this likely imposed selective pressure favoring the evolution of increased virulence in this pathogen. IntroductionPathogenic bacteria must overcome several physiological and immunological challenges to successfully infect even a single type of host, such as a mammal. It is remarkable, then, that bacteria transmitted by blood-feeding arthropods are capable of infecting two very different hosts during their life cycle: an invertebrate (usually an insect or tick) and a mammal. As if this were not enough of a challenge, it is not sufficient that an arthropod-borne bacterium successfully infect both vector and host. It must establish a transmissible infection in both; that is, it must infect the vector in such a way as to be transmitted during a blood meal, and it must infect the mammal in a way that allows uptake by a blood-feeding arthropod. This feat of evolution has occurred relatively rarely, but nonetheless arthropod-borne transmission has developed independently in a phylogenetically diverse group of microorganisms, including the rickettsiae, spirochetes in the genus Borrelia, and the Gram-negative bacteria.Compared to the ancient relationship of rickettsiae and spirochetes with arthropods, the vector relationship between Y. pestis and fleas is new. Population genetics and comparative genomics analyses indicate that Y. pestis is a clonal variant of Y. pseudotuberculosis that diverged only within the last 1,500 to 20,000 years (Achtman et Hinchcliffe et al., 2003;Chain et al., 2004). Presumably, the change from the food-and water-borne transmission of the Y. pseudotuberculosis ancestor to the flea-borne transmission of Y. pestis occurred during this evolutionarily short period of time. The monophyletic relationship of these two sister-species implies that the genetic changes that underlie the ability of Y. pestis to use the flea for its transmission vector are relatively few and discrete. Therefore, the Y. pseudotuberculosis -Y. pestis species complex provides an interesting case study in the evolution of arthropod-borne transm...

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Virulence of pPst+ and pPst- strains of Yersinia pestis for guinea-pigs

Cited by 39 publications

References 25 publications

Current Trends in Plague Research: From Genomics to Virulence

Current Trends in Plague Research: From Genomics to Virulence

Plague in Guinea Pigs and Its Prevention by Subunit Vaccines

The Evolution of Flea-borne Transmission inYersinia pestis

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