Cat-Transmitted Fatal Pneumonic Plague in a Person who Traveled from Colorado to Arizona *

Doll, John M.; Zeitz, Paul; Ettestad, Paul; Bucholtz, Ann; Davis, Ted; Gage, Kenneth L.

doi:10.4269/ajtmh.1994.51.109

Cited by 183 publications

(118 citation statements)

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“…Horizontally acquired DNA may be signi®cant in having enabled Y. pestis to adapt to new hosts; conversely, the identi®cation of gene remnants produced through genome decay may be associated with a redundant enteric lifestyle. Given the historical importance of plague and the need to understand the evolution and pathogenesis of such a potentially devastating pathogen, we undertook the genome sequencing of Y. pestis CO92 (biovar Orientalis), a strain recently isolated from a fatal human case of primary pneumonic plague contracted from an infected cat 5 .…”

mentioning

confidence: 99%

Genome sequence of Yersinia pestis, the causative agent of plague

Parkhill

Wren

Thomson

et al. 2001

Nature

1,123

965

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mentioning

confidence: 99%

Genome sequence of Yersinia pestis, the causative agent of plague

Parkhill

Wren

Thomson

et al. 2001

Nature

1,123

965

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“…In addition, extensive neutrophilic infiltrate and fibrin deposition have been observed, and in some cases a complete loss of recognizable alveolar architecture results from the infection (3,4). Studies of experimental primary pneumonic plague in monkeys, mice, and guinea pigs showed similar pathologic effects, including extensive intraalveolar edema, massive bacterial proliferation in the small airways, and numerous neutrophils in the alveoli (5)(6)(7)(8).…”

mentioning

confidence: 99%

Progression of primary pneumonic plague: A mouse model of infection, pathology, and bacterial transcriptional activity

Lathem

Crosby

Miller

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

269

363

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Although pneumonic plague is the deadliest manifestation of disease caused by the bacterium Yersinia pestis, there is surprisingly little information on the cellular and molecular mechanisms responsible for Y. pestis-triggered pathology in the lung. Therefore, to understand the progression of this unique disease, we characterized an intranasal mouse model of primary pneumonic plague. Mice succumbed to a purulent multifocal severe exudative bronchopneumonia that closely resembles the disease observed in humans. Analyses revealed a strikingly biphasic syndrome, in which the infection begins with an antiinflammatory state in the first 24 -36 h that rapidly progresses to a highly proinflammatory state by 48 h and death by 3 days. To assess the adaptation of Y. pestis to a mammalian environment, we used DNA microarray technology to analyze the transcriptional responses of the bacteria during interaction with the mouse lung. Included among the genes up-regulated in vivo are those comprising the yop-ysc type III secretion system and genes contained within the chromosomal pigmentation locus, validating the use of this technology to identify loci essential to the virulence of Y. pestis.inflammation ͉ microarray ͉ Yersinia pestis P neumonic plague is the deadliest manifestation of disease caused by the bacterium Yersinia pestis. Although rare compared with the bubonic form of plague, which is acquired by skin penetration, primary pneumonic plague is highly contagious and almost always fatal. The current worldwide incidence of plague is low by historical standards, but the possible combination of widespread aerosol dissemination and rapid disease progression are of particular concern for defense against bioterrorism (1).In cases of primary pneumonic plague in humans, microscopic examination of lung tissue reveals multiple histological patterns, including acute pneumonia, intraalveolar hemorrhage and edema, and the presence of extracellular bacteria in the alveoli but not the interstitium (2). In addition, extensive neutrophilic infiltrate and fibrin deposition have been observed, and in some cases a complete loss of recognizable alveolar architecture results from the infection (3, 4). Studies of experimental primary pneumonic plague in monkeys, mice, and guinea pigs showed similar pathologic effects, including extensive intraalveolar edema, massive bacterial proliferation in the small airways, and numerous neutrophils in the alveoli (5-8).How Y. pestis triggers pulmonary pathology is largely unexplored, as are the bacterial responses to this dramatically changing host environment. DNA microarray technology has been widely used to assess transcriptional changes in bacterial gene expression in vitro, but analyses of the bacterial transcriptome during host infection have been hampered by two significant problems (9). These include the excess amounts of copurified eukaryotic RNA that may produce nonspecific hybridization signals on the microarray, and the oftenlimiting amounts of bacterial RNA extracted from an animal, which w...

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“…The fully virulent Y. pestis strain CO92 37,38 and the variants CO92 ⌬F1 20 and CAC1 39 have been previously described. The ⌬F1 variant of Y. pestis CO92 carries a deletion of the caf1 gene, which encodes the F1 (Caf1) pilin subunit of plague bacteria.…”

Section: Bacterial Strains and Plasmidsmentioning

confidence: 99%

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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Cat-Transmitted Fatal Pneumonic Plague in a Person who Traveled from Colorado to Arizona *

Cited by 183 publications

References 0 publications

Genome sequence of Yersinia pestis, the causative agent of plague

Genome sequence of Yersinia pestis, the causative agent of plague

Progression of primary pneumonic plague: A mouse model of infection, pathology, and bacterial transcriptional activity

Plague in Guinea Pigs and Its Prevention by Subunit Vaccines

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