Susceptibility of the Langur Monkey (Semnopithecus entellus) to Experimental Plague: Pathology and Immunity

Chen, T. H.; Meyer, K. F.

doi:10.1093/infdis/115.5.456

Cited by 12 publications

(4 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The saturation of the filtering capacity of the spleen and liver coupled with massive in situ bacterial multiplication subsequently leads to a terminal septicemia with an invasion of the entire body, as attested by a luminescent signal emitted from the whole animal. This terminal septicemic stage of bubonic plague has been largely documented, both in human victims [4], [27], [30], [31] and in non-human hosts [5], [8], [9], [29], [32], [33].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Imaging of Bubonic Plague Dynamics by In Vivo Tracking of Bioluminescent Yersinia pestis

Nham¹,

Filali²,

Danne³

et al. 2012

PLoS ONE

View full text Add to dashboard Cite

Yersinia pestis dissemination in a host is usually studied by enumerating bacteria in the tissues of animals sacrificed at different times. This laborious methodology gives only snapshots of the infection, as the infectious process is not synchronized. In this work we used in vivo bioluminescence imaging (BLI) to follow Y. pestis dissemination during bubonic plague. We first demonstrated that Y. pestis CO92 transformed with pGEN-luxCDABE stably emitted bioluminescence in vitro and in vivo, while retaining full virulence. The light produced from live animals allowed to delineate the infected organs and correlated with bacterial loads, thus validating the BLI tool. We then showed that the first step of the infectious process is a bacterial multiplication at the injection site (linea alba), followed by a colonization of the draining inguinal lymph node(s), and subsequently of the ipsilateral axillary lymph node through a direct connection between the two nodes. A mild bacteremia and an effective filtering of the blood stream by the liver and spleen probably accounted for the early bacterial blood clearance and the simultaneous development of bacterial foci within these organs. The saturation of the filtering capacity of the spleen and liver subsequently led to terminal septicemia. Our results also indicate that secondary lymphoid tissues are the main targets of Y. pestis multiplication and that colonization of other organs occurs essentially at the terminal phase of the disease. Finally, our analysis reveals that the high variability in the kinetics of infection is attributable to the time the bacteria remain confined at the injection site. However, once Y. pestis has reached the draining lymph nodes, the disease progresses extremely rapidly, leading to the invasion of the entire body within two days and to death of the animals. This highlights the extraordinary capacity of Y. pestis to annihilate the host innate immune response.

show abstract

Section: Discussionmentioning

confidence: 99%

“…[5]–[9], the most widely used being the mouse experimental model. This model is appropriate and reliable to study a natural Y. pestis infection, as rodents are the normal hosts for Y. pestis .…”

Section: Introductionmentioning

confidence: 99%

Imaging of Bubonic Plague Dynamics by In Vivo Tracking of Bioluminescent Yersinia pestis

Nham¹,

Filali²,

Danne³

et al. 2012

PLoS ONE

View full text Add to dashboard Cite

show abstract

“…In studies of the pathogenesis of Y. pestis infection workers have used a number of different animal models (4,5,13,14,19,31,37). Currently, there is no consensus concerning which model system is best.…”

Section: Discussionmentioning

confidence: 99%

“…In previous studies workers used a number of different hosts to experimentally study Y. pestis infection, including nonhuman primates, cats, and rodents (mice and rats), each of which has advantages and disadvantages (4,5,13,14,19,31,37). The utility of rodent models, particularly mice, make them attractive models, as rodents are natural hosts of Y. pestis and have been used extensively in studies of both pathogenesis and the efficacy of vaccines against Y. pestis infection using both bubonic (22,26) and pneumonic (36,39) models.…”

mentioning

confidence: 99%

Delayed Inflammatory Response to Primary Pneumonic Plague Occurs in Both Outbred and Inbred Mice

2007

View full text Add to dashboard Cite

Yersinia pestis is the causative agent of plague, a disease that can manifest as either bubonic or pneumonic plague. An interesting feature of plague is that it is a rapidly progressive disease, suggesting that Y. pestis either evades and/or suppresses the innate immune response to infection. Therefore, the early host response during the course of primary pneumonic plague was investigated in two mouse strains, the outbred strain CD1 and the inbred strain C57BL/6. A comparative analysis of the course of disease in these two strains of mice indicated that they are susceptible to intranasal Y. pestis CO92 infection and have similar 50% lethal doses and kinetics of infection with respect to colonization of the lung, liver, and spleen. Significantly, in both strains of mice, robust neutrophil recruitment to the lungs was not observed until 48 h after infection, suggesting that there was a delay in inflammatory cell recruitment to the site of infection. In addition, proinflammatory cytokines (interleukin-6 [IL-6], tumor necrosis factor alpha, gamma interferon, IL-12p70, monocyte chemoattractant protein 1) and chemokines (KC, MIP-2) in the bronchoalveolar lavage fluids were not readily detected until 48 h after infection, which coincided with the increase in polymorphonuclear leukocyte (PMN) recruitment to the lungs. In comparison, CD1 mice with gram-negative pneumonia caused by Klebsiella pneumoniae exhibited strong inflammatory responses early in infection, with PMNs comprising the majority of the cells in the bronchoalveolar lavage fluid 24 h postinfection, indicating that PMN recruitment to the lungs could occur earlier in this infection than in Y. pestis infection. Together, our results indicate that there is a delay in the recruitment of neutrophils to the lungs in the mouse model of primary plague pneumonia that correlates with delayed expression of proinflammatory cytokines and chemokines in both outbred and inbred mice.

show abstract

Defense Against Biological Weapons (Biodefense)

Georgiev

2009

National Institute of Allergy and Infectious Diseases, NIH

View full text Add to dashboard Cite

Susceptibility of the Langur Monkey (Semnopithecus entellus) to Experimental Plague: Pathology and Immunity

Cited by 12 publications

References 0 publications

Imaging of Bubonic Plague Dynamics by In Vivo Tracking of Bioluminescent Yersinia pestis

Imaging of Bubonic Plague Dynamics by In Vivo Tracking of Bioluminescent Yersinia pestis

Delayed Inflammatory Response to Primary Pneumonic Plague Occurs in Both Outbred and Inbred Mice

Defense Against Biological Weapons (Biodefense)

Contact Info

Product

Resources

About