Journal articles: 'Plague Plague Plague Yersinia pestis'

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Theilmann, John, and Frances Cate. "A Plague of Plagues: The Problem of Plague Diagnosis in Medieval England." Journal of Interdisciplinary History 37, no. 3 (2007): 371–93. http://dx.doi.org/10.1162/jinh.2007.37.3.371.

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Recent works by historians and biologists have called into doubt whether the great epidemic of 1348/49 in England was the plague. Examination of the biological evidence, however, shows their arguments to be faulty. The great epidemic of 1348/49 may have included other diseases, but it was clearly yersinia pestis.

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Daniszewski, Piotr. "Pestis (Yersinia pestis) - As Biological Weapons." International Letters of Social and Humanistic Sciences 9 (September 2013): 84–94. http://dx.doi.org/10.18052/www.scipress.com/ilshs.9.84.

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Yersinia pestis (formerly Pasteurella pestis) is a type of bacterium. It is believed to have been responsible for plagues of the early 1300s. More accurately, it is a Gram-negative rod-shaped coccobacillus. It is a facultative anaerobe that can infect humans and other animals. Human Y. pestis infection takes three main forms: pneumonic, septicemic, and bubonic plagues. All three forms are widely believed to have been responsible for a number of high-mortality epidemics throughout human history, including the Justinianic Plague of the sixth century and the Black Death that accounted for the death of at least one-third of the European population between 1347 and 1353. It has now been shown conclusively that these plagues originated in rodent populations in China. More recently, Y. pestis has gained attention as a possible biological warfare agent and the CDC has classified it as a category A pathogen requiring preparation for a possible terrorist attack. Every year, thousands of cases of plague are still reported to the World Health Organization, although, with proper treatment, the prognosis for victims is now much better. A five- to six-fold increase in cases occurred in Asia during the time of the Vietnam war, possibly due to the disruption of ecosystems and closer proximity between people and animals. Plague also has a detrimental effect on non-human mammals. In the United States of America, animals such as the black-tailed prairie dog and the endangered black-footed ferret are under threat from the disease.

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Titball, R. W., J. Hill, D. G. Lawton, and K. A. Brown. "Yersinia pestis and plague." Biochemical Society Transactions 31, no. 1 (2003): 104–7. http://dx.doi.org/10.1042/bst0310104.

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Yersinia pestis is the aetiological agent of plague, a disease of humans that has potentially devastating consequences. Evidence indicates that Y. pestis evolved from Yersinia pseudotuberculosis, an enteric pathogen that normally causes a relatively mild disease. Although Y. pestis is considered to be an obligate pathogen, the lifestyle of this organism is surprisingly complex. The bacteria are normally transmitted to humans from a flea vector, and Y. pestis has a number of mechanisms which allow survival in the flea. Initially, the bacteria have an intracellular lifestyle in the mammalian host, surviving in macrophages. Later, the bacteria adopt an extracellular lifestyle. These different interactions with different host cell types are regulated by a number of systems, which are not well characterized. The availability of the genome sequence for this pathogen should now allow a systematic dissection of these regulatory systems.

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Titball, Richard W., and E. Diane Williamson. "Yersinia pestis (plague) vaccines." Expert Opinion on Biological Therapy 4, no. 6 (2004): 965–73. http://dx.doi.org/10.1517/14712598.4.6.965.

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Sun, Wei, Kenneth L. Roland, and Roy Curtiss III. "Developing live vaccines against plague." Journal of Infection in Developing Countries 5, no. 09 (2011): 614–27. http://dx.doi.org/10.3855/jidc.2030.

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Three great plague pandemics caused by the gram-negative bacterium Yersinia pestis have killed nearly 200 million people and it has been linked to biowarfare in the past. Plague is endemic in many parts of the world. In addition, the risk of plague as a bioweapon has prompted increased research to develop plague vaccines against this disease. Injectable subunit vaccines are being developed in the United States and United Kingdom. However, the live attenuated Y. pestis-EV NIIEG strain has been used as a vaccine for more than 70 years in the former Soviet Union and in some parts of Asia and provides a high degree of efficacy against plague. This vaccine has not gained general acceptance because of safety concerns. In recent years, modern molecular biological techniques have been applied to Y. pestis to construct strains with specific defined mutations designed to create safe, immunogenic vaccines with potential for use in humans and as bait vaccines to reduce the load of Y. pestis in the environment. In addition, a number of live, vectored vaccines have been reported using attenuated viral vectors or attenuated Salmonella strains to deliver plague antigens. Here we summarize the progress of live attenuated vaccines against plagu

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Rollins, MD, Sarah E., Sean M. Rollins, PhD, and Edward T. Ryan, MD. "Yersinia pestis and the Plague." Pathology Patterns Reviews 119 (June 1, 2003): 78–85. http://dx.doi.org/10.1309/dqm93r8qnqwbfyu8.

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Bai, Guangchun, Andrey Golubov, Eric A. Smith, and Kathleen A. McDonough. "The Importance of the Small RNA Chaperone Hfq for Growth of Epidemic Yersinia pestis, but Not Yersinia pseudotuberculosis, with Implications for Plague Biology." Journal of Bacteriology 192, no. 16 (2010): 4239–45. http://dx.doi.org/10.1128/jb.00504-10.

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ABSTRACT Yersinia pestis, the etiologic agent of plague, has only recently evolved from Yersinia pseudotuberculosis. hfq deletion caused severe growth restriction at 37°C in Y. pestis but not in Y. pseudotuberculosis. Strains from all epidemic plague biovars were similarly affected, implicating Hfq, and likely small RNAs (sRNAs), in the unique biology of the plague bacillus.

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Drancourt, Michel, and Didier Raoult. "Genotyping Yersinia pestis in historical plague." Lancet Infectious Diseases 11, no. 12 (2011): 894–95. http://dx.doi.org/10.1016/s1473-3099(11)70292-4.

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Perry, R. D., and J. D. Fetherston. "Yersinia pestis--etiologic agent of plague." Clinical Microbiology Reviews 10, no. 1 (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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Perry, R. D., and J. D. Fetherston. "Yersinia pestis--etiologic agent of plague." Clinical microbiology reviews 10, no. 1 (1997): 35–66. http://dx.doi.org/10.1128/cmr.10.1.35-66.1997.

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Titball, Richard W. "Plague: A natural history of Yersinia pestis." Biochemist 26, no. 2 (2004): 11–14. http://dx.doi.org/10.1042/bio02602011.

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Yersinia pestis is the aetiological agent of plague, a disease that has a place in history as one the major causes of death from the 14th to the 17th Centuries1. It is estimated that, during the Black Death pandemic, approximately 30% of the population of Europe died of plague, and so great in number were the corpses that, in many parts of Europe, the dead were placed in burial pits rather than receiving individual burials. Y. pestis has also been responsible for two other pandemics of disease. The first of these, the Justinian plague, occurred during the 1st Century. The third pandemic occurred during the latter part of the 19th Century and was confined mainly to South-East Asia1. Even today, several thousand cases of plague are reported to the World Health Organization each year, mainly from South-East Asia, the southwestern parts of the USA, Madagascar and Africa.

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Sebbane, Florent, Vladimir N. Uversky, and Andrey P. Anisimov. "Yersinia pestis Plasminogen Activator." Biomolecules 10, no. 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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Cornelius, Claire A., Lauriane E. Quenee, Derek Elli, Nancy A. Ciletti, and Olaf Schneewind. "Yersinia pestis IS1541 Transposition Provides for Escape from Plague Immunity." Infection and Immunity 77, no. 5 (2009): 1807–16. http://dx.doi.org/10.1128/iai.01162-08.

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ABSTRACTYersinia pestisis perhaps the most feared infectious agent due to its ability to cause epidemic outbreaks of plague disease in animals and humans with high mortality. Plague infections elicit strong humoral immune responses against the capsular antigen (fraction 1 [F1]) ofY. pestis, and F1-specific antibodies provide protective immunity. Here we asked whetherY. pestisgenerates mutations that enable bacterial escape from protective immunity and isolated a variant with an IS1541insertion incaf1Aencoding the F1 outer membrane usher. Thecaf1A::IS1541insertion prevented assembly of F1 pili and provided escape from plague immunity via F1-specific antibodies without a reduction in virulence in mouse models of bubonic or pneumonic plague. F1-specific antibodies interfere withY. pestistype III transport of effector proteins into host cells, an inhibitory effect that was overcome by thecaf1A::IS1541insertion. These findings suggest a model in which IS1541insertion intocaf1Aprovides for reversible changes in envelope structure, enablingY. pestisto escape from adaptive immune responses and plague immunity.

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Drancourt, Michel, and Didier Raoult. "Yersinia pestis and the three plague pandemics." Lancet Infectious Diseases 14, no. 10 (2014): 918–19. http://dx.doi.org/10.1016/s1473-3099(14)70877-1.

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Green, Monica H., Lori Jones, Lester K. Little, Uli Schamiloglu, and George D. Sussman. "Yersinia pestis and the three plague pandemics." Lancet Infectious Diseases 14, no. 10 (2014): 918. http://dx.doi.org/10.1016/s1473-3099(14)70878-3.

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Atshabar, B., S. T. Nurtazhin, A. Shevtsov, et al. "POPULATIONS OF THE MAJOR CARRIER RHOMBOMYS OPIMUS, VECTORS OF XENOPSYLLA FLEAS AND THE CAUSATIVE AGENT OF YERSINIA PESTIS IN THE CENTRAL ASIAN DESERT NATURAL FOCUS OF PLAGUE." BULLETIN 389, no. 1 (2021): 26–34. http://dx.doi.org/10.32014/2021.2518-1467.4.

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In the Central Asia desert natural focus of plague, the major carrier of the Yersinia pestis agent is the great gerbil Rhombomys opimus, and its vectors include fleas of the Xenopsylla genus. Phenotypical and genotypical properties of the R. opimus populations, Xenopsylla fleas and Yersinia pestis strains have been studied in the Central Asia desert natural focus of plague. Phenotypic distinctions and population discreteness have been identified in R. opimus on the cytochrome b gene of the mitochondrial genome from three autonomous plague foci: Pre-Balkhash, Betpakdala and Pre-Ustyurt. Phenotypic distinctions have been found in Xenopsylla fleas in the Central Asia desert natural focus of plague, and the genotype of X. gerbilli minax fleas on the Cox2 gene of the mitochondrial DNA; these had been captured in the Betpakdala autonomous focus. The repertoire diversity in phenotypical properties of Y. pestis strains from different natural foci of plague has been demonstrated, and population discreteness of Y. pestis strains has been determined using the next-generation sequencing method for single nucleotide polymorphism genes. Results of the study suggest that geographical and environmental isolation and natural selection have led to heterogeneity in the three populations of the great gerbil, vector fleas and Y. pestis.

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Ben Ari, Tamara, Alexander Gershunov, Kenneth L. Gage, et al. "Human plague in the USA: the importance of regional and local climate." Biology Letters 4, no. 6 (2008): 737–40. http://dx.doi.org/10.1098/rsbl.2008.0363.

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A 56-year time series of human plague cases ( Yersinia pestis ) in the western United States was used to explore the effects of climatic patterns on plague levels. We found that the Pacific Decadal Oscillation (PDO), together with previous plague levels and above-normal temperatures, explained much of the plague variability. We propose that the PDO's impact on plague is conveyed via its effect on precipitation and temperature and the effect of precipitation and temperature on plague hosts and vectors: warmer and wetter climate leading to increased plague activity and thus an increased number of human cases. Our analysis furthermore provides insights into the consistency of plague mechanisms at larger scales.

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Eppinger, Mark, Zhaobiao Guo, Yinong Sebastian, et al. "Draft Genome Sequences of Yersinia pestis Isolates from Natural Foci of Endemic Plague in China." Journal of Bacteriology 191, no. 24 (2009): 7628–29. http://dx.doi.org/10.1128/jb.01227-09.

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ABSTRACT To gain insights into the evolutionary origin, emergence, and pathogenicity of the etiologic agent of plague, we have sequenced the genomes of four Yersinia pestis strains isolated from the zoonotic rodent reservoir in foci of endemic plague in China. These resources enable in-depth studies of Y. pestis sequence variations and detailed whole-genome comparisons of very closely related genomes from the supposed site of the origin and the emergence of global pandemics of plague.

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DeBord, Kristin L., Deborah M. Anderson, Melanie M. Marketon, et al. "Immunogenicity and Protective Immunity against Bubonic Plague and Pneumonic Plague by Immunization of Mice with the Recombinant V10 Antigen, a Variant of LcrV." Infection and Immunity 74, no. 8 (2006): 4910–14. http://dx.doi.org/10.1128/iai.01860-05.

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ABSTRACT In contrast to Yersinia pestis LcrV, the recombinant V10 (rV10) variant (lacking residues 271 to 300) does not suppress the release of proinflammatory cytokines by immune cells. Immunization with rV10 generates robust antibody responses that protect mice against bubonic plague and pneumonic plague, suggesting that rV10 may serve as an improved plague vaccine.

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Quenee, Lauriane E., Claire A. Cornelius, Nancy A. Ciletti, Derek Elli, and Olaf Schneewind. "Yersinia pestis caf1 Variants and the Limits of Plague Vaccine Protection." Infection and Immunity 76, no. 5 (2008): 2025–36. http://dx.doi.org/10.1128/iai.00105-08.

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ABSTRACT Yersinia pestis, the highly virulent agent of plague, is a biological weapon. Strategies that prevent plague have been sought for centuries, and immunization with live, attenuated (nonpigmented) strains or subunit vaccines with F1 (Caf1) antigen is considered effective. We show here that immunization with live, attenuated strains generates plague-protective immunity and humoral immune responses against F1 pilus antigen and LcrV. Y. pestis variants lacking caf1 (F1 pili) are not only fully virulent in animal models of bubonic and pneumonic plague but also break through immune responses generated with live, attenuated strains or F1 subunit vaccines. In contrast, immunization with purified LcrV, a protein at the tip of type III needles, generates protective immunity against the wild-type and the fully virulent caf1 mutant strain, in agreement with the notion that LcrV can elicit vaccine protection against both types of virulent plague strains.

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Born, Friederike, Peter Braun, Holger C. Scholz, and Gregor Grass. "Specific Detection of Yersinia pestis Based on Receptor Binding Proteins of Phages." Pathogens 9, no. 8 (2020): 611. http://dx.doi.org/10.3390/pathogens9080611.

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The highly pathogenic bacterium Yersinia pestis is the causative agent of plague, a notorious infectious zoonotic disease. When transmitted from person to person as pneumonic plague via droplets, Y. pestis is highly contagious and in most cases is fatal if left untreated. Thus, when plague is suspected, rapid diagnosis is crucial, as a serious course of the infection is only averted by early antibiotic therapy. The bacterium is easy to cultivate, accessible and has a high potential for nefarious use such as bioterrorism. Highly specific, rapid and easy-to-use confirmatory diagnostic methods are required to reliably identify the pathogen independently from PCR-based methods or F1 antigen-based immunological detection. Yersinia pestis specific phages such as L-413C and ΦA1122 are already used for detection of Y. pestis in bacterial plaque or biosensor assays. Here, we made use of the host specificities conferred by phage receptor binding (or tail fiber/spike) proteins (RBP) for developing a specific, fast and simple fluorescence-microscopy-based detection method for Y. pestis. Genes of putative RBP of phages L-413C (gpH) and ΦA1122 (gp17) were fused with those of fluorescent proteins and recombinant receptor-reporter fusion proteins were produced heterologously in Escherichia coli. When first tested on attenuated Y. pestis strain EV76, RBP-reporters bound to the bacterial cell surface. This assay could be completed within a few minutes using live or formaldehyde-inactivated cells. Specificity tests using cultures of closely related Yersinia species and several inactivated fully virulent Y. pestis strains exhibited high specificities of the RBP-reporters against Y. pestis. The L-413C RBP proved to be especially specific, as it only detected Y. pestis at all temperatures tested, whereas the RBP of ΦA1122 also bound to Y. pseudotuberculosis strains at 37 °C (but not at 28, 20 or 6 °C). Finally, the Y. pestis-specific capsule, produced when grown at 37 °C, significantly reduced binding of phage ΦA1122 RBP, whereas the capsule only slightly diminished binding of L-413C RBP.

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Amedei, Amedeo, Elena Niccolai, Luigi Marino, and Mario Milco D'Elios. "Role of immune response in Yersinia pestis infection." Journal of Infection in Developing Countries 5, no. 09 (2011): 628–39. http://dx.doi.org/10.3855/jidc.1999.

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Yersinia pestis (Y. Pestis) is an infamous pathogen causing plague pandemics throughout history and is a selected agent of bioterrorism threatening public health. Y. pestis was first isolated by Alexandre Yersin in 1894 in Hong Kong and in the years to follow from all continents. Plague is enzootic in different rodents and their fleas in Africa, North and South America, and Asia such as Middle/Far East and ex-USSR countries. Comprehending the multifaceted interaction between Y. pestis and the host immune system will enable us design more effective vaccines. Innate immune response and both component (humoral and cellular) of adaptive immune response contribute to host defense against Y.pestis infection, but the bacterium possess different mechanisms to counteract the immune response. The aims of this review are to analyze the role of immune response versus Yersinia pestis infection and to highlight the various stratagems adopted by Y. pestis to escape the immunological defenses.

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Lindler, Luther E. "Typing Methods for the Plague Pathogen, Yersinia pestis." Journal of AOAC INTERNATIONAL 92, no. 4 (2009): 1174–83. http://dx.doi.org/10.1093/jaoac/92.4.1174.

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Abstract Phenotypic and genotypic methodologies have been used to differentiate the etiological agent of plague, Yersinia pestis. Historically, phenotypic methods were used to place isolates into one of three biovars based on nitrate reduction and glycerol fermentation. Classification of Y. pestis into genetic subtypes is problematic due to the relative monomorphic nature of the pathogen. Resolution into groups is dependent on the number and types of loci used in the analysis. The last 510 years of research and analysis in the field of Y. pestis genotyping have resulted in a recognition by Western scientists that two basic types of Y. pestis exist. One type, considered to be classic strains that are able to cause human plague transmitted by the normal flea vector, is termed epidemic strains. The other type does not typically cause human infections by normal routes of infection, but is virulent for rodents and is termed endemic strains. Previous classification schemes used outside the Western hemisphere referred to these latter strains as Pestoides varieties of Y. pestis. Recent molecular analysis has definitely shown that both endemic and epidemic strains arose independently from a common Yersinia pseudotuberculosis ancestor. Currently, 11 major groups of Y. pestis are defined globally.

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Hill, Jim, Jim E. Eyles, Stephen J. Elvin, Gareth D. Healey, Roman A. Lukaszewski, and Richard W. Titball. "Administration of Antibody to the Lung Protects Mice against Pneumonic Plague." Infection and Immunity 74, no. 5 (2006): 3068–70. http://dx.doi.org/10.1128/iai.74.5.3068-3070.2006.

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ABSTRACT Intratracheal delivery of aerosolized monoclonal antibodies with specificity for Yersinia pestis LcrV and F1 antigens protected mice in a model of pneumonic plague. These data support the utility of inhaled antibodies as a fast-acting postexposure treatment for plague.

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Uittenbogaard, Annette M., Tanya Myers-Morales, Amanda A. Gorman, et al. "Temperature-dependence of yadBC phenotypes in Yersinia pestis." Microbiology 160, no. 2 (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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Congleton, Yasemin H. K., Christine R. Wulff, Edward J. Kerschen та Susan C. Straley. "Mice Naturally Resistant to Yersinia pestis Δpgm Strains Commonly Used in Pathogenicity Studies". Infection and Immunity 74, № 11 (2006): 6501–4. http://dx.doi.org/10.1128/iai.00597-06.

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ABSTRACT We report that females of some substrains of inbred mouse strain 129 are resistant to systemic plague due to conditionally virulent Δpgm strains of Yersinia pestis; however, fully virulent Y. pestis is not attenuated in these mice. Therefore, these mice offer a powerful system in which to map in parallel host resistance traits and opposing bacterial virulence properties for plague.

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Parent, Michelle A., Kiera N. Berggren, Lawrence W. Kummer, et al. "Cell-Mediated Protection against Pulmonary Yersinia pestis Infection." Infection and Immunity 73, no. 11 (2005): 7304–10. http://dx.doi.org/10.1128/iai.73.11.7304-7310.2005.

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ABSTRACT Pulmonary infection with the bacterium Yersinia pestis causes pneumonic plague, an often-fatal disease for which no vaccine is presently available. Antibody-mediated humoral immunity can protect mice against pulmonary Y. pestis infection, an experimental model of pneumonic plague. Little is known about the protective efficacy of cellular immunity. We investigated the cellular immune response to Y. pestis in B-cell-deficient μMT mice, which lack the capacity to generate antibody responses. To effectively prime pulmonary cellular immunity, we intranasally vaccinated μMT mice with live replicating Y. pestis. Vaccination dramatically increased survival of μMT mice challenged intranasally with a lethal Y. pestis dose and significantly reduced bacterial growth in pulmonary, splenic, and hepatic tissues. Vaccination also increased numbers of pulmonary T cells, and administration of T-cell-depleting monoclonal antibodies at the time of challenge abrogated vaccine-induced survival. Moreover, the transfer of Y. pestis-primed T cells to naive μMT mice protected against lethal intranasal challenge. These findings establish that vaccine-primed cellular immunity can protect against pulmonary Y. pestis infection and suggest that vaccines promoting both humoral and cellular immunity will most effectively combat pneumonic plague.

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Watson, R. P., T. W. Blanchard, M. G. Mense, and P. W. Gasper. "Histopathology of Experimental Plague in Cats." Veterinary Pathology 38, no. 2 (2001): 165–72. http://dx.doi.org/10.1354/vp.38-2-165.

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Formalin-fixed paraffin-embedded archival tissues of seven adult cats of both sexes that died after being experimentally infected with Yersinia pestis were examined light microscopically to characterize the lesions. The cats were exposed in two groups using two routes of infection: ingestion of Y. pestis-infected rodent or a subcutaneous injection of Y. pestis to simulate a flea bite. Immunohistochemistry was performed on tissues from all organ systems from a representative cat from each group to determine the distribution of Y. pestis bacilli during infection. In all seven cats, bubonic plague lesions were seen. The lesions of pneumonic plague were present in two cats. Septicemic plague was confirmed in all seven cats by bacteriologic culture. Aggregations of bacteria were seen in lymphoid tissue in all cats and in lung tissues from the two cats with pneumonic plague. The most consistent histologic finding was necrosuppurative inflammation in the lymph nodes. Invariably, Y. pestis bacteria were present in large numbers at affected sites. Orally infected cats had more numerous lesions in the lymph nodes of the head and neck regions. These experimentally induced cases of feline plague document that cats are unique among carnivores in exhibiting bubonic, pneumonic, and septicemic plague following exposure to Y. pestis. The lesions of the orally infected cats were consistent with those previously described for naturally occurring Y. pestis infections in cats and corroborate the contention that cats most commonly contract plague by eating Y. pestis-infected rodents and not via flea bite. The histopathology of Y. pestis disease in these cats is comparable to that described for human plague.

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Kutyrev, V., R. J. Mehigh, V. L. Motin, M. S. Pokrovskaya, G. B. Smirnov, and R. R. Brubaker. "Expression of the Plague Plasminogen Activator in Yersinia pseudotuberculosis andEscherichia coli." Infection and Immunity 67, no. 3 (1999): 1359–67. http://dx.doi.org/10.1128/iai.67.3.1359-1367.1999.

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ABSTRACT Enteropathogenic yersiniae (Yersinia pseudotuberculosisand Yersinia enterocolitica) typically cause chronic disease as opposed to the closely related Yersinia pestis, the causative agent of bubonic plague. It is established that this difference reflects, in part, carriage by Y. pestis of a unique 9.6-kb pesticin or Pst plasmid (pPCP) encoding plasminogen activator (Pla) rather than distinctions between shared ∼70-kb low-calcium-response, or Lcr, plasmids (pCD in Y. pestisand pYV in enteropathogenic yersiniae) encoding cytotoxic Yops and anti-inflammatory V antigen. Pla is known to exist as a combination of 32.6-kDa (α-Pla) and slightly smaller (β-Pla) outer membrane proteins, of which at least one promotes bacterial dissemination in vivo and degradation of Yops in vitro. We show here that only α-Pla accumulates in Escherichia coli LE392/pPCP1 cultivated in enriched medium and that either autolysis or extraction of this isolate with 1.0 M NaCl results in release of soluble α and β forms possessing biological activity. This process also converted cell-bound α-Pla to β-Pla and smaller forms in Y. pestis KIM/pPCP1 and Y. pseudotuberculosis PB1/+/pPCP1 but did not promote solubilization. Pla-mediated posttranslational hydrolysis of pulse-labeled Yops in Y. pseudotuberculosis PB1/+/pPCP1 occurred more slowly than that in Y. pestis but was otherwise similar except for accumulation of stable degradation products of YadA, a pYV-mediated fibrillar adhesin not encoded in frame by pCD. Carriage of pPCP by Y. pseudotuberculosis did not significantly influence virulence in mice.

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Gilbert, M. Thomas P., Jon Cuccui, William White, et al. "Absence of Yersinia pestis-specific DNA in human teeth from five European excavations of putative plague victims." Microbiology 150, no. 2 (2004): 341–54. http://dx.doi.org/10.1099/mic.0.26594-0.

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This study reports the results of a collaborative study undertaken by two independent research groups to (a) confirm recent PCR-based detection of Yersinia pestis DNA in human teeth from medieval plague victims in France, and (b) to extend these observations over five different European burial sites believed to contain plague victims dating from the late 13th to 17th centuries. Several different sets of primers were used, including those previously documented to yield positive results on ancient DNA extracts. No Y. pestis DNA could be amplified from DNA extracted from 108 teeth belonging to 61 individuals, despite the amplification of numerous other bacterial DNA sequences. Several methods of extracting dentine prior to the DNA extraction were also compared. PCR for bacterial 16S rDNA indicated the presence of multiple bacterial species in 23 out of 27 teeth DNA extracts where dentine was extracted using previously described methods. In comparison, positive results were obtained from only five out of 44 teeth DNA extracts for which a novel contamination-minimizing embedding technique was used. Therefore, high levels of environmental bacterial DNA are present in DNA extracts where previously described methods of tooth manipulation are used. To conclude, the absence of Y. pestis-specific DNA in an exhaustive search using specimens from multiple putative European plague burial sites does not allow us to confirm the identification of Y. pestis as the aetiological agent of the Black Death and subsequent plagues. In addition, the utility of the published tooth-based ancient DNA technique used to diagnose fatal bacteraemias in historical epidemics still awaits independent corroboration.

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Lopatina, N. V., and B. N. Mishankin. "Study of Interactions of Microscopic Fungi Isolated from Burrow Microbiotopes of Great Gerbil and Little Souslik with Plague Agent and its Vectors." Epidemiology and Vaccine Prevention 16, no. 6 (2017): 32–37. http://dx.doi.org/10.31631/2073-3046-2017-16-6-32-37.

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At present there is strong evidence of the long-term persistence of Yersinia pestis in soil during interepizootic period in nonculturable and L-forms of bacteria. This information helps to reveal the mechanisms of emergence, establishment and extinction of plague foci. Deciphering causes of transformation of plague microbe in rodent burrows is possible only under condition of detailed study of biocenotic relations of plague causative agent with each of the multiple biocenosis components, including microorganisms -permanent inhabitants of the burrow microbiotopes in natural plague foci. Purpose of the study: Study of interactions of microscopic fungi-micromycetes iso-lated from burrow microbiotopes of great gerbil and little souslik in the Ural-Emba interfluve and in Nogai steppe with plague agent and its vectors. Materials and methods: The effect of 74 micromycete species, isolated in natural plague foci, on Yersinia pestis virulent strains was studied in vitro and in vivo (in organisms of X. skrjabini fleas). In the experiments in vitro fungi metabolites were applied on the lawns of Y. pestis test-cultures with subsequent recording of the size of lysed zones. Fleas were challenged in tubes with filtering-paper strips impregnated by fungal cultural liquid and then LT100 value was calculated. In the experiments in vivo fungus conidia were applied on the surface of insect cuticle; flea challenging with plague was carried out on agonizing white mice infected by plague microbe. Insect challenge with plague and fungal conidia was alternated in different succession. Results and discussion: Of 74 micromycete strains 78.4% produced antagonistic effect in relation to 1-5 Y. pestis strains. Ashergillus versicolor, A. clavatus, A. sulfereus, Mucor racematus, Penicillium baarnensens, P. sp. relative to P. charlesii, P. sp. relative to P. martensii, P. insectus, P. chrysogenum fungi induced growth suppression of all five test strains of Y. pestis. High antibiotic activity of fungi metabolites was accompanied by insecticidal activity against Xenopsylla skrjabini fleas. Microscopic fungi P. funiculosum, P. cyclopium, P. chrisogenum, P. charlesii. P. canescens, A. versicolor induced 100% flea death on 4-6 day. As a result of insect pretreatment by conidia of P. funiculosum with subsequent challenging with plague microbe block formation in fleas decreased 14 times, and the number of Y. pestis cells after 12 days was 25-33 times less independent of succession, in which insects were challenged with microorganisms. Conclusion. It is supposed that micromycetes could play an important role in natural plague foci, adjusting epizootic activity of plague vectors and causative agent.

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Shen, Xiaona, Qi Wang, Lianxu Xia, et al. "Complete Genome Sequences of Yersinia pestis from Natural Foci in China." Journal of Bacteriology 192, no. 13 (2010): 3551–52. http://dx.doi.org/10.1128/jb.00340-10.

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ABSTRACT Yersinia pestis, the causative agent of plague, is a deadly bacterium that affects humans. Strain D106004 was isolated from a new plague focus in Yulong County, China, in 2006. To gain insights into the epidemic origin, we have sequenced the genomes of D106004 and strains Z176003 and D182038, isolated from neighboring regions.

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Vityazeva, S. A., T. P. Starovoitova, G. B. Mukhturgin, V. I. Dubrovina, and S. V. Balakhonov. "Pathological Changes in Respiratory Part of Lungs White Mice with Experimental Plague." Epidemiology and Vaccine Prevention 14, no. 5 (2015): 67–71. http://dx.doi.org/10.31631/2073-3046-2015-14-5-67-71.

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The paper presents data on changes in the respiratory part of lungs of white mice with experimental plague caused by Yersinia рestis strains with different plasmid composition of Tuva and Gorno-Altaisk natural foci of plague and breeding clones. Morphological and structural changes in the lungs, which appear different degree of activation of the immune response and the severity of the pathological process caused by Y. pestis subsp. altaica and Y. pestis subsp. pestis and their isogenic plasmid options.

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Hill, Jim, Catherine Copse, Sophie Leary, Anthony J. Stagg, E. Diane Williamson, and Richard W. Titball. "Synergistic Protection of Mice against Plague with Monoclonal Antibodies Specific for the F1 and V Antigens of Yersinia pestis." Infection and Immunity 71, no. 4 (2003): 2234–38. http://dx.doi.org/10.1128/iai.71.4.2234-2238.2003.

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ABSTRACT Monoclonal antibodies specific for Yersinia pestis V antigen and F1 antigen, administered singly or in combination, protected mice in models of bubonic and pneumonic plague. Antibodies showed synergy when administered prophylactically and as a therapy 48 h postinfection. Monoclonal antibodies therefore have potential as a treatment for plague.

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Sazanova, E. V., T. A. Malyukova, and Yu A. Popov. "Dummy Yersinia pestis Strains: Selection Criteria, Usage Guidelines." Problems of Particularly Dangerous Infections, no. 3 (September 20, 2014): 38–41. http://dx.doi.org/10.21055/0370-1069-2014-3-38-41.

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Objective of the work was to develop selection criteria for the dummy Y. pestis strains, as well as principles of the setting-up a panel and its application for practicing laboratory and differential diagnostics of plague. Studied were the RF regulations, statutory documents and methodological recommendations on the laboratory diagnostics of plague and safety of works with microorganisms; training courses for specialists to qualify for work with the agents of particularly dangerous infections. Research method: analytical. Consequently, established were the term for “dummy strain”; selection criteria for the Y. pestis strains used in the practical course within the frames of the training programme “Microbiology and Laboratory Diagnosis of Plague”; and algorithm of the course application in view of biological risk mitigation during the process of education.

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Namouchi, Amine, Meriam Guellil, Oliver Kersten, 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 (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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Pechous, Roger D., Vijay Sivaraman, Nikolas M. Stasulli, and William E. Goldman. "Pneumonic Plague: The Darker Side of Yersinia pestis." Trends in Microbiology 24, no. 3 (2016): 190–97. http://dx.doi.org/10.1016/j.tim.2015.11.008.

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Nemeth, J., and S. C. Straley. "Effect of Yersinia pestis YopM on experimental plague." Infection and immunity 65, no. 3 (1997): 924–30. http://dx.doi.org/10.1128/iai.65.3.924-930.1997.

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Tsiamis, Costas, Effie Poulakou-Rebelakou, and Eleni Petridou. "The Red Sea and the Port of Clysma. A Possible Gate of Justinian’s Plague." Gesnerus 66, no. 2 (2009): 209–17. http://dx.doi.org/10.1163/22977953-06602002.

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The aim of this study is to present the sea and land commercial routes of the Byzantine Egypt and their role in the dissemination of the plague bacteria Yersinia pestis from the Red Sea to Mediterranean ports.The Mediterranean port of Pelusium was considered as the starting point of the first plague pandemic, according to the historical and archaeological data; the port of Clysma in the Red Sea, however, can also be assumed as possible entrance gate of the Yersinia pestis. Indeed, it is proposed that the port of Clysma is most likely to have been the gateway of Yersinia pestis in the Byzantine Egypt when the epidemic broke out, given its geographic position and close trade relationship at the time of the epidemic in Pelusium.

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Lee-Lewis, Hanni, and Deborah M. Anderson. "Absence of Inflammation and Pneumonia during Infection with Nonpigmented Yersinia pestis Reveals a New Role for the pgm Locus in Pathogenesis." Infection and Immunity 78, no. 1 (2009): 220–30. http://dx.doi.org/10.1128/iai.00559-09.

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ABSTRACT Yersinia pestis causes primary pneumonic plague in many mammalian species, including humans, mice, and rats. Virulent Y. pestis strains undergo frequent spontaneous deletion of a 102-kb chromosomal DNA fragment, known as the pigmentation (pgm) locus, when grown in laboratory media, yet this locus is present in every virulent isolate. The pgm locus encodes, within a high-pathogenicity island, siderophore biosynthesis genes that are required for growth in the mammalian host when inoculated by peripheral routes. Recently, higher challenge doses of nonpigmented Y. pestis were reported to cause fatal pneumonic plague in mice, suggesting a useful model for studies of virulence and immunity. In this work, we show that intranasal infection of BALB/c mice with nonpigmented Yersinia pestis does not result in pneumonic plague. Despite persistent bacterial colonization of the lungs and the eventual death of infected mice, pulmonary inflammation was generally absent, and there was no disease pathology characteristic of pneumonic plague. Iron given to mice at the time of challenge, previously shown to enhance the virulence of pgm-deficient strains, resulted in an accelerated disease course, with less time to bacteremia and lethality, but lung inflammation and pneumonia were still absent. We examined other rodent models and found differences in lung inflammatory responses, some of which led to clearance and survival even when high challenge doses were used. Together, the results suggest that the Y. pestis pgm locus encodes previously unappreciated virulence factors required for the induction of pneumonic plague that are independent of iron scavenging from the mammalian host.

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Philipovskiy, Alexander V., and Stephen T. Smiley. "Vaccination with Live Yersinia pestis Primes CD4 and CD8 T Cells That Synergistically Protect against Lethal Pulmonary Y. pestis Infection." Infection and Immunity 75, no. 2 (2006): 878–85. http://dx.doi.org/10.1128/iai.01529-06.

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ABSTRACT Vaccination with live attenuated Yersinia pestis confers protection against pneumonic plague but is not considered safe for general use. Subunit plague vaccines containing the Y. pestis F1 and LcrV proteins prime robust antibody responses but may not provide sufficient protection. To aid the development of a safe and effective plague vaccine, we are investigating roles for T cells during defense against Y. pestis infection. Here we demonstrate that vaccination of mice with live Y. pestis primes specific CD4 and CD8 T cells that, upon purification and direct transfer to naïve mice, synergistically protect against lethal intranasal Y. pestis challenge. While not preventing extrapulmonary dissemination, the coadministered T cells promote bacterial clearance and reduce bacteremia. These observations strongly suggest that development of pneumonic plague vaccines should strive to prime both CD4 and CD8 T cells. Finally, we demonstrate that vaccination with live Y. pestis primes CD4 and CD8 T cells that respond to Y. pestis strains lacking the capacity to express F1, LcrV, and all pCD1/pPCP-encoded proteins, suggesting that protective T cells likely recognize antigens distinct from those previously defined as targets for humoral immunity.

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Elbroch, L. Mark, T. Winston Vickers, and Howard B. Quigley. "Plague, pumas and potential zoonotic exposure in the Greater Yellowstone Ecosystem." Environmental Conservation 47, no. 2 (2020): 75–78. http://dx.doi.org/10.1017/s0376892920000065.

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SummaryWe tested for plague (Yersinia pestis) in a puma population in the Greater Yellowstone Ecosystem (GYE) over 9 years, overlapping a case when a boy in the area became infected with plague. Antibodies to Y. pestis were detected in 8 of 17 (47%) pumas tested by complement-enzyme-linked immunosorbent assay, and the organism itself was detected in 4 of 11 (36%) pumas tested after necropsy. Neither puma sex nor age was significantly associated with Y. pestis exposure or mortality, although our sample size was small. The overall prevalence of exposure we recorded was similar to that found along the western slope of Colorado, which is adjacent to the Four Corners region, a known plague hotspot in the USA. This suggests that: (1) Y. pestis may be present at higher levels in the GYE than previously assumed; (2) plague is a significant source of mortality for local pumas (6.6% of sub-adult and adult mortality); and (3) pumas may be a useful sentinel for potential risk of plague exposure to humans throughout the West. We would also emphasize that hunters and others handling pumas in this region should be made aware of the possibility of exposure.

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Perry, Robert D., Alexander G. Bobrov, and Jacqueline D. Fetherston. "The role of transition metal transporters for iron, zinc, manganese, and copper in the pathogenesis of Yersinia pestis." Metallomics 7, no. 6 (2015): 965–78. http://dx.doi.org/10.1039/c4mt00332b.

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Knirel, Yu A., and A. P. Anisimov. "Lipopolysaccharide of Yersinia Pestis, the Cause of Plague: Structure, Genetics, Biological Properties." Acta Naturae 4, no. 3 (2012): 46–58. http://dx.doi.org/10.32607/20758251-2012-4-3-46-58.

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The present review summarizes data pertaining to the composition and structure of the carbohydrate moiety (core oligosaccharide) and lipid component (lipid A) of the various forms of lipopolysaccharide (LPS), one of the major pathogenicity factors of Yersinia pestis, the cause of plague. The review addresses the functions and the biological significance of genes for the biosynthesis of LPS, as well as the biological properties of LPS in strains from various intraspecies groups of Y. pestis and their mutants, including the contribution of LPS to the resistance of bacteria to factors of the innate immunity of both insect-vectors and mammal-hosts. Special attention is paid to temperature-dependent variations in the LPS structure, their genetic control and roles in the pathogenesis of plague. The evolutionary aspect is considered based on a comparison of the structure and genetics of the LPS of Y. pestis and other enteric bacteria, including other Yersinia species. The prospects of development of live plague vaccines created on the basis of Y. pestis strains with the genetically modified LPS are discussed.

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Ziegler, Michelle. "The Black Death and the Future of the Plague." Medieval Globe 1, no. 1 (2015): 259–83. http://dx.doi.org/10.17302/tmg.1-1.10.

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This essay summarizes what we know about the spread of Yersinia pestis today, assesses the potential risks of tomorrow, and suggests avenues for future collaboration among scientists and humanists. Plague is both a re-emerging infectious disease and a developed biological weapon, and it can be found in enzootic foci on every inhabited continent except Australia. Studies of the Black Death and successive epidemics can help us to prepare for and mitigate future outbreaks (and other pandemics) because analysis of medieval plagues provides a crucial context for modern scientific discoveries and theories. These studies prevent us from stopping at easy answers, and they force us to acknowledge that there is still much that we do not understand.

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Korytov, K. M., V. V. Voitkova, V. I. Dubrovina, et al. "Efficiency of Human Plague Vaccination in Tuvinian Natural Plague Focus." Acta Biomedica Scientifica 4, no. 5 (2019): 31–37. http://dx.doi.org/10.29413/abs.2019-4.5.5.

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Background. Plague is an especially dangerous natural focal infectious disease belonging to a group of quarantine infections. There are eleven natural plague foci in Russian Federation. In Republic Tyva plague endemic territories include Ovyur, Mongun-Taigin and Tes-Hem areas where Y. pestis strains are intermittently isolated from Citellus undulates. Population living at the territory of the natural foci get immunoprophylaxis against plague at complication of epizootic and epidemic conditions.This paper presents the results of monitoring indicators of the immune status of people vaccinated with the plague vaccine living in the territory of the Tuva natural focus.Materials and methods. The study involved 76 volunteers who had not previously been vaccinated. The study included the determination of production IFN-γ, IL-4, TNF-α by blood cells, titers of specific IgG antibodies to the capsule F1 antigen of the Yersinia pestis, and concentrations of immunoglobulins in serum blood, as well as immunophenotyping of blood lymphocytes.Results. In the course of a comprehensive immunological study, features of the development of cellular and humoral reactions in people living in the territory of the Tuva natural plague focus were established in the first months after vaccination. Changes in the concentration dynamics of the main classes of immunoglobulins were accompanied by an increase in the level of specific IgGs to the F1 within 6 months after immunization. In the same period, a significant increase in the production of cytokines, as well as significant changes in terms of the subpopulation composition of the vaccinated blood.Conclusion. It is necessary to note the importance of studying of the human immune status in 1–3 months after plague vaccination as this period coincides with potentially dangerous season from epidemiological point of view. Nevertheless, much important role for improvement of tactics of the specific prevention measures plays the data received after the revaccination.

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Byvalov, A. A., L. G. Dudina, S. G. Litvinets, and E. A. Martinson. "IMMUNOCHEMICAL STUDY OF RECEPTION OF PLAGUE BACTERIOPHAGE POKROVSKY." Journal of microbiology, epidemiology and immunobiology, no. 4 (August 28, 2016): 16–21. http://dx.doi.org/10.36233/0372-9311-2016-4-16-21.

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Aim. Study of mechanism of reception of plague bacteriophage Pokrovsky to cells of Yersinia pestis using a panel of monoclonal antibodies. Materials and methods. Using a method of competitive inhibition, the ability of monoclonal antibodies against antigenic epitopes of outer membrane of Yersinia genus bacteria to inhibit adhesion of the studied bacteriophage to cells of Y. pestis EV strain, was evaluated. Results. A key role of structure of carbohydrate nature in reception of Pokrovsky bacteriophage was confirmed. Among 5 lines of monoclonal antibodies against protein epitopes 2 were established to cause significant inactivation of bacteriophage adhesion to bacterial cells. Conclusion. An assumption is proposed regarding participation of a structure of polypeptide nature in reception of Pokrovsky bacteriophage by cells of plague microbe.

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Dai, Ruixia, Jian He, Xi Zha, et al. "A novel mechanism of streptomycin resistance in Yersinia pestis: Mutation in the rpsL gene." PLOS Neglected Tropical Diseases 15, no. 4 (2021): e0009324. http://dx.doi.org/10.1371/journal.pntd.0009324.

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Streptomycin is considered to be one of the effective antibiotics for the treatment of plague. In order to investigate the streptomycin resistance of Y. pestis in China, we evaluated streptomycin susceptibility of 536 Y. pestis strains in China in vitro using the minimal inhibitory concentration (MIC) and screened streptomycin resistance-associated genes (strA and strB) by PCR method. A clinical Y. pestis isolate (S19960127) exhibited high-level resistance to streptomycin (the MIC was 4,096 mg/L). The strain (biovar antiqua) was isolated from a pneumonic plague outbreak in 1996 in Tibet Autonomous Region, China, belonging to the Marmota himalayana Qinghai–Tibet Plateau plague focus. In contrast to previously reported streptomycin resistance mediated by conjugative plasmids, the genome sequencing and allelic replacement experiments demonstrated that an rpsL gene (ribosomal protein S12) mutation with substitution of amino-acid 43 (K43R) was responsible for the high-level resistance to streptomycin in strain S19960127, which is consistent with the mutation reported in some streptomycin-resistant Mycobacterium tuberculosis strains. Streptomycin is used as the first-line treatment against plague in many countries. The emergence of streptomycin resistance in Y. pestis represents a critical public health problem. So streptomycin susceptibility monitoring of Y. pestis isolates should not only include plasmid-mediated resistance but also include the ribosomal protein S12 gene (rpsL) mutation, especially when treatment failure is suspected due to antibiotic resistance.

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Bossi, P., A. Tegnell, A. Baka, et al. "Bichat guidelines for the clinical management of plague and bioterrorism-related plague." Eurosurveillance 9, no. 12 (2004): 23–24. http://dx.doi.org/10.2807/esm.09.12.00501-en.

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Yersinia pestis appears to be a good candidate agent for a bioterrorist attack. The use of an aerosolised form of this agent could cause an explosive outbreak of primary plague pneumonia. The bacteria could be used also to infect the rodent population and then spread to humans. Most of the therapeutic guidelines suggest using gentamicin or streptomycin as first line therapy with ciprofloxacin as optional treatment. Persons who come in contact with patients with pneumonic plague should receive antibiotic prophylaxis with doxycycline or ciprofloxacin for 7 days. Prevention of human-to-human transmission via patients with plague pneumonia can be achieved by implementing standard isolation procedures until at least 4 days of antibiotic treatment have been administered. For the other clinical types of the disease, patients should be isolated for the first 48 hours after the initiation of treatment.

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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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Journal articles on the topic 'Plague Plague Plague Yersinia pestis'

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