Wikipedia

Yersinia pestis

Yersinia pestis (formerly Pasteurella pestis) is a Gram-negative rod-shaped coccobacillus, a facultative anaerobic bacterium that can infect humans and animals.[1]

Human Y. pestis infection takes three main forms: pneumonic, septicemic, and bubonic plagues.[1] All three forms were responsible for a number of high-mortality epidemics throughout human history, including the sixth century's Plague of Justinian, the Black Death, which accounted for the death of at least one-third of the European population between 1347 and 1353, and the 19th century's Third Pandemic.[2][3][4][5] It has now been shown that these plagues probably originated in rodent populations in China.[5][6]

Y. pestis was discovered in 1894 by Alexandre Yersin, a Swiss/French physician and bacteriologist from the Pasteur Institute, during an epidemic of plague in Hong Kong.[7] Yersin was a member of the Pasteur school of thought. Kitasato Shibasaburō, a German-trained Japanese bacteriologist who practiced Koch's methodology, was also engaged at the time in finding the causative agent of plague.[8] However, it was Yersin who actually linked plague with Yersinia pestis. Originally named Pasteurella pestis, the organism was renamed in 1967.

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.

Historical outbreaks[edit]

Plague of Justinian[edit]

During the mid 6th century, the pandemic known as the Plague of Justinian wiped out roughly one third of the Byzantine Empire's population, creating major military and financial difficulties. Modern historians named this plague incident after the Eastern Roman Emperor Justinian I, who held power in the Byzantine capital of Constantinople at the time of the initial outbreak. The primary years of the plague were 541–542 AD, although plague returned throughout the Mediterranean basin in successive generations, until about 750.

The waves of disease had a major effect on the future course of European history. The plague's social and cultural impact during the Justinian period is comparable to that of the Black Death.

The most commonly accepted cause of the pandemic has been bubonic plague.[9] A genetic study suggests that the Plague of Justinian (and others from antiquity) arose from either now-extinct strains of Y. pestis, genetically distinct from the strain that broke out in the 14th century pandemic, or from pathogens entirely unrelated to bubonic plague.[10][11]

Role in Black Death[edit]

In 2000, Didier Raoult and others reported finding Y. pestis DNA by performing a "suicide PCR" on tooth pulp tissue from a fourteenth-century plague cemetery in Montpellier.[12]

A study by an international team of researchers published in October 2010 confirmed that Y. pestis was the cause of the Black Death and later epidemics on the entire European continent over a period of 400 years. The team used ancient DNA and proteins recovered from the bodies of plague victims buried in Hereford in England, in Saint-Laurent-de-la-Cabrerisse in France, and Bergen op Zoom in the Netherlands to identify the pathogen.[13] They found two previously unknown, older strains of Y. pestis that had spread from China by two different routes, rather than the modern Orientalis and Medievalis.[14]

Three biovars of Y. pestis were originally thought to correspond to one of the historical pandemics of bubonic plague.[15] Biovar Antiqua is thought to correspond to the Plague of Justinian; it is not known whether this biovar also corresponds to earlier or smaller epidemics of bubonic plague, or whether these were even truly bubonic plague.[16] Biovar Mediaevalis was formerly thought to correspond to the Black Death, while Biovar Orientalis was thought to correspond to the Third Pandemic and the majority of modern outbreaks of plague. However, calculations of Y pestis's evolutionary age, found using the number of synonymous single nucleotide polymorphisms (SNPs) in conjunction with molecular clock rates, date the emergence of the biovars prior to any of the historical epidemics due to the length of time needed to accumulate such mutations.[17] Additional evidence against this hypothesis includes the fact that Mediaevalis is likely too young to have produced the Black Death due to its recent divergence from Orientalis.[18]

Use in biological warfare[edit]

Y. pestis is potentially one of the first examples of biological warfare in history, when in 1347 plague victims were catapulted by the Mongols over the city walls of Caffa, a town currently known as Feodosiya located in present day Ukraine. It is possible that infected inhabitants may have fled to Italy, thus spreading the Black Death to Europe, though this is likely only one of a few routes that could have brought the Plague from the East.[19]

Y. pestis has been used as a biological weapon in World War II, when on October 4, 1940 a Japanese airplane flying over Chushien, Chekiang Province, China released rice and wheat plus rat fleas carrying Y. pestis. A second plane load was released 3 weeks later. These actions led to a local plague that killed 121 people.[20] Leon A. Fox from the U.S. Army Medical Corps had suggested a similar approach in 1933 proposing to drop infested rats from planes.[20]

General characteristics[edit]

Y. pestis is a non-motile, rod-shaped, facultative anaerobe with bipolar staining (giving it a safety pin appearance).[21] Similar to other Yersinia members, it tests negative for urease, lactose fermentation, and indole.[22] The closest relative is the gastrointestinal pathogen Yersinia pseudotuberculosis, and more distantly Yersinia enterocolitica.

Genome[edit]

The complete genomic sequence is available for two of the three sub-species of Y. pestis: strain KIM (of biovar Medievalis),[23] and strain CO92 (of biovar Orientalis, obtained from a clinical isolate in the United States).[24] As of 2006, the genomic sequence of a strain of biovar Antiqua has been recently completed.[25] Similar to the other pathogenic strains, there are signs of loss of function mutations. The chromosome of strain KIM is 4,600,755 base pairs long; the chromosome of strain CO92 is 4,653,728 base pairs long. Like its cousins Y. pseudotuberculosis and Y. enterocolitica, Y. pestis is host to the plasmid pCD1. In addition, it also hosts two other plasmids, pPCP1 (also called pPla or pPst) and pMT1 (also called pFra) that are not carried by the other Yersinia species. pFra codes for a phospholipase D that is important for the ability of Y. pestis to be transmitted by fleas.[26] pPla codes for a protease, Pla, that activates plasminogen in human hosts and is a very important virulence factor for pneumonic plague.[27] Together, these plasmids, and a pathogenicity island called HPI, encode several proteins that cause the pathogenesis, for which Y. pestis is famous. Among other things, these virulence factors are required for bacterial adhesion and injection of proteins into the host cell, invasion of bacteria in the host cell (via a Type III secretion system), and acquisition and binding of iron that is harvested from red blood cells (via siderophores). Y. pestis is thought to be descendant from Y. pseudotuberculosis, differing only in the presence of specific virulence plasmids.

A comprehensive and comparative proteomics analysis of Y. pestis strain KIM was performed in 2006.[28] The analysis focused on the transition to a growth condition mimicking growth in host cells.

Pathogenics and immunity[edit]

Oriental rat flea (Xenopsylla cheopis) infected with the Yersinia pestis bacterium which appears as a dark mass in the gut. The foregut (proventriculus) of this flea is blocked by a Y. pestis biofilm; when the flea attempts to feed on an uninfected host, Y. pestis is regurgitated into the wound, causing infection.

In the urban and sylvatic (forest) cycles of Y. pestis, most of the spreading occurs between rodents and fleas. In the sylvatic cycle, the rodent is wild, but, in the urban cycle, the rodent is domestic. In addition, Y. pestis can spread from the urban environment and back. Infected animal carcasses can transmit pestis to humans through blood and tissue. If the disease has progressed to the pneumonic form, humans can spread the bacterium to others by coughing and possibly sneezing.

In reservoir hosts[edit]

The reservoir commonly associated with Y. pestis is several species of rodents. In the steppes, the reservoir species is believed to be principally the marmot. In the south western United States, several species of rodents are thought to maintain Y. pestis. However, the expected disease dynamics have not been found in any rodent. It is known that rodent populations will have a variable resistance, which could lead to a carrier status.[29] There is evidence that fleas from other mammals have a role in human plague outbreaks.[30]

This lack of knowledge of the dynamics of plague in mammal species is also true among susceptible rodents such as the black-tailed prairie dog (Cynomys ludovicianus), in which plague can cause colony collapse, resulting in a massive effect on prairie food webs.[31] However, the transmission dynamics within prairie dogs does not follow the dynamics of blocked fleas; carcasses, unblocked fleas, or another vector could possibly be important instead.[32]

In other regions of the world, the reservoir of the infection is not clearly identified, which complicates prevention and early warning programs. One such example was seen in a 2003 outbreak in Algeria.[33]

Vector[edit]

The transmission of Y. pestis by fleas is well characterized.[34] Initial acquisition of Y. pestis by the vector occurs during feeding on an infected animal. Several proteins then contribute to the maintenance of the bacteria in the flea digestive tract, among them the hemin storage (Hms) system and Yersinia murine toxin (Ymt).

Although Yersinia murine toxin is highly toxic to rodents and was once thought to be produced to ensure reinfection of new hosts, it has been demonstrated that Ymt is important for the survival of Y. pestis in fleas.[26]

The Hms system plays an important role in the transmission of Y. pestis back to a mammalian host.[35] While in the insect vector, proteins encoded by Hms genetic loci induce biofilm formation in the proventriculus, a valve connecting the midgut to the esophagus.[36] Aggregation in the biofilm inhibits feeding, as a mass of clotted blood and bacteria forms (referred to as "Bacot's block" [37]). Transmission of Y. pestis occurs during the futile attempts of the flea to feed. Ingested blood is pumped into the esophagus, where it dislodges bacteria lodged in the proventriculus and is regurgitated back into the host circulatory system.

In humans and other susceptible hosts[edit]

Pathogenesis due to Y. pestis infection of mammalian hosts is due to several factors including an ability of these bacteria to suppress and avoid normal immune system responses such as phagocytosis and antibody production. Flea bites allow for the bacteria to pass the skin barrier. Y. pestis expresses the yadBC gene, which is similar to adhesins in other Yersinia species, allowing for adherence and invasion of epithelial cells.[38] Y. pestis expresses a plasminogen activator that is an important virulence factor for pneumonic plague and that might degrade on blood clots in order to facilitate systematic invasion.[27] Many of the bacteria's virulence factors are anti-phagocytic in nature. Two important anti-phagocytic antigens, named F1 (Fraction 1) and V or LcrV, are both important for virulence.[21] These antigens are produced by the bacterium at normal human body temperature. Furthermore, Y. pestis survives and produces F1 and V antigens while it is residing within white blood cells such as monocytes, but not in neutrophils. Natural or induced immunity is achieved by the production of specific opsonic antibodies against F1 and V antigens; antibodies against F1 and V induce phagocytosis by neutrophils.[39]

In addition, the Type III secretion system (T3SS) allows Y. pestis to inject proteins into macrophages and other immune cells. These T3SS-injected proteins are called Yops (Yersinia Outer Proteins) and include Yop B/D, which form pores in the host cell membrane and have been linked to cytolysis. The YopO, YopH, YopM, YopT, YopJ, and YopE are injected into the cytoplasm of host cells via T3SS into the pore created in part by YopB and YopD.[40] The injected Yop proteins limit phagocytosis and cell signaling pathways important in the innate immune system, as discussed below. In addition, some Y. pestis strains are capable of interfering with immune signaling (e.g., by preventing the release of some cytokines).

Yersinia pestis proliferates inside lymph nodes where it is able to avoid destruction by cells of the immune system such as macrophages. The ability of Yersinia pestis to inhibit phagocytosis allows it to grow in lymph nodes and cause lymphadenopathy. YopH is a protein tyrosine phosphatase that contributes to the ability of Yersinia pestis to evade immune system cells.[41] In macrophages, YopH has been shown to dephosphorylate p130Cas, Fyb (Fyn binding protein) SKAP-HOM and Pyk, a tyrosine kinase homologous to FAK. YopH also binds the p85 subunit of phosphoinositide 3-kinase, the Gab1, the Gab2 adapter proteins, and the Vav guanine nucleotide exchange factor.

YopE functions as a GTPase activating protein for members of the Rho family of GTPases such as RAC1. YopT is a cysteine protease that inhibits RhoA by removing the isoprenyl group, which is important for localizing the protein to the cell membrane. It has been proposed that YopE and YopT may function to limit YopB/D-induced cytolysis.[42] This might limit the function of YopB/D to create the pores used for Yop insertion into host cells and prevent YopB/D-induced rupture of host cells and release of cell contents that would attract and stimulate immune system responses.

YopJ is an acetyltransferase that binds to a conserved α-helix of MAPK kinases.[43] YopJ acetylates MAPK kinases at serines and threonines that are normally phosphorylated during activation of the MAP kinase cascade.[44][45] YopJ is activated in eukaryotic cells by interaction with target cell Phytic acid (IP6).[46] This disruption of host cell protein kinase activity causes apoptosis of macrophages, and it has been proposed that this is important for the establishment of infection and for evasion of the host immune response. YopO is a protein kinase also known as Yersinia protein kinase A (YpkA). YopO is a potent inducer of human macrophage apoptosis.[47]

Immunity[edit]

A formalin-inactivated vaccine once was available in the United States for adults at high risk of contracting the plague until removal from the market by the U.S. Food and Drug Administration. It was of limited effectiveness and could cause severe inflammation. Experiments with genetic engineering of a vaccine based on F1 and V antigens are underway and show promise. However, bacteria lacking antigen F1 are still virulent, and the V antigens are sufficiently variable, such that vaccines composed of these antigens may not be fully protective.[48] United States Army Medical Research Institute of Infectious Diseases (USAMRIID) have found that an experimental F1/V antigen-based vaccine protects cynomolgus macaques but fails to protect African green monkeys.[49] A systematic review by the Cochrane Collaboration found no studies of sufficient quality to make any statement on the efficacy of the vaccine.[50]

Clinical aspects[edit]

Symptoms and disease progression[edit]

  • Bubonic plague
    • Incubation period of 2–6 days, when the bacteria is actively replicating.
    • General malaise
    • Fever
    • Headache and chills occur suddenly at the end of the incubation period
    • Swelling of lymph nodes resulting in buboes, the classic sign of bubonic plague. Most flea bites will occur on the legs, so the inguinal nodes are most frequently affected ("boubon" is Greek for "groin.")
    • Death can occur in less than 2 weeks

If this occurs with the classic buboes, this is considered primary, while secondary occurs after symptoms of bubonic or pneumonic infection. Since the bacteria are blood-borne, several organs can be affected, including the spleen and brain. The diffuse infection can cause an immunologic cascade to occur, leading to disseminated intravascular coagulation (DIC), which in turn results in bleeding and necrotic skin and tissue. Such a disseminated infection increases mortality to 22%.

With the exception of the buboes, the initial symptoms of plague are very similar to many other diseases, making diagnosis difficult.[52]

ICD-9 codes for the diseases caused by Y. pestis:

  • 020.0 Bubonic plague
  • 020.2 Septicemic plague
  • 020.3 Primary pneumonic plague
  • 020.4 Secondary pneumonic plague
  • 020.5 Unspecified pneumonic plague

Clinical determination[edit]

Gram's stains can confirm the presence of gram-negative rods, and in some cases the identification of the double-curved shape. An anti-F1 serology test can differentiate between different species of Yersinia, and Polymerase chain reaction (PCR) can be used to identify Y. pestis.

The protein H of the tail fiber of the bacteriophage Yersinia phage L-413C permits the differenciation between Y. pestis and Y. pseudotuberculosis", the gastro-intestinal corrolary (Kane et al.).[53]

Treatment[edit]

The traditional first line treatment for Y. pestis has been streptomycin,[54][55] chloramphenicol, tetracycline,[56] and fluoroquinolones. There is also good evidence to support the use of doxycycline or gentamicin.[57] Resistant strains have been isolated; treatment should be guided by antibiotic sensitivities where available. Antibiotic treatment alone is insufficient for some patients, who may also require circulatory, ventilator, or renal support.

In an emergency department setting, Harrison's Principles of Internal Medicine outlines the following treatment course.[58] Antibiotics within the first 24 hours are very beneficial, with intravenous being preferred in pulmonary or advanced cases. Streptomycin or gentamicin are the first-line drugs, with chloramphenicol for critically ill patients, or rarely for suspected neuro-involvement.

Recent events[edit]

In September 2009, the death of Malcolm Casadaban, a molecular genetics professor at the University of Chicago, was linked to his work on a weakened laboratory strain of Y. pestis.[59] Hemochromatosis was hypothesised to be a predisposing factor in Casadaban's death from this attenuated strain used for research.[60]

In 2012, researchers in Germany collected samples of Yersinia pestis from gravesites with a view to reconstructing the DNA of the bacterium.[61]

Notes[edit]

  1. ^ a b Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 484–488. ISBN 0-8385-8529-9. 
  2. ^ Austin Alchon, Suzanne (2003). A pest in the land: new world epidemics in a global perspective. University of New Mexico Press. p. 21. ISBN 0-8263-2871-7. 
  3. ^ Harbeck, Michaela; Seifert, Lisa; Hänsch, Stephanie; Wagner, David M.; Birdsell, Dawn; Parise, Katy L.; Wiechmann, Ingrid; Grupe, Gisela; Thomas, Astrid; Keim, Paul; Zöller, Lothar; Bramanti, Barbara; Riehm, Julia M.; Scholz, Holger C. (2013). "Yersinia pestis DNA from Skeletal Remains from the 6th Century AD Reveals Insights into Justinianic Plague". PLoS Pathogens 9 (5): e1003349. doi:10.1371/journal.ppat.1003349. PMID 23658525. Lay summaryScienceDaily (May 10, 2013). 
  4. ^ Carter, Adam (Jan 27, 2014). "Black Death mysteries unlocked by McMaster scientists". CBC News. 
  5. ^ a b Nicholas Wade (October 31, 2010). "Europe's Plagues Came From China, Study Finds". New York Times. Retrieved November 1, 2010. 
  6. ^ G. Morelli, Y. Song, C.J. Mazzoni, M. Eppinger, P. Roumagnac, D.M. Wagner et al. (2010). "Phylogenetic diversity and historical patterns of pandemic spread of Yersinia pestis". Nature Genetics 42 (12): 1140–3. doi:10.1038/ng.705. PMC 2999892. PMID 21037571. 
  7. ^ Bockemühl J (1994). "100 years after the discovery of the plague-causing agent--importance and veneration of Alexandre Yersin in Vietnam today". Immun Infekt 22 (2): 72–5. PMID 7959865. 
  8. ^ Howard-Jones N (1973). "Was Kitasato Shibasaburō the discoverer of the plague bacillus?". Perspect Biol Med 16 (2): 292–307. PMID 4570035. 
  9. ^ "Europe’s Plagues Came From China, Study Finds". The New York Times. October 31, 2010. Retrieved 2010-11-01. 
  10. ^ McGrath, Matt (12 October 2011). "Black Death Genetic Code 'Built'". BBC World Service. Retrieved 12 October 2011. 
  11. ^ Bos, Kirsten; Schuenemann, Verena J.; Golding, G. Brian; Burbano, Hernán A.; Waglechner, Nicholas; Coombes, Brian K.; McPhee, Joseph B.; Dewitte, Sharon N.; Meyer, Matthias; Schmedes, Sarah; Wood, James; Earn, David J. D.; Herring, D. Ann; Bauer, Peter; Poinar, Hendrik N.; Krause, Johannes (12 October 2011). "A draft genome of Yersinia pestis from victims of the Black Death". Nature 478 (7370): 506–510. Bibcode:2011Natur.478..506B. doi:10.1038/nature10549. PMC 3690193. PMID 21993626. 
  12. ^ Drancourt M, Aboudharam G, Signolidagger M, Dutourdagger O, Raoult D. (2002). "Detection of 400-year-old Yersinia pestis DNA in human dental pulp: An ory of plague". Microbes Infect. 4 (1): 105–9. doi:10.1016/S1286-4579(01)01515-5. PMID 11825781. 
  13. ^ Haensch, Stephanie; Bianucci, Raffaella; Signoli, Michel; Rajerison, Minoarisoa; Schultz, Michael; Kacki, Sacha; Vermunt, Marco; Weston, Darlene A.; Hurst, Derek; Achtman, Mark; Carniel, Elisabeth; Bramanti, Barbara (2010). "Distinct Clones of Yersinia pestis Caused the Black Death". PLoS Pathogens 6 (10): e1001134. doi:10.1371/journal.ppat.1001134. PMID 20949072. 
  14. ^ "Black Death Blamed on Bacteria". Associated Free Press (Discovery). October 8, 2010. Retrieved October 11, 2010. 
  15. ^ Zhou D, Tong Z, Song Y, Han Y, Pei D, Pang X, Zhai J, Li M, Cui B, Qi Z, Jin L, Dai R, Du Z, Wang J, Guo Z, Wang J, Huang P, Yang R (2004). "Genetics of Metabolic Variations between Yersinia pestis Biovars and the Proposal of a New Biovar, microtus". J Bacteriol 186 (15): 5147–52. doi:10.1128/JB.186.15.5147-5152.2004. PMC 451627. PMID 15262951. 
  16. ^ Guiyoule A, Grimont F, Iteman I, Grimont P, Lefèvre M, Carniel E (1994). "Plague pandemics investigated by ribotyping of Yersinia pestis strains". J Clin Microbiol 32 (3): 634–41. PMC 263099. PMID 8195371. 
  17. ^ Parkhill, J., B. W. Wren, N. R. Thomson, R. W. Titball, M. T. G. Holden, M. B. Prentice, M. Sebaihia et al. (2001). "Genome sequence of Yersinia pestis, the causative agent of plague". Nature 413 (6855): 523–527. doi:10.1038/35097083. PMID 11586360. 
  18. ^ Achtman M, Morelli G, Zhu P, Wirth T, Diehl I, Kusecek B et al. (2004). "Microevolution and history of the plague bacillus, Yersinia pestis". Proc Natl Acad Sci U S A 101 (51): 17837–42. Bibcode:2004PNAS..10117837A. doi:10.1073/pnas.0408026101. PMC 535704. PMID 15598742. 
  19. ^ Wheelis, Mark (September 2002). "Biological Warfare at the 1346 Siege of Caffa". Emerging Infectious Diseseases 8 (9): 971–75. doi:10.3201/eid0809.010536. PMC 2732530. PMID 12194776. 
  20. ^ a b Drisdelle R. Parasites. Tales of Humanity's Most Unwelcome Guests. Univ. of California Publishers, 2010. p. 162f. ISBN 978-0-520-25938-6. 
  21. ^ a b Collins FM (1996). Pasteurella, Yersinia, and Francisella. In: Baron's Medical Microbiology (Baron S et al, eds.) (4th ed.). Univ. of Texas Medical Branch. ISBN 0-9631172-1-1. 
  22. ^ Stackebrandt, Erko; Dworkin, Martin; Falkow, Stanley; Rosenberg, Eugene; Karl-Heinz Schleifer (2005). The Prokaryotes: A Handbook on the Biology of Bacteria:Volume 6: Proteobacteria: Gamma Subclass. Berlin: Springer. ISBN 0-387-25499-4. 
  23. ^ Deng W et al. (2002). "Genome Sequence of Yersinia pestis KIM". Journal of Bacteriology 184 (16): 4601–4611. doi:10.1128/JB.184.16.4601-4611.2002. PMC 135232. PMID 12142430. 
  24. ^ Parkhill J et al. (2001). "Genome sequence of Yersinia pestis, the causative agent of plague". Nature 413 (6855): 523–527. doi:10.1038/35097083. PMID 11586360. 
  25. ^ Chain PS, Hu P, Malfatti SA et al. (2006). "Complete Genome Sequence of Yersinia pestis Strains Antiqua and Nepal516: Evidence of Gene Reduction in an Emerging Pathogen". J. Bacteriol. 188 (12): 4453–63. doi:10.1128/JB.00124-06. PMC 1482938. PMID 16740952. 
  26. ^ a b Hinnebusch BJ, Rudolph AE, Cherepanov P, Dixon JE, Schwan TG, Forsberg A; Rudolph; Cherepanov; Dixon; Schwan; Forsberg (2002). "Role of Yersinia murine toxin in survival of Yersinia pestis in the midgut of the flea vector". Science 296 (5568): 733–5. Bibcode:2002Sci...296..733H. doi:10.1126/science.1069972. PMID 11976454. 
  27. ^ a b Lathem WW, Price PA, Miller VL, Goldman WE; Price; Miller; Goldman (2007). "A plasminogen-activating protease specifically controls the development of primary pneumonic plague". Science 315 (5811): 509–13. Bibcode:2007Sci...315..509L. doi:10.1126/science.1137195. PMID 17255510. 
  28. ^ Hixson K et al. (2006). "Biomarker candidate identification in Yersinia pestis using organism-wide semiquantitative proteomics". Journal of Proteome Research 5 (11): 3008–3017. doi:10.1021/pr060179y. PMID 16684765. 
  29. ^ MEYER KF (1957). "The natural history of plague and psittacosis: The R. E. Dyer Lecture". Public Health Rep 72 (8): 705–19. doi:10.2307/4589874. JSTOR 4589874. PMC 2031327. PMID 13453634. 
  30. ^ von Reyn CF, Weber NS, Tempest B et al. (1977). "Epidemiologic and clinical features of an outbreak of bubonic plague in New Mexico". J. Infect. Dis. 136 (4): 489–94. doi:10.1093/infdis/136.4.489. PMID 908848. 
  31. ^ Pauli JN, Buskirk SW, Williams ES, Edwards WH (2006). "A plague epizootic in the black-tailed prairie dog (Cynomys ludovicianus)". J. Wildl. Dis. 42 (1): 74–80. doi:10.7589/0090-3558-42.1.74. PMID 16699150. 
  32. ^ Webb CT, Brooks CP, Gage KL, Antolin MF; Brooks; Gage; Antolin (2006). "Classic flea-borne transmission does not drive plague epizootics in prairie dogs". Proc. Natl. Acad. Sci. U.S.A. 103 (16): 6236–41. Bibcode:2006PNAS..103.6236W. doi:10.1073/pnas.0510090103. PMC 1434514. PMID 16603630. 
  33. ^ Bertherat E, Bekhoucha S, Chougrani S et al. (2007). "Plague Reappearance in Algeria after 50 Years, 2003". Emerging Infect. Dis. 13 (10): 1459–1462. doi:10.3201/eid1310.070284. PMC 2851531. PMID 18257987. 
  34. ^ Zhou D, Han Y, Yang R (2006). "Molecular and physiological insights into plague transmission, virulence and etiology". Microbes Infect. 8 (1): 273–84. doi:10.1016/j.micinf.2005.06.006. PMID 16182593. 
  35. ^ B.J. Hinnebusch, R.D. Perry and T.G. Schwan (1996). "Role of the Yersinia pestis hemin storage (hms) locus in the transmission of plague by fleas". Science. 273 (5237): 367–70. Bibcode:1996Sci...273..367H. doi:10.1126/science.273.5273.367. PMID 8662526. 
  36. ^ Erickson, D. L., N. R. Waterfield, V. Vadyvaloo, D. Long, E. R. Fischer, R. ffrench-Constant, and B. J. Hinnebusch (2007). "Acute oral toxicity of yersinia pseudotuberculosis to fleas: Implications for the evolution of vector-borne transmission of plague". Cellular Microbiology 9 (11): 2658–2666. doi:10.1111/j.1462-5822.2007.00986.x. PMID 17587333. 
  37. ^ Pepper, C., M. Nascarella, E. Marsland, J. Montford, L. Wood, S. Cox, C. Bradford, T. Burns, and S. Presley. 2004. Threatened or endangered? Keystone species or public health threat? The black-tailed prairie dog, the Endangered Species Act, and the imminent threat of bubonic plague. Journal of Land, Resources, and Environmental Law 24: 355-391.
  38. ^ Forman S, Wulff CR, Myers-Morales T, Cowan C, Perry RD, Straley SC (2008). "yadBC of Yersinia pestis, a New Virulence Determinant for Bubonic Plague". Infect. Immun. 76 (2): 578–87. doi:10.1128/IAI.00219-07. PMC 2223446. PMID 18025093. 
  39. ^ Salyers AA, Whitt DD (2002). Bacterial Pathogenesis: A Molecular Approach (2nd ed.). ASM Press. pp. 207-12. 
  40. ^ Viboud GI, Bliska JB (2005). "Yersinia outer proteins: role in modulation of host cell signaling responses and pathogenesis". Annu. Rev. Microbiol. 59: 69–89. doi:10.1146/annurev.micro.59.030804.121320. PMID 15847602. 
  41. ^ de la Puerta ML, Trinidad AG, del Carmen Rodríguez M, Bogetz J, Sánchez Crespo M, Mustelin T, Alonso A, Bayón Y; Trinidad; Rodríguez; Bogetz; Sánchez Crespo; Mustelin; Alonso; Bayón (February 2009). "Characterization of New Substrates Targeted By Yersinia Tyrosine Phosphatase YopH". In Bozza, Patricia. PLoS ONE 4 (2): e4431. Bibcode:2009PLoSO...4.4431D. doi:10.1371/journal.pone.0004431. PMC 2637541. PMID 19221593. 
  42. ^ Mejía E, Bliska JB, Viboud GI (February 2009). "Yersinia Controls Type III Effector Delivery into Host Cells by Modulating Rho Activity". PLoS ONE 4 (2): e4431. doi:10.1371/journal.ppat.0040003. PMC 2186360. PMID 18193942. 
  43. ^ Hao YH, Wang Y, Burdette D, Mukherjee S, Keitany G, Goldsmith E, Orth K; Wang; Burdette; Mukherjee; Keitany; Goldsmith; Orth (January 2008). "Structural Requirements for Yersinia YopJ Inhibition of MAP Kinase Pathways". In Kobe, Bostjan. PLoS ONE 2 (3): e1375. Bibcode:2008PLoSO...3.1375H. doi:10.1371/journal.pone.0001375. PMC 2147050. PMID 18167536. 
  44. ^ Mukherjee, S.; Keitany, Gladys; Li, Yan; Wang, Yong; Ball, Haydn L.; Goldsmith, Elizabeth J.; Orth, Kim (2006). "Yersinia YopJ Acetylates and Inhibits Kinase Activation by Blocking Phosphorylation". Science 312 (5777): 1211. Bibcode:2006Sci...312.1211M. doi:10.1126/science.1126867. PMID 16728640. 
  45. ^ Mittal, R.; Peak-Chew, S.-Y.; McMahon, H. T. (2006). "Acetylation of MEK2 and I B kinase (IKK) activation loop residues by YopJ inhibits signaling". Proceedings of the National Academy of Sciences 103 (49): 18574. Bibcode:2006PNAS..10318574M. doi:10.1073/pnas.0608995103. 
  46. ^ Mittal R, Peak-Chew SY, Sade RS, Vallis Y, McMahon HT (2010). "The Acetyltransferase Activity of the Bacterial Toxin YopJ of Yersinia Is Activated by Eukaryotic Host Cell Inositol Hexakisphosphate". J Biol Chem 285 (26): 19927–34. doi:10.1074/jbc.M110.126581. PMC 2888404. PMID 20430892. 
  47. ^ Park H, Teja K, O'Shea JJ, Siegel RM (May 2007). "The Yersinia effector protein YpkA induces apoptosis independently of actin depolymerization". J Immunol. 178 (10): 6426–6434. PMID 17475872. 
  48. ^ Welkos S et al. (2002). "Determination of the virulence of the pigmentation-deficient and pigmentation-/plasminogen activator-deficient strains of Yersinia pestis in non-human primate and mouse models of pneumonic plague". Vaccine 20 (17–18): 2206–2214. doi:10.1016/S0264-410X(02)00119-6. PMID 12009274. 
  49. ^ Pitt ML (October 2004). Non-human primates as a model for pneumonic plague. In: Animals Models and Correlates of Protection for Plague Vaccines Workshop. 
  50. ^ Jefferson T, Demicheli V, Pratt M (2000). "Vaccines for preventing plague". In Jefferson, Tom. Cochrane Database Syst Rev (2): CD000976. doi:10.1002/14651858.CD000976. PMID 10796565. 
  51. ^ Info taken from "Harrison's Principles of Internal Medicine 16th Edition"[page needed]
  52. ^ Prentice, Michael B; Rahalison, Lila (2007). "Plague". The Lancet 369 (9568): 1196. doi:10.1016/S0140-6736(07)60566-2. 
  53. ^ Garcia, E et al. (2008). "Molecular characterization of L-413C, a P2-related plague diagnostic bacteriophage". Virology 372 (1): 85–96. doi:10.1016/j.virol.2007.10.032. PMID 18045639. 
  54. ^ Wagle PM. (1948). "Recent advances in the treatment of bubonic plague". Indian J Med Sci 2: 489–94. 
  55. ^ Meyer KF. (1950). "Modern therapy of plague". JAMA 144 (12): 982–5. doi:10.1001/jama.1950.02920120006003. PMID 14774219. 
  56. ^ Kilonzo BS, Makundi RH, Mbise TJ. (1992). "A decade of plague epidemiology and control in the Western Usambara mountains, north-east Tanzania". Acta Tropica 50 (4): 323–9. doi:10.1016/0001-706X(92)90067-8. PMID 1356303. 
  57. ^ Mwengee W, Butler T, Mgema S et al. (2006). "Treatment of plague with gentamicin or doxycycline in a randomized clinical trial in Tanzania". Clin Infect Dis 42 (5): 614–21. doi:10.1086/500137. PMID 16447105. 
  58. ^ Jameson, J. N. St C.; Dennis L. Kasper; Harrison, Tinsley Randolph; Braunwald, Eugene; Fauci, Anthony S.; Hauser, Stephen L; Longo, Dan L. (2005). Harrison's principles of internal medicine. New York: McGraw-Hill Medical Publishing Division. ISBN 0-07-140235-7. 
  59. ^ Sadovi, Carlos (2009-09-19). "U. of C. researcher dies after exposure to plague bacteria". Chicago Breaking News Center. Retrieved 2010-03-03. 
  60. ^ Randall, Tom (Feb 25, 2011). "Plague Death Came Within Hours, Spurred by Scientist's Medical Condition". 
  61. ^ Harbeck M, Seifert L, Hänsch S, et al. (2013). "Yersinia pestis DNA from skeletal remains from the 6(th) century AD reveals insights into Justinianic Plague". PLoS Pathogens 9 (5): e1003349. doi:10.1371/journal.ppat.1003349. PMC 3642051. PMID 23658525. 
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Sylvatic plague

Sylvatic plague is an infectious disease caused by the bacterium Yersinia pestis that primarily affects rodents. It is primarily transmitted by fleas and contact with infected tissue or fluids. Sylvatic refers specifically to the form of plague in rural wildlife while Urban plague refers to the form in urban wildlife. Sylvatic plague is most commonly found in prairie dog colonies and some mustelids like the highly endangered black-footed ferret.[1] The disease is found primarily in rural regions of Asia, Africa, and western states in America.

Transmission[edit]

Sylvatic plague is primarily transmitted through bites from rodent fleas. Other ways of transmission are through direct contact with contaminated fluids or tissue, which in wildlife means predation or scavenging, and through infectious airborne droplets. Humans can get infected with plague from contact with infected live or dead animals, including pets and fleas. This is particularly important for hunters or researchers who handle animal carcasses.[1]

Clinical signs and symptoms[edit]

Cats are highly susceptible to sylvatic plague. Feline symptoms include painful, swollen lymph nodes, enlarged tonsils, high fever and inflammation, vomiting, diarrhea and dehydration, anorexia, visible weight loss, swelling in the head and neck area, and coma. Cats infected with plague bacteria have only a 50 percent survival rate. Some animals affected may not show symptoms of the disease.[2][3]

Humans affected by the disease can develop one of three types of disease: bubonic plague, sepsis, and pneumonic plague. Symptoms may include high fever, bubo (swollen lymph gland), chills, malaise, muscle pain, severe headache, and seizures. If immediate action is not taken, death can occur as soon as 24 hours after first appearance of symptoms.[2]

Geographic distribution[edit]

The likely origin for all types of plague is Central Asia, from which it has gradually spread worldwide to every continent except Australia and Antarctica. Sylvatic plague typically arises in regions where there is sufficient populations of rodents and fleas, and is most common in tropical/subtropical regions between 50N° and 40S° latitude.

It also occurs in warmer temperate zones, like the North American west; enzootic plague in the United States occurs mainly west of 100° longitude, and is most prevalent in the southwestern states. The disease was introduced to the U.S in San Francisco around the year 1900 and continues to spread east.[1] According to the Centers for Disease Control and Prevention, the majority of human cases have occurred in the western half of the United States.[4] Usually, plague occurs in rural/semi-rural areas of the western U.S., since rodent populations are larger in semi-arid forests and grasslands, but the disease does occur in dense urban areas with large population sizes of rats and mice.[5]

Effects on wildlife populations[edit]

Sylvatic plague affects over 50 species of rodents worldwide and various predators (especially Felids) and humans that come into contact with them, vectored by variety of different flea species. Some of the non-rodent animals susceptible to the disease include shrews, Lagomorphs, ferrets, badgers, skunks, weasels, coyotes, domestic dogs and cats, bobcats, mountain lions, camels, goats, sheep, pigs, deer, nonhuman primates and humans. Birds are not known to be susceptible.[6]

Sylvatic plague is enzootic - occurring at regular or predictable/expected rates in populations or specific areas. However, at times the disease becomes epizootic - arising in outbreaks that occur at unexpected times or places, or in an infrequent basis; this, or shortly after, is when transmission to humans is most likely. High densities of rodents, multiple species of rodents in a particular area, and multiple rodent species in diverse habitats are all factors for epizootic events. Epizootic outbreaks more likely to occur in southwest US in cooler summers following wet winters.[2]

Plague has an indirect effect on many western wildlife species in the U.S and direct devastating effects on certain populations. More than 50% of the International Union for Conservation of Nature rodent species of concern in the U.S are within the range of historic plague flare ups.[7] Of particular concern in the United States are the effects of the disease on prairie dog and black-footed ferret populations. Black footed ferrets, once considered extinct, are considered highly endangered and are the subject of a major reintroduction and rehabilitation effort. Ferrets are vulnerable to plague from direct transmission from fleas and from preying on infected prairie dogs, their main food source.[6]

Prairie dog populations have also been greatly affected by plague; affected colonies subject to near 100% mortality rates during outbreaks. This threat has compounded with factors like habitat loss and recreational shooting to cause drastic declines in numbers of all species of prairie dogs. Given prairie dogs' vital role as the primary prey of black footed ferrets and their likely role as a keystone species, developing methods to control plague is of high concern for preserving ferrets and the conservation of Western prairie and grassland ecosystems.[1]

Disease Control/Prevention[edit]

Dusting rodent dens with pesticides, such as pyrethroids, like DeltaDust® (0.05% deltamethrin; Bayer, Montvale, NJ), to kill fleas is currently the main method of controlling sylvatic plague in the wild. However, due to the labor this practice requires and its limited sustainability, there is considerable interest in using vaccines to control plague in wild populations.[8]

An injectable vaccine has been used with some populations of black-footed ferrets, developed from a vaccine for humans created by the United States Army Medical Research Institute of Infectious Diseases. Subcutaneous injection of recombinant fusion protein called F1-V consisting of two antigens expressed by Y. pestis protects ferrets against plague. All captive-borne ferrets have been vaccinated since 2008, and the vaccine has been administered in some instances to wild kits and adults as an emergency preventive measure against outbreaks.[1]

An oral live vaccine for prairie dogs was developed by the U.S. Geological Survey, National Wildlife Health Center, Madison, WI from a recombinant raccoon poxvirus expressing plague antigens, originally developed by a Fort Detrick, CO company in 2003 which showed it protected mice against lethal plague [9] The oral vaccine uses fraction 1 (F1) and a truncated form of the V protein-V307, and is currently tested. Preliminary results show the vaccine to be effective in preventing the disease;[10] if effective in the wild it might be distributed across prairie dog colonies, especially with ferret populations. Successful vaccination of prairie dogs could increase their numbers, providing a more stable food source for black-footed ferrets.[11]

Treating pets for fleas can prevent the spread into homes.[12] Controlling rat populations in urban areas, including insecticide applications to rodent dens, helps to interrupt plague transmission.

Treatments for affected humans[edit]

If human plague is contracted from an animal and diagnosed, it can be treated with antibiotics. It is important to treat plague as early as possible to fully recover. Other methods for killing the bacterium are with sulfadiazine, streptomycin, tetracycline, and chloramphenicol.[1] Acquired resistance can be gained through humoral therapy.[13]

See also[edit]

References[edit]

  1. ^ a b c d e f Abbott, R.C.; Rocke, T.E (2012). Plague: U.S. Geological Survey Circular 1372. 
  2. ^ a b c "Plague Symptoms". Center for Disease Control. 
  3. ^ "Plague Fact Sheet". Center for Disease Control. 
  4. ^ http://www.cdc.gov/plague/maps/index.html.  Missing or empty |title= (help)accessed Dec 14, 2013
  5. ^ . Center for Disease Control http://www.cdc.gov/plague/transmission/index.html.  Missing or empty |title= (help)
  6. ^ a b "History of the Black Footed Ferret". Black-footed Ferret Recovery Implementation Team. Retrieved 25 Oct 2013. 
  7. ^ "Protecting Black-footed Ferrets". National Wildlife Health Center. 
  8. ^ USGS (July 2013). "Sylvatic Plague Immunization in Black-footed Ferrets and Prairie Dogs.". USGS National Wildlife Health Center. 
  9. ^ Osorio JE, Powell TD, Frank RS, Moss K, Haanes EJ, Smith SR, Rocke TE, Stinchcomb DT. Recombinant raccoon pox vaccine. Vaccine. 2003 Mar 7;21(11-12):1232-8.
  10. ^ Rocke TE, Pussini N, Smith SR, Williamson J, Powell B, Osorio JE. Consumption of baits containing raccoon pox-based plague vaccines protects black-tailed prairie dogs (Cynomys ludovicianus).Vector Borne Zoonotic Dis. 2010 Jan-Feb;10(1):53-8. doi: 10.1089/vbz.2009.0050.
  11. ^ Abbott, R.C.; Osorio, J. E ; Bunck, C. M. ; Rocke, T. E. (2012). "Sylvatic plague vaccine: a new tool for conservation of threatened and endangered species?". EcoHealth 9 (3): 243–50. 
  12. ^ "Prevention of Plague". Center for Disease Control. 
  13. ^ Collins, Frank (1996). Medical Microbiology: chapter 29. Galveston Texas: University of Texas Medical Branch at Galveston. 
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Urban plague

Urban plague is an infectious disease among rodent species that live in close association with humans in urban areas. It is caused by the bacterium Yersinia pestis which is the same bacterium that causes bubonic and pneumonic plague in humans. Plague was first introduced into the United States in 1900 by rat–infested steamships that had sailed from affected areas, mostly from Asia. Urban plague spread from urban rats to rural rodent species, especially among prairie dogs in the western United States.[1][2]

Vector reservoir[edit]

Common vectors for urban plague are house mice, black rats, and Norway rats.[3]

Transmission[edit]

Urban plague spreads via flea bites.

See also[edit]

References[edit]

  1. ^ "A Plague Epizootic In The Black-Tailed Prairie Dog (Cynomys Ludovicianus)". Jwildlifedis.org. 2006-01-01. Retrieved 2013-07-28. 
  2. ^ "CDC - Maps & Statistics - Plague". Cdc.gov. 2013-04-23. Retrieved 2013-07-28. 
  3. ^ Cockrum, E. Lendell, Rabies, Lyme Diseases, Hanta Virus and other Animal-Borne Human Diseases in the United States and Canada. Fisher Books, Tucson, Arizona. 1997. Page 36.
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