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| __NOTOC__
| | #REDIRECT [[Yersinia pestis]] |
| {{Yersinia pestis infection}}
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| {{CMG}}; Assistant Editors-In-Chief: Esther Lee, M.A.; {{Rim}}
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| ==Overview==
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| ''[[Yersinia pestis]]'' (''Y. pestis''), a rod-shaped [[facultative anaerobe]] with bipolar staining (giving it a safety pin appearance) causes the infection in mammals and humans.<ref name=Baron>{{cite book | author = Collins FM | title = Pasteurella, Yersinia, and Francisella. ''In:'' Baron's Medical Microbiology ''(Baron S ''et al'', eds.)| edition = 4th | publisher = Univ. of Texas Medical Branch | year = 1996 | url = http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.section.1611 | isbn = 0-9631172-1-1 }}</ref> The bacteria maintain their existence in a cycle involving rodents and their fleas. The genus Yersinia is [[gram-negative]], bipolar staining coccobacilli, and, similarly to other [[Enterobacteriaceae]], it has a fermentative metabolism. ''Y. pestis'' produces an antiphagocytic slime. The organism is motile when isolated, but becomes nonmotile in the mammalian host.
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| ==Taxonomy==
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| [[Bacteria]]; [[Eubacteria]]; [[Proteobacteria]]; [[Proteobacteria#Gammaproteobacteria|Gammaproteobacteria]]; ''[[Yersinia]]''; Yersinia pestis
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| ==Transmission==
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| Transmission of Y. pestis to an uninfected individual is possible by any of the following means.<ref name="PM">Plague Manual: Epidemiology, Distribution, Surveillance and Control, pp. 9 and 11. WHO/CDS/CSR/EDC/99.2</ref>
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| * Droplet contact – coughing or sneezing on another person
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| * Direct physical contact – touching an infected person, including sexual contact
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| * Indirect contact – usually by touching [[soil contamination]] or a contaminated surface
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| * Airborne transmission – if the microorganism can remain in the air for long periods
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| * Fecal-oral transmission – usually from contaminated food or water sources
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| * Vector borne transmission – carried by insects or other animals
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| Pneumonic plague can be transmitted from person to person; bubonic plague cannot. Pneumonic [[plague]] affects the [[lungs]] and is transmitted when a person breathes in Y. pestis particles in the air. Bubonic plague is transmitted through the bite of an infected flea or exposure to infected material through a break in the skin.
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| ===Flea Bites===
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| Plague [[bacteria]] are most often transmitted by the bite of an infected flea. During plague epizootics, many rodents die, causing hungry fleas to seek other sources of [[blood]]. People and animals that visit places where rodents have recently died from plague are at risk of being infected from flea bites. Dogs and cats may also bring plague-infected fleas into the home. Flea bite exposure may result in primary bubonic plague or septicemic plague.
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| ===Contact with Contaminated Fluid or Tissue===
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| Humans can become infected when handling tissue or body fluids of a plague-infected animal. For example, a hunter skinning a rabbit or other infected animal without using proper precautions could become infected with plague [[bacteria]]. This form of exposure most commonly results in bubonic plague or septicemic plague.
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| ===Infectious Droplets===
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| When a person has plague [[pneumonia]], they may cough droplets containing the plague bacteria into air. If these bacteria-containing droplets are breathed in by another person they can cause pneumonic plague. Typically this requires direct and close contact with the person with pneumonic plague. Transmission of these droplets is the only way that plague can spread between people. This type of spread has not been documented in the United States since 1924, but still occurs with some frequency in developing countries. Cats are particularly susceptible to plague, and can be infected by eating infected rodents. Sick cats pose a risk of transmitting infectious plague droplets to their owners or to veterinarians. Several cases of human plague have occurred in the United States in recent decades as a result of contact with infected cats.
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| ==Genome==
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| The complete [[genome|genomic]] sequence is available for two of the three sub-species of yersinia pestis: strain KIM (of biovar Medievalis),<ref>{{cite journal | author = Deng W| title = Genome Sequence of Yersinia pestis KIM | journal = Journal of Bacteriology | year = 2002 | volume = 184 | issue = 16 | pages = 4601–4611 | doi= 10.1128/JB.184.16.4601-4611.2002 | pmid=12142430 | pmc = 135232 | author-separator = , | display-authors = 1 | last2 = Burland | first2 = V. | last3 = Plunkett Iii | first3 = G. | last4 = Boutin | first4 = A. | last5 = Mayhew | first5 = G. F. | last6 = Liss | first6 = P. | last7 = Perna | first7 = N. T. | last8 = Rose | first8 = D. J. | last9 = Mau | first9 = B.}}</ref> and strain CO92 (of biovar Orientalis, obtained from a clinical isolate in the United States).<ref>{{cite journal | author = Parkhill J| title = Genome sequence of Yersinia pestis, the causative agent of plague | journal = Nature | year = 2001 | volume = 413 | issue = 6855| pages = 523–527 | doi = 10.1038/35097083 | pmid = 11586360 | author-separator = , | display-authors = 1 | last2 = Wren | first2 = B. W. | last3 = Thomson | first3 = N. R. | last4 = Titball | first4 = R. W. | last5 = Holden | first5 = M. T. G. | last6 = Prentice | first6 = M. B. | last7 = Sebaihia | first7 = M. | last8 = James | first8 = K. D. | last9 = Churcher | first9 = C.}}</ref> As of 2006, the genomic sequence of a strain of biovar Antiqua has been recently completed.<ref name="pmid16740952">{{cite journal |author=Chain PS |title=Complete Genome Sequence of Yersinia pestis Strains Antiqua and Nepal516: Evidence of Gene Reduction in an Emerging Pathogen |journal=J. Bacteriol. |volume=188 |issue=12 |pages=4453–63 |year=2006 |pmid=16740952 |doi=10.1128/JB.00124-06 |pmc=1482938 |author-separator=, |author2=Hu P |author3=Malfatti SA |display-authors=3 |last4=Radnedge |first4=L. |last5=Larimer |first5=F. |last6=Vergez |first6=L. M. |last7=Worsham |first7=P. |last8=Chu |first8=M. C. |last9=Andersen |first9=G. L.}}</ref> 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 [[Yersinia pseudotuberculosis|Yersinia pseudotuberculosis]] and [[Yersinia enterocolitica|Yersinia enterocolitica]], Yersinia 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 Yersinia pestis to be transmitted by fleas. pPla codes for a [[protease]], Pla, that activates [[plasminogen]] in human hosts and is a very important [[virulence factor]] for pneumonic plague.<ref name="pmid17255510">{{cite journal| author=Lathem WW, Price PA, Miller VL, Goldman WE| title=A plasminogen-activating protease specifically controls the development of primary pneumonic plague. | journal=Science | year= 2007 | volume= 315 | issue= 5811 | pages= 509-13 | pmid=17255510 | doi=10.1126/science.1137195 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17255510 }} </ref> Together, these plasmids, and a [[pathogenicity island]] called HPI, encode several proteins that cause the pathogenesis, for which Yersinia 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). Yersinia pestis is thought to be descendant from Yersinia pseudotuberculosis, differing only in the presence of specific virulence plasmids.
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| A comprehensive and comparative [[proteomics]] analysis of Yersinia pestis strain KIM was performed in 2006.<ref>{{cite journal | author = Hixson K| title = Biomarker candidate identification in Yersinia pestis using organism-wide semiquantitative proteomics | journal = Journal of Proteome Research | year = 2006 | volume = 5 | issue = 11 | pages = 3008–3017 | pmid = 16684765 | doi = 10.1021/pr060179y | author-separator = , | display-authors = 1 | last2 = Adkins | first2 = Joshua N. | last3 = Baker | first3 = Scott E. | last4 = Moore | first4 = Ronald J. | last5 = Chromy | first5 = Brett A. | last6 = Smith | first6 = Richard D. | last7 = McCutchen-Maloney | first7 = Sandra L. | last8 = Lipton | first8 = Mary S. | last9 = Heffron | first9 = F}}</ref> The analysis focused on the transition to a growth condition mimicking growth in host cells.
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| ==References==
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| {{Reflist|2}}
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| [[Category:Dermatology]]
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| [[Category:Infectious disease]]
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| [[Category:Pulmonology]]
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| [[Category:Hematology]]
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| [[Category:Disease]]
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| [[Category:Needs content]]
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| {{WH}}
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| {{WS}}
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