Yersinia pestis 34367 223089542 2008-07-02T14:54:43Z 140.139.35.250 /* In humans and other susceptible hosts */ {{Mergefrom|bubonic plague|date=May 2008}} {{Taxobox | color =very light gray <!-- Please read [[WP:Taxobox_usage#Color]] before making any changes to the taxobox color. --> | name = ''Yersinia pestis'' | image = Yersinia pestis.jpg | image_width = 250px | image_caption = A scanning electron micrograph depicting a mass of ''Yersinia pestis'' bacteria | regnum = [[Bacterium|Eubacteria]] | phylum = [[Proteobacteria]] | classis = [[Proteobacteria#Gammaproteobacteria|Gammaproteobacteria]] | ordo = [[Enterobacteriaceae|Enterobacteriales]] | familia = [[Enterobacteriaceae]] | genus = ''[[Yersinia]] | species = '''''Y. pestis''''' | binomial = ''Yersinia pestis'' | binomial_authority = (Lehmann &amp; Neumann, 1896)<br>van Loghem 1944 }} '''''Yersinia pestis''''' (formerly '''''Pasteurella pestis''''') is a [[Gram-negative]] [[bacillus|rod-shaped]] [[bacterium]] belonging to the family [[Enterobacteriaceae]]. It is a [[facultative anaerobe]] that can infect humans and other animals. Human ''Y. pestis'' infection takes three main forms: [[pneumonic plague|pneumonic]], [[septicemic plague|septicemic]], and the famous [[bubonic plague|bubonic]] plagues.<ref name=Sherris>{{cite book | author = Ryan KJ; Ray CG (editors) | title = Sherris Medical Microbiology | edition = 4th ed. | pages = pp. 484-8 | publisher = McGraw Hill | year = 2004 | id = ISBN 0-8385852-9-9 }}</ref> All three forms have been responsible for high mortality rates in [[epidemics]] throughout human history, including the [[Black Death]] (a bubonic plague) that accounted for the death of approximately one-third of the [[Europe]]an population in [[1347]] to [[1353]]. Recently ''Y. pestis'' has gained attention as a possible biological warfare agent and the CDC has classified it as [[Bioterrorism|category A pathogen]] requiring preparation for a possible terrorist attack. ==History== ''Y. pestis'' was discovered in [[1894]] by [[Alexandre Yersin]], a [[Switzerland|Swiss]]/[[France|French]] [[physician]] and [[bacteriologist]] from the [[Pasteur Institute]], during an [[epidemic]] of plague in [[Hong Kong]].<ref name=Bockemühl_1994>{{cite journal |author=Bockemühl J |title=[100 years after the discovery of the plague-causing agent--importance and veneration of Alexandre Yersin in Vietnam today] |journal=Immun Infekt |volume=22 |issue=2 |pages=72–5 |year=1994 |pmid = 7959865}}</ref> Yersin was a member of the [[Louis Pasteur|Pasteur]] school of thought. [[Shibasaburo Kitasato]], a [[Germany|German]]-trained [[Japan]]ese bacteriologist who practiced [[Robert Koch|Koch's methodology]] was also engaged at the time in finding the causative agent of plague.<ref name="Ho">{{cite journal |author=Howard-Jones N |title=Was Shibasaburo Kitasato the discoverer of the plague bacillus? | journal=Perspect Biol Med |volume=16 |issue=2 |pages=292–307 |year=1973 |pmid = 4570035}}</ref> However, it was Yersin who actually linked plague with ''Yersinia pestis''. Originally named ''Pasteurella pestis'', the organism was renamed in 1967. Three [[biovar]]s of ''Y. pestis'' are known, each thought to correspond to one of the historical pandemics of bubonic plague.<ref name=Zhou_2004>{{cite journal |author=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 |title=Genetics of metabolic variations between Yersinia pestis biovars and the proposal of a new biovar, microtus |journal=J Bacteriol |volume=186 |issue=15 |pages=5147–52 |year=2004 |url= http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=8195371 | pmid = 15262951 | doi = 10.1128/JB.186.15.5147-5152.2004 <!--Retrieved from CrossRef by DOI bot-->}}</ref> Biovar '''Antiqua''' is thought to correspond to the [[Plague of Justinian]]; it is not known whether this biovar also corresponds to earlier, smaller epidemics of bubonic plague, or whether these were even truly bubonic plague.<ref name=Guiyoule_1994>{{cite journal |author=Guiyoule A, Grimont F, Iteman I, Grimont P, Lefèvre M, Carniel E |title=Plague pandemics investigated by ribotyping of Yersinia pestis strains |journal=J Clin Microbiol |volume=32 |issue=3 |pages=634–41 |year=1994 |pmid=8195371}}</ref> Biovar '''Medievalis''' is thought to correspond to the [[Black Death]]. Biovar '''Orientalis''' is thought to correspond to the [[Third Pandemic]] and the majority of modern outbreaks of plague. ''Y. pestis'' was transmitted by [[flea]]s infesting [[rat]]s. ===Controversy=== The role of ''Y. pestis'' in the Black Death is debated among historians; some have suggested that the Black Death spread far too rapidly to be caused by ''Y. pestis''. DNA from ''Y. pestis'' is alleged to have been found in the teeth of an individual who supposedly died from the Black Death, however, and medieval corpses who died from other causes did test positive for ''Y. pestis''.<ref>{{cite journal | author = Drancourt M, Aboudharam G, Signolidagger M, Dutourdagger O, Raoult D.| title = Detection of 400-year-old ''Yersinia pestis'' DNA in human dental pulp: An approach to the diagnosis of ancient septicemia | journal = PNAS | year = 1998| volume = 95 | issue = 21 | pages = 12637&ndash;12640 | url= http://www.pnas.org/cgi/content/abstract/95/21/12637} | pmid = 9770538 }}</ref><ref>{{cite journal | author = Drancourt M; Raoult D.| title = Molecular insights into the history of plague. | journal = Microbes Infect. | year = 2002 | volume = 4| issue = | pages = 105&ndash;9 | pmid = 11825781 | doi = 10.1016/S1286-4579(01)01515-5 <!--Retrieved from CrossRef by DOI bot-->}}</ref> This suggests that ''Y. pestis'' was, at the very least, a contributing factor in some (though possibly not all) of the European plagues. It is possible that the selective pressures induced by the plague might have changed how the pathogen manifests in humans, selecting against the individuals or populations which were the most susceptible. ==General characteristics== ''Y. pestis'' is a rod-shaped facultative anaerobe with bipolar staining (giving it a [[safety pin]] appearance).<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 ed. | publisher = Univ of Texas Medical Branch | year = 1996 | url = http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.section.1611 | id = ISBN 0-9631172-1-1 }}</ref> Similar to other ''[[Yersinia]]'' members, it tests negative for [[urease test|urease]], [[lactose fermentation]], and [[indole test|indole]].<ref name="isbn0-387-25499-4">{{cite book |author=Stackebrandt, Erko; Dworkin, Martin; Falkow, Stanley; Rosenberg, Eugene; Karl-Heinz Schleifer |title=The Prokaryotes: A Handbook on the Biology of Bacteria:Volume 6: Proteobacteria: Gamma Subclass |publisher=Springer |location=Berlin |year= |pages= |isbn=0-387-25499-4 |oclc= |doi=}}</ref> The closest relative is the gastrointestinal pathogen ''[[Yersinia pseudotuberculosis| Yersinia pseudotuberculosis]]'', and more distantly ''[[Yersinia enterocolitica]].'' ===Genome=== The complete [[genome|genomic]] sequence is available for two of the three sub-species of ''Y. pestis'': strain KIM (of biovar Medievalis),<ref>{{cite journal | author = Deng W ''et al.''.| title = Genome Sequence of ''Yersinia pestis KIM'' | journal = Journal of Bacteriology | year = 2002 | volume = 184 | issue = 16 | pages = 4601&ndash;4611 | doi= 10.1128/JB.184.16.4601-4611.2002 | pmid=12142430}}</ref> and strain CO92 (of biovar Orientalis, obtained from a clinical isolate in the United States)<ref>{{cite journal | author = Parkhill J ''et al.''.| title = Genome sequence of ''Yersinia pestis'', the causative agent of plague | journal = Nature | year = 2001 | volume = 413 | issue = | pages = 523&ndash;527 | doi = 10.1038/35097083 | pmid = 11586360}}</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, Hu P, Malfatti SA, ''et al'' |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}}</ref> Similar to the other pathogenic strains, there are signs of loss of function. 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|Y. pseudotuberculosis]]'' and ''[[Yersinia enterocolitica|Y. enterocolitica]]'', ''Y. pestis'' is host to the [[plasmid]] pCD1. In addition, it also hosts two other plasmids, pPCP1 and pMT1 which are not carried by the other ''Yersinia'' species. Together, these plasmids, and a [[pathogenicity island]] called HPI, encode several proteins which 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 into the host cell, and acquisition and binding of iron harvested from red blood cells. ''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;<ref>{{cite journal | author = Hixson K ''et al.''.| 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 <!--Retrieved from CrossRef by DOI bot-->}}</ref> this analysis focused on the transition to a growth condition mimicking growth in host cells. ==Pathogenics and immunity== ===In reservoir host=== The reservoir commonly associated with ''Y. pestis'' are several species of rodents. In the [[steppe]]s, the [[Natural reservoir| reservoir species]] is principally believed to be the [[marmots|marmot]]. In the United States, several species of [[Rodent|rodents]] are thought maintain ''Y. pestis''. However, the case is not very clear because the expected disease dynamics have not been found in any rodent species. It is known that some individuals in a rodent population will have a different resistance, which could lead to a [[Asymptomatic carrier|carrier]] status.<ref name="pmid13453634">{{cite journal |author=MEYER KF |title=The natural history of plague and psittacosis |journal=[[Public Health Rep]] |volume=72 |issue=8 |pages=705–19 |year=1957 |pmid=13453634 |doi=}}</ref> There is some evidence that fleas from other mammals have a role in human plague outbreaks.<ref name="pmid908848">{{cite journal |author=von Reyn CF, Weber NS, Tempest B, ''et al'' |title=Epidemiologic and clinical features of an outbreak of bubonic plague in New Mexico |journal=J. Infect. Dis. |volume=136 |issue=4 |pages=489–94 |year=1977 |pmid=908848 |doi=}}</ref> 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.<ref name="pmid16699150">{{cite journal |author=Pauli JN, Buskirk SW, Williams ES, Edwards WH |title=A plague epizootic in the black-tailed prairie dog (Cynomys ludovicianus) |journal=J. Wildl. Dis. |volume=42 |issue=1 |pages=74–80 |year=2006 |pmid=16699150 |doi=}}</ref> 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.<ref name="pmid16603630">{{cite journal |author=Webb CT, Brooks CP, Gage KL, Antolin MF |title=Classic flea-borne transmission does not drive plague epizootics in prairie dogs |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=103 |issue=16 |pages=6236–41 |year=2006 |pmid=16603630 |doi=10.1073/pnas.0510090103}}</ref> 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.<ref name="pmid18257987">{{cite journal |author=Bertherat E, Bekhoucha S, Chougrani S, ''et al'' |title=Plague Reappearance in Algeria after 50 Years, 2003 |journal=Emerging Infect. Dis. |volume=13 |issue=10 |pages=1459–1462 |year=2007 |pmid=18257987 |doi=}}</ref> ===In vector=== The transmission of ''Y. pestis'' by [[fleas]] is well characterized<ref name="pmid16182593">{{cite journal |author=Zhou D, Han Y, Yang R |title=Molecular and physiological insights into plague transmission, virulence and etiology |journal=Microbes Infect. |volume=8 |issue=1 |pages=273–84 |year=2006 |pmid=16182593 |doi=10.1016/j.micinf.2005.06.006}}</ref>. 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 Ymt is highly toxic to rodents and was once thought to be produced to insure reinfection of new hosts, it has been demonstrated that murine toxin is important for the survival of ''Y. pestis'' in fleas.<ref name="pmid11976454">{{cite journal |author=Hinnebusch BJ, Rudolph AE, Cherepanov P, Dixon JE, Schwan TG, Forsberg A |title=Role of Yersinia murine toxin in survival of Yersinia pestis in the midgut of the flea vector |journal=Science |volume=296 |issue=5568 |pages=733–5 |year=2002 |pmid=11976454 |doi=10.1126/science.1069972}}</ref> The Hms system plays an important role in the transmission of ''Y. pestis'' back to a mammalian host<ref name="pmid8662526">{{cite journal |author=B.J. Hinnebusch, R.D. Perry and T.G. Schwan |title=Role of the Yersinia pestis hemin storage (hms) locus in the transmission of plague by fleas |journal=Science. |volume=8 |issue=1 |pages=367–70 |year=1996 |pmid=8662526 |doi=}}</ref>. The proteins encoded by Hms genetic loci aggregate in the esophagus and proventriculus of the flea, which is a structure that ruptures blood cells. Aggregation of Hms proteins inhibits feeding and causes the flea to feel hungry. 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 growing there and is regurgitated back into the host circulatory system. ===In humans and other susceptible hosts=== Pathogenesis of Y. pestis in mammalian hosts is due to several factors, which predominately focus on the initial immune response. Flea bites allow for the bacteria to enter through the skin. ''Y. pestis'' expresses the yadBC gene, which is similar to Invasin in other Yersinia species, allowing for adherence and invasion of epithelium.<ref name="pmid18025093">{{cite journal |author=Forman S, Wulff CR, Myers-Morales T, Cowan C, Perry RD, Straley SC |title=yadBC of Yersinia pestis, a new virulence determinant for bubonic plague |journal=Infect. Immun. |volume=76 |issue=2 |pages=578–87 |year=2008 |pmid=18025093 |doi=10.1128/IAI.00219-07}}</ref> There are reports that isolates from the pneumatic plague patients have a [[plasminogen]] activator, which can remove clots in order to facilitate systematic invasion. <ref>{{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 |volume=315 |issue=5811 |pages=509–13 |year=2007 |pmid=17255510 |doi=10.1126/science.1137195}}</ref> The majority of the bacteria's virulence factors are anti-[[phagocytosis|phagocytic]] in nature. Two important anti-phagocytic [[antigens]], named F1 (Fraction 1) and V or [[LcrV]], are both important for [[virulence]].<ref name=Baron/> 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 [[blood]] cells such as [[monocyte]]s, but not in [[neutrophils]]. Natural or induced [[immunity (medical)|immunity]] is achieved by the production of specific [[opsonin|opsonic]] [[antibody|antibodies]] against F1 and V antigens; antibodies against F1 and V induce [[phagocytosis]] by neutrophils.<ref>{{cite book | author = Salyers AA, Whitt DD | title = Bacterial Pathogenesis: A Molecular Approach | edition = 2nd ed. | publisher = ASM Press | year = 2002 | id = pp. 207-12}}</ref> Additionally, the [[Secretion#Type III secretion system (T3SS)|Type III secretion system]] allows ''y. pestis'' to inject six different substances into macrophages and other immune cells. These are collectively call YOPs (Yersinia Outercoat Proteins) and include Yop B/D for [[cytolysis]] , YpkA for serine/threonine kinase activity, YopO, YopH, YopM for platelet aggregation, YopT, YopJ for [[apoptosis]], and YopE for actin microfilament disruption. These proteins are injected via a long syringe into a pore created in part by YopB and YopD. <ref>{{cite journal |author=Viboud GI, Bliska JB |title=Yersinia outer proteins: role in modulation of host cell signaling responses and pathogenesis |journal=Annu. Rev. Microbiol. |volume=59 |issue= |pages=69–89 |year=2005 |pmid=15847602 |doi=10.1146/annurev.micro.59.030804.121320}}</ref> These proteins limit phagocytosis by targeting [[actin]] and other cell singling pathways important in the [[innate immune system]]. ===Immunity=== A [[formalin]]-inactivated [[vaccine]] once was available for adults at high risk of contracting the plague until removal from the market by the [[FDA]]. It was of limited effectiveness and may 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, that vaccines composed of these antigens may not be fully protective<ref>{{cite journal | author = Welkos S ''et al.''.| title = 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 | journal = Vaccine | year = 2002 | volume = 20 | issue = | pages = 2206&ndash;2214 | pmid = 12009274 | doi = 10.1016/S0264-410X(02)00119-6 <!--Retrieved from CrossRef by DOI bot-->}}</ref>. ==Clinical aspects== ===Symptoms and disease progression=== *Bubonic plague **Incubation period of 2-6 days, when the bacteria is actively replicating in lymph nodes **Universally a general lack of energy **Fever **Headache and chills occur suddenly at the end of the incubation period. From this point the infection is resolved or lethal. **Swelling of lymph nodes resulting of buboes, this is the classic sign of bubonic plague *Septicemic plague **[[Hypotension]] **[[Hepatosplenomegaly]] **[[Delirium]] **Seizures in children **Shock **Universally a general lack of energy **Fever **Symptoms of Bubonic or Pneumonic Plague, not always present *Pneumonic plague **Fever **Chills **Cough **Chest pain **Dyspnea **Hemoptysis **Lethargy **Hypotension **Shock **Symptoms of bubonic or septicemic plague, not always present <ref>Info taken from "Harrison's Principles of Internal Medicine 16th Edition"</ref> If this occurs with the classic [[bubo]]es, this is considered primary, while secondary occurs after symptoms of bubonic or pneumonic infection. Since the bacteria blood-bourne, 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%. Pneumonic plague can be spread from one human to another directly by aerosol. Rarely bubonic and even more rarely septicemic plague can gain pneumonic characteristics. As with the other forms of plague, after the incubation period there is a sudden onset of coughing, high temperature, and lack of energy. From this point the infection increases in severity. Due to its high replication rates, plague proves fatal in roughly 50% of cases even with medical treatment, and is almost universally fatal without treatment.<ref name="pmid16200159">{{cite journal |author=Riedel S |title=Plague: from natural disease to bio-terrorism |journal=Proc (Bayl Univ Med Cent) |volume=18 |issue=2 |pages=116–24 |year=2005 |pmid=16200159 |doi=}}</ref> With the exception of the buboes, the initial symptoms of plague are very similar to many other disease, making diagnosis difficult<ref name="pmid17416264">{{cite journal |author=Prentice MB, Rahalison L |title=Plague |journal=Lancet |volume=369 |issue=9568 |pages=1196–207 |year=2007 |pmid=17416264 |doi=10.1016/S0140-6736(07)60566-2 |url=http://linkinghub.elsevier.com/retrieve/pii/S0140-6736(07)60566-2}}</ref>. ICD-9 codes for the diseases caused by ''Y. pestis'': *020.0 Bubonic plague *020.2 Septicemic plague *020.5 Unspecified pneumonic plague *020.3 Primary pneumonic plague *020.4 Secondary pneumonic plague ===Clinical determination=== Grams stains can confirm the presence of gram negative rods, and in some cases the identification of the double curved shape. More definitive test is a Anti-F1 serology test, which can differentiate between different species of Yersinia. ===Treatment=== The traditional first line treatment for ''Y. pestis'' has been [[streptomycin]],<ref>{{cite journal | author=Wagle PM. | title=Recent advances in the treatment of bubonic plague | journal=Indian J Med Sci | year=1948 | volume=2 | pages=489&ndash;94 }}</ref><ref>{{cite journal | author=Meyer KF. | title=Modern therapy of plague | journal=JAMA | year=1950 | volume=144 | pages=982&ndash;5 | pmid = 14774219}}</ref> [[chloramphenicol]], [[tetracycline]],<ref>{{cite journal | author=Kilonzo BS, Makundi RH, Mbise TJ. | title= A decade of plague epidemiology and control in the Western Usambara mountains, north-east Tanzania | journal=Acta Tropica | year=1992 | volume=50 | pages=323&ndash;9 | pmid = 1356303 | doi = 10.1016/0001-706X(92)90067-8 <!--Retrieved from CrossRef by DOI bot-->}}</ref> and [[fluoroquinolones]]. There is also good evidence to support the use of [[doxycycline]] or [[gentamicin]].<ref>{{cite journal | author=Mwengee W, Butler T, Mgema S, ''et al.'' | title=Treatment of plague with gentamicin or doxycycline in a randomized clinical trial in Tanzania | journal=Clin Infect Dis | year=2006 | volume=42 | pages=614&ndash;21 | pmid = 16447105 | doi = 10.1086/500137 <!--Retrieved from CrossRef by DOI bot-->}}</ref> 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<ref name="isbn0-07-140235-7">{{cite book |author=Jameson, J. N. St C.; Dennis L. Kasper; Harrison, Tinsley Randolph; Braunwald, Eugene; Fauci, Anthony S.; Hauser, Stephen L; Longo, Dan L. |title=Harrison's principles of internal medicine |publisher=McGraw-Hill Medical Publishing Division |location=New York |year=2005 |pages= |isbn=0-07-140235-7 |oclc= |doi=}}</ref>. Antibiotics within the first 24 hours is very beneficial, with intravenous being preferred in pulmonary or advance cases. Streptomycin or gentamicin are the first-line drugs, with chloramphenicol for critically ill patients, or rarely for suspected neuro-involvement. ==External links== {{wikispecies|Yersinia pestis}} {{commons|Yersinia pestis}} * [http://www.bacteriamuseum.org/species/ypestis.shtml ''Yersinia pestis'']. Virtual Museum of Bacteria. * Genome information is available from the [http://www.ericbrc.org NIAID Enteropathogen Resource Integration Center (ERIC)] * A list of variant strains and information on synonyms (and much more) is available through the [http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=632 NCBI taxonomy browser]. *CDC's Home page for Plague [http://www.cdc.gov/ncidod/dvbid/plague/index.htm] ==References== {{Reflist|2}} [[Category:Enterobacteria]] [[Category:Bacterial diseases]] [[br:Yersinia pestis]] [[cs:Yersinia pestis]] [[cy:Yersinia pestis]] [[da:Yersinia pestis]] [[de:Yersinia pestis]] [[es:Yersinia pestis]] [[fa:یرسینیا پستیس]] [[fr:Yersinia pestis]] [[it:Yersinia pestis]] [[he:Yersinia pestis]] [[ku:Peşte]] [[la:Yersinia pestis]] [[nl:Yersinia pestis]] [[ja:ペスト菌]] [[no:Yersinia pestis]] [[pl:Pałeczka dżumy]] [[pt:Yersinia pestis]] [[ru:Yersinia pestis]] [[simple:Yersinia pestis]] [[sl:Yersinia pestis]] [[sv:Yersinia pestis]] [[vi:Yersinia pestis]] [[tr:Yersinia pestis]] [[uk:Yersinia pestis]] [[zh:鼠疫桿菌]]