Yersinia pestis infection causes: Difference between revisions

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* fecal-oral transmission – usually from contaminated food or water sources
* fecal-oral transmission – usually from contaminated food or water sources
* vector borne transmission – carried by insects or other animals.
* vector borne transmission – carried by insects or other animals.
===Genome===
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&ndash;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&ndash;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.<ref name="pmid11976454" /> 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" /> 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.
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.


==References==
==References==

Revision as of 16:32, 18 December 2012

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Assistant Editors-In-Chief: Esther Lee, M.A.

Causes

Yersinia pestis, a rod-shaped facultative anaerobe with bipolar staining (giving it a safety pin appearance).[1] causes the infection in mammals and humans.

Transmission of Y. pestis to an uninfected individual is possible by any of the following means.[2]

  • droplet contact – coughing or sneezing on another person
  • direct physical contact – touching an infected person, including sexual contact
  • indirect contact – usually by touching soil contamination or a contaminated surface
  • airborne transmission – if the microorganism can remain in the air for long periods
  • fecal-oral transmission – usually from contaminated food or water sources
  • vector borne transmission – carried by insects or other animals.

References

  1. 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.
  2. Plague Manual: Epidemiology, Distribution, Surveillance and Control, pp. 9 and 11. WHO/CDS/CSR/EDC/99.2

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