Yersinia pseudotuberculosis

From MicrobeWiki, the student-edited microbiology resource

Jump to: navigation, search
This student page has not been curated.

A Microbial Biorealm page on the genus Yersinia pseudotuberculosis

Contents

Classification

Higher order taxa

Bacteria; Proteobacteria; Gammaproteobacteria; Enterobacteriales; Enterobacteriaceae (1)

Species

Yersinia pseudotuberculosis (1)

Description and significance

Yersinia pseudotuberculosis is a rod-shaped bacteria that has flagella. (16, 17)

Y. pseudotuberculosis has a pillus that extends from one pole and is used for adhesion and pathogenicity. (18) The increased G+C content of the DNA encoding the pil operon indicates that it was likely aquired via a horizontal gene transfer. (18)

Y. pseudotuberculosis is related to Y. pestis which is the bacteria responsible for the bubonic plague. (2) Y. pestis evolved from Y. pseudotuberculosis. Y. pseudotuberculosis is a pathogen of the gut. (3)

Genome structure

The genome of Y. pseudotuberculosis is contained in one circular chromosome and two plasmids. The circular chromosome has 4.7 million base pairs. (3) One of the plasmids is responsible for the bacteria's virulence. The other plasmid encodes mobilization information. This second plasmid can replicate and transmit itself independently from the main chromosome. It does not serve a virulence function. (3) The virulence plasmid has 68,000 base pairs and the other plasmid has 28,000 base pairs. The whole genome has been sequenced. (3) 75% of the genes on the main chromosome of Y. pseudotuberculosis are also found on the chromosome of Y. pestis. (3)

Cell structure and metabolism

Y. pseudotuberculosis is a Gram-negative bacterium. (4) The acyl chains of the LPSs in Y. pseudotuberculosis are very fluid and this increases the permeability of the outer membrane of the bacteria. (4) These bacteria potentially have efflux systems that pump out hydrophobic compounds. (4)

Y. pseudotuberculosis is a chemoheterotroph. (3) When restricted to a two-carbon carbon source such as acetate Y. pseudotuberculosis is able to synthesize isocitrate lyase and malate synthase, the two enzymes of the glyoxylate bypass pathway. (20) Y. pestis uses palmitic acid as its primary carbon source. (19)

Y. pseudotuberculosis has not been shown to produce siderophores in low Fe3+ conditions. Instead the bacteria have developed a method to uptake hemin, an iron transport protoporphyrin used by Haemophilus influenzae, as an alternative iron source. (21)

Ecology

Wild rodents historically have been important reservoir disease hosts for Yersinia species. The availability of rodent hosts in Europe, Africa, and Asia throughout the 2nd millenium enabled Yersinia pestis to infect and kill millions of people. (10)

The transmission of Yersinia pestis by fleas is affected by climate. (11) Temperature, rainfall, humidity, wind, and duration of daylight all affect bacterial and flea reproduction. Successful transmission requires that the bacterial replication time is shorter than the lifetime of the host. (11)

Y. pseudotuberculosis use quorum sensing to trigger motility and pathogenicity. (12) This means they secrete molecules into their environment and measure the concentration of those molecules to estimate the number of bacterial cells in the vicinity. If there are a sufficient number present, the group will proceed to move or infect.

Pathology

Y. pseudotuberculosis infects eukaryotic hosts through a type III secretion system. The secretion system involves the transport of proteins through the bacterial envelope and past the host cell plasma membrane. (5) The secretion is part of a highly regulated system that is indirectly modulated by temperature changes and by a Ca2+ dependency. (5) The calcium requirement indicates that infection is dependent on cell to cell contact. (6) The secretion system, regulatory pathways, and toxic proteins are all encoded on the virulence plasmid. (6)

Y. pseudotuberculosis is usually a food-borne pathogen. (8) It is relatively resistant to the non-specific human immune response. (6) Y. pseudotuberculosis infects the intestinal tract, liver, spleen, and lymph nodes and causes these tissues to become inflammed. (7,6) Typical symptoms of a Y. pseudotuberculosis infection include joint or back pain, abdominal cramps, and diarrhea. (8) The O:3 strain of Y. pseudotuberculosis can cause reactive arthritis. (9)

Yersinia pestis can be transmitted via direct contact with an infected mammal, inhalation of the bacteria, or by a flea bite. (11)

Application to Biotechnology

The V-antigen from Yersinia species could be used as a vaccination against the plague. The V-antigen from Y. pestis was extracted, purified and administered as an effective vaccine. During the purification the V-antigen broke down. The V-antigen from Y. pseudotuberculosis is more stable. Perhaps a plague vaccine will be more easily isolated from Y. pseudotuberculosis. (13)

Y. pestis is a potential bacteria to be used as biowarfare. (14) In September of 2003 a plague scientist from Texas Tech, Dr. Thomas Butler, was on trial for illegally transporting 30 vials containing Y. pestis and lying about the fates of those vials. (15) The severity of the legal response to Dr. Butler’s actions indicates two things. The first is that the biowarfare of Y. pestis is at least perceived as a grave threat and warrants in depth scientific study of the organism. The second is that the regulations and legal boundaries imposed on the study of threatening organisms such as Y. pestis may disuade scientists from studying them.

Current Research

====Intranasal inoculation of mice with Yersinia pseudotuberculosis causes a lethal lung infection that is dependent on Yersinia outer proteins and PhoP.==== (22) This study was conducted to analyze the pathway of a lung infection by Y. pseudotuberculosis in mice. Lung infections in humans by Y. pseudotuberculosis are uncommon. Typically, a lung infection only results after transmission of the bacteria from a systemic infection. Once the bacteria are in the lungs, they can be recovered. In this study, mice were inoculated intranasally to attempt to induce lung infections. The mice that were infected with Y. pseudotuberculosis reacted with pneumonia and subsequent death. The mice gave essentially the same symptoms when inoculated with Y. pestis, however, the symptoms took half as long to develop compared to Y. pseudotuberculosis infected mice. Both bacteria had very low infectious doses in the mice. Various virulent genes of Y. pseudotuberculosis were altered to prioritize the role of these genes in lung infections versus systemic infections. A mutation in the yopB gene disabled Y. pseudotuberculosis from effectively infecting the mice through intranasal inoculation. However, six weeks later these mice had granulomas and collagen deposits in their lungs that were not present in the mice infected with the wild type Y. pseudotuberculosis. This study provided a model for lung infections by Y. pseudotuberculosis through intranasal inoculation.

====Yersinia pseudotuberculosis adhesins regulate tissue-specific colonization and immune cell localization in a mouse model of systemic infection.==== (23) The purpose of this study was to assess the importance of invasin and YadA in Y. pseudotuberculosis colonization of host tissues. Invasin and YadA are outer membrane proteins that are responsible for the attachment to and penetration of host cells by Y. pseudotuberculosis. Strains of Y. pseudotuberculosis were produced that lacked typical virulence properties including the type III secretion system. From these strains various alterations were made to invasin and YadA to assess their role in tissue colonization. This allowed for the study of colonization properties independent from virulence properties. No significant difference was shown between strains during a systemic infection. These strains were then tested specifically for liver, spleen, and lung colonization. YadA and invasin inhibited liver colonization. Invasin also inhibited spleen colonization. YadA, however, increased the ability of Y. pseudotuberculosis to colonize the lungs. Invasin and YadA may be targets of the host immune response. This is supported by the observation of increased pathogenicity of Y. pestis, which lack YadA and invasin proteins.

====Evaluation of Ribotyping as a Tool for Molecular Typing of Yersinia pseudotuberculosis Strains of Worldwide Origin.==== (24) This study evaluated the power of ribotyping to delineate between different strains of Y. pseudotuberculosis. In ribotyping, DNA coding for rRNA is put through two restriction digests. There are EcoR1 sites at the 5’ end of each rRNA operon. The varition in fragment size indicates diversity. 80 strains of Y. pseudotuberculosis were evaluated by this method. This first digest produced 5 common patterns, which accounted for about %65 of the strains tested. The DNA from each of the strains was then digested by EcoRV. This produced a total of 17 profiles. Neither digest pattern correlated very well with the serotypes already assigned to the bacterial strains. High conservation of certain band sizes between strains gave information about fragment position. The ribotype combines information from both digests to find patterns between the strains. 27 ribotypes were identified. 21 of these ribotypes were associated with just one serotype. This classification system can help distinguish different ribotypes within a serotype. With the exception of Russia, which has a specific ribotype of Y. pseudotuberculosis found only there, there was no geographical link between ribotype and location of isolation of the strain.

References

1 http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi

2 Achtman, M., Zurth, K., Morelli, G., Torrea, G., Guiyoule, A. & Carniel, E. Yersinia pestis, the cause of plague, is a recently emerged clone of Yersinia pseudotuberculosis. Proc Natl Acad Sci U S A. 1999 Nov 23. Volume 96(24). p. 14043–14048.

3 P. S. G. Chain, E. Carniel, F. W. Larimer, J. Lamerdin, P. O. Stoutland, W. M. Regala, A. M. Georgescu, L. M. Vergez, M. L. Land, V. L. Motin, R. R. Brubaker, J. Fowler, J. Hinnebusch, M. Marceau, C. Medigue, M. Simonet, V. Chenal-Francisque, B. Souza, D. Dacheux, J. M. Elliott, A. Derbise, L. J. Hauser, and E. Garcia. “Insights into the evolution of Yersinia pestis through whole-genome comparison with Yersinia pseudotuberculosis. Proc Natl Acad Sci U S A. 2004 Sept 21. Volume 101(38). p. 13826-13831.

4 JA Bengoechea, K Brandenburg, U Seydel, R Diaz, and I Moriyon. Yersinia pseudotuberculosis and Yersinia pestis show increased outer membrane permeability to hydrophobic agents which correlates with lipopolysaccharide acyl-chain fluidity.” Microbiology. 1998 June. Volume 144(6). p. 1517-1526.

5 Matthew S. Francis, Scott A. Lloyd, Hans Wolf-Watz. “The type III secretion chaperone LcrH co-operates with YopD to establish a negative, regulatory loop for control of Yop synthesis in Yersinia pseudotuberculosis Molecular Microbiology. 2001 Nov. Volume 42(4). p. 1075–1093.

6 Guy R Cornelis, Hans Wolf-Watz. “The Yersinia Yop virulon: a bacterial system for subverting eukaryotic cells.” Molecular Microbiology. 1997 Mar. Volume 23(5). p. 861–867.

7 Lauren K. Logsdon and Joan Mecsas. “The Proinflammatory Response Induced by Wild-Type Yersinia pseudotuberculosis Infection Inhibits Survival of yop Mutants in the Gastrointestinal Tract and Peyer's Patches.” Infect Immun. 2006 Mar. Volume 74(3). p. 1516–1527.

8 Katri Jalava, S. Hallanvuo, U.-M. Nakari, P. Ruutu, E. Kela, T. Heinäsmäki, A. Siitonen, and J. P. Nuorti. “Multiple Outbreaks of Yersinia pseudotuberculosis Infections in Finland.” Journal of Clinical Microbiology. 2004 June. Volume 42(6). p. 2789-2791.

9 T Hannu, L Mattila, J Nuorti, P Ruutu, J Mikkola, A Siitonen, and M Leirisalo-Repo. “Reactive arthritis after an outbreak of Yersinia pseudotuberculosis serotype O:3 infection.” Ann Rheum Dis. 2003 Sept. Volume 62(9). p. 866–869.

10 Isaäcson M, Taylor P, Arntzen L. “Ecology of plague in Africa: response of indigenous wild rodents to experimental plague infection.” Bull World Health Organ. 1983. Volume 62(2). p. 339-44.

11 Gubler DJ, Reiter P, Ebi KL, Yap W, Nasci R, Patz JA. “Climate variability and change in the United States: potential impacts on vector- and rodent-borne diseases.” Environ Health Perspect. 2001 May. Volume 109 (Suppl 2). p. 223-33.

12 Atkinson S, Chang CY, Sockett RE, Cámara M, Williams P. “Quorum sensing in Yersinia enterocolitica controls swimming and swarming motility.” J Bacteriol. 2006 Feb. Volume 188(4). p. 1451-61.

13 Leary SE, Williamson ED, Griffin KF, Russell P, Eley SM, Titball RW. “Active immunization with recombinant V antigen from Yersinia pestis protects mice against plague.” Infect Immun. 1995 Aug. Volume 63(8). p. 2854-8.

14 Rebecca J. Eisen, Scott W. Bearden, Aryn P. Wilder, John A. Montenieri, Michael F. Antolin, and Kenneth L. Gage. “Early-phase transmission of Yersinia pestis by unblocked fleas as a mechanism explaining rapidly spreading plague epizootics.” Proc Natl Acad Sci U S A. 2006 October 17. Volume 103(42). p. 15380–15385.

15 Gregory A Petsko. “The usual suspects.” Genome Biol. 2003. Volume 4(10). p. 118.

16 Lewenza S, Vidal-Ingigliardi D, Pugsley AP. “Direct visualization of red fluorescent lipoproteins indicates conservation of the membrane sorting rules in the family Enterobacteriaceae.” J Bacteriol. 2006 May. Volume 188(10). p. 3516-24.

17 Chen TH, Elberg SS. “Scanning electron microscopic study of virulent Yersinia pestis and Yersinia pseudotuberculosis type 1.” Infect Immun. 1977 Mar. Volume 15(3). p. 972-7.

18 Collyn F, Léty MA, Nair S, Escuyer V, Ben Younes A, Simonet M, Marceau M. Yersinia pseudotuberculosis harbors a type IV pilus gene cluster that contributes to pathogenicity.” Infect Immun. 2002 Nov. Volume 70(11). p. 6196-205.

19 Moncla BJ, Hillier SL, Charnetzky WT. “Constitutive uptake and degradation of fatty acids by Yersinia pestis.” J Bacteriol. 1983 Jan. Volume 153(1). p. 340-4.

20 Hillier S, Charnetzky WT. “Glyoxylate bypass enzymes in Yersinia species and multiple forms of isocitrate lyase in Yersinia pestis.” J Bacteriol. 1981 Jan. Volume 145(1). p. 452-8.

21 Perry RD, Brubaker RR. “Accumulation of iron by yersiniae.” J Bacteriol. 1979 Mar. Volume 137(3). p. 1290-8.

22 Fisher ML, Castillo C, Mecsas J. “Intranasal inoculation of mice with Yersinia pseudotuberculosis causes a lethal lung infection that is dependent on Yersinia outer proteins and PhoP.” Infect Immun. 2007 Jan. Volume 75(1). p. 429-42.

23 Hudson KJ, Bouton AH. Yersinia pseudotuberculosis adhesins regulate tissue-specific colonization and immune cell localization in a mouse model of systemic infection.” Infect Immun. 2006 Nov. Volume 74(11). p. 6487-90

24 Voskressenskaya E, Leclercq A, Tseneva G, Carniel E. “Evaluation of ribotyping as a tool for molecular typing of Yersinia pseudotuberculosis strains of worldwide origin.” J Clin Microbiol. 2005 Dec. Volume 43(12). p. 6155-60.


Edited by Jennifer Jacobsen

Personal tools