Difference between revisions of "Rickettsia conorii"

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"Rickettsiae" just like other bacteria enter into non-phagocytic host cells and adhere to it's vacuole(Hackstadt, 1996). Within the cytoplasm, "rickettsiae" begin to divide and able to polymerize host actin filaments to drive themselves to be linked intra- and intercellularly (Gouin et al., 2004; Gouin et al., 1999; Heinzen et al., 1993; Teysseire et al., 1992).  
 
"Rickettsiae" just like other bacteria enter into non-phagocytic host cells and adhere to it's vacuole(Hackstadt, 1996). Within the cytoplasm, "rickettsiae" begin to divide and able to polymerize host actin filaments to drive themselves to be linked intra- and intercellularly (Gouin et al., 2004; Gouin et al., 1999; Heinzen et al., 1993; Teysseire et al., 1992).  
  
To internalize rickettsiae is associated with a phospholipase A2 activity and host actin polymerization (Silverman et al., 1992; Walker et al., 2001; Walker, 1984). R. conorii invades non-phagocytic cells. Some proteins are able to control actin dynamics during R. conorii invasion reveals that the Arp2/3 complex is recruited to the entry site.  R. conorii uses pathways involving Cdc42, PI 3-kinase, c-Src and other PTK activities to enter non-phagocytic cells and that signals from these pathways may be coordinated to activate the Arp2/3 complex.  Various signaling pathways by activating one signal to either supress or futher activate the Arp2/3 complex . Internalization of R. conorii most likely involves R. conorii surface protein(s) with an unidentified host cell receptor(s) [[Image:JCS01382F8.gif|frame|none|
+
To internalize rickettsiae is associated with a phospholipase A2 activity and host actin polymerization (Silverman et al., 1992; Walker et al., 2001; Walker, 1984). R. conorii invades non-phagocytic cells. Some proteins are able to control actin dynamics during R. conorii invasion reveals that the Arp2/3 complex is recruited to the entry site.  R. conorii uses pathways involving Cdc42, PI 3-kinase, c-Src and other PTK activities to enter non-phagocytic cells and that signals from these pathways may be coordinated to activate the Arp2/3 complex.  Various signaling pathways by activating one signal to either supress or futher activate the Arp2/3 complex . Internalization of R. conorii most likely involves R. conorii surface protein(s) with an unidentified host cell receptor(s) [[Image:JCS01382F8.gif|frame|none]]
  
 
This picture shows the interactions involved in the uptake of Rickettsia conorii in non-phagocytic mammalian cells.
 
This picture shows the interactions involved in the uptake of Rickettsia conorii in non-phagocytic mammalian cells.

Revision as of 18:07, 2 June 2007

A Microbial Biorealm page on the genus Rickettsia conorii

Preincubation of Vero cells with cytochalasin D diminished the ability of R. conorii to invade. Bar, 2 µm.


Classification

Higher order taxa:

Bacteria ; Proteobacteria ; Alphaproteobacteria ; Rickettsiales ; Rickettsiaceae ; Rickettsieae ; Rickettsia ; spotted fever group ; Rickettsia conorii

Gene Classification based on COG functional categories

Species:

Orientia tsutsugamushi;
spotted fever group: Candidatus R. principis; Israeli tick typhus rickettsia; R. aeschimannii; R. africae; R. akari; R. amblyommii; R. andeana; R. australis; R. conorii; R. cooleyi; R. felis; R. heilongjiangensis; R. heilongjiangii; R. helvtica; R. honei; R. hulinensis; R. hulinii; R. japonica; R. martinet; R. massiliae; R. monacensis; R. montanensis; R. moreli; R. parkeri; R. peacockii; R. rhipicephali; R. rickettsii; R. sibirica subgroup; R. slovaca; R. sp.
Typhus group: R. canadensis; R. prowazekii; R. typhi
Unclassified
Rickettsia: Candidatus R. tarasevichiae; R. bellii; R. publicis; R. sp.

NCBI: Taxonomy Genome: -R. conorii str. Malish 7 -R. prowazekii str. Madrid E

Description and Significance

Rickettsia bacteria are a pathogen transmitted to humans by Rhipicephalus ticks.[1] Rickettsia conorii are known as a cause of "Mediterranean spotted fever, Astrakhan fever, Israeli spotted fever, and Indian tick typhus in the Mediterranean basin and Africa, Southern Russia, Middle East, and India, respectively."[1] Israeli spotted fever and Mediterranean spotted fever overlap among clinical features and are characterized by a rash. The differences lies at an inoculation eschar,Indochina scrub typhus, is rarely in Astrakhan fever and Israeli spotted fever but common in Mediterranean spotted fever and is contracted by contact with infected brown dog ticks.

Genome Structure

The genome of Rickettsia conorii is 1,268,755 base pairs in length and contains 1374 protein-coding genes.(2) In anaerobic glycolysis, there are no genes in the biosynthesis and regulation of amino acids and no genes in the nucleosides of free-living bacteria. Rickettsia are intracellular small gram-negative proteobacteria in a subdivision associated with different arthropod hosts. The genomes and the mitochondria of Rickettsia are small, highly derived, "products of several types of reductive evolution" (Andersson et al. 1998). The R. conorii genome sequence relates closely with its relative Rickettsia prowazekii shows a new type of "coding" mobile element (Rickettsia-specific palindromic element, RPE)mostly found inserted in frame within open reading frames (ORFs). All bacterial palindromic repeats appeared exclusively in noncoding regions. There are 656 interspersed repeated sequences in 10 distinct families. Among the 10 families, three palindromic sequence families showed clear cases of insertions into open reading frames (ORFs). The in-frame insertion located to be compatible with three dimentional encoded protein.

Cell Structure and Metabolism

"Rickettsiae" just like other bacteria enter into non-phagocytic host cells and adhere to it's vacuole(Hackstadt, 1996). Within the cytoplasm, "rickettsiae" begin to divide and able to polymerize host actin filaments to drive themselves to be linked intra- and intercellularly (Gouin et al., 2004; Gouin et al., 1999; Heinzen et al., 1993; Teysseire et al., 1992).

To internalize rickettsiae is associated with a phospholipase A2 activity and host actin polymerization (Silverman et al., 1992; Walker et al., 2001; Walker, 1984). R. conorii invades non-phagocytic cells. Some proteins are able to control actin dynamics during R. conorii invasion reveals that the Arp2/3 complex is recruited to the entry site. R. conorii uses pathways involving Cdc42, PI 3-kinase, c-Src and other PTK activities to enter non-phagocytic cells and that signals from these pathways may be coordinated to activate the Arp2/3 complex. Various signaling pathways by activating one signal to either supress or futher activate the Arp2/3 complex . Internalization of R. conorii most likely involves R. conorii surface protein(s) with an unidentified host cell receptor(s)

JCS01382F8.gif

This picture shows the interactions involved in the uptake of Rickettsia conorii in non-phagocytic mammalian cells.

Ecology

Subsequent proliferation of SFG rickettsiae at the site of inoculation, typically in endothelial cells, results in the characteristic dermal and epidermal necrosis known as `eschar' or `tache noire' (Walker et al., 1988). Injury to the vascular endothelium leads to an increase in vascular permeability and leakage of fluid into the interstitial space, resulting in the characteristic dermal rash (Hand et al., 1970; Walker et al., 1988). Bacteria can then spread via lymphatic vessels to the lymph nodes and via the bloodstream to various other tissues including the lungs, spleen, liver, kidneys and heart (Walker and Gear, 1985).

Based upon the antigenicity of their lipopolysaccharide (LPS) and the differences in the diseases that they cause, members are divided into two groups, the spotted fever group (SFG) and the typhus group (TG) (Vishwanath, 1991). Both groups have been classified by the National Institute of Allergy and Infectious Diseases (NIAID) as `select agents' for bioterrorism (http://www2.niaid.nih.gov/biodefense/bandc_priority.htm).

Pathology

Below are tables of different groups of Ricketsia along with the diseases that each species cause and their general geological distribution. From The University of South Carolina.

Spotted Fever Group

Organism Disease Distribution
R. rickettsii Rocky Mountain spotted fever Western hemisphere
R. akari Rickettsialpox USA, former Soviet Union
R. conorii Boutonneuse fever Mediterranean countries, Africa, India, Southwest Asia
R. sibirica Siberian tick typhus Siberia, Mongolia, nothern China
R. australis Australian tick typhus Australia
R. japonica Oriental spotted fever Japan

Typhus Group

Organism Disease Distribution
R. prowazekii

Epidemic typhus
Recrudescent typhus
Sporadic typhus

South America and Africa
Worldwide
United States
R. typhi Murine typhus Worldwide

Scrub typhus group

Organism Disease Distribution
R. tsutsugamushi Scrub typhus Asia, northern Australia, Pacific Islands

References

General:

Cell Structure and Metabolism

  • Juan J. Martinez and Pascale Cossart. 2004. "Early signaling events involved in the entry of Rickettsia conorii into mammalian cells."Journal of Cell Science 117, 5097-5106
  • Silverman, D. J., Santucci, L. A., Meyers, N. and Sekeyova, Z. (1992). Penetration of host cells by Rickettsia rickettsii appears to be mediated by a phospholipase of rickettsial origin. Infect. Immun. 60, 2733-2740.[Abstract/Free Full Text]
  • Hackstadt, T. (1996). The biology of rickettsiae. Infect. Agents Dis. 5, 127-143.[Medline]
  • Gouin, E., Egile, C., Dehoux, P., Villiers, V., Adams, J., Gertler, F., Li, R. and Cossart, P. (2004). The RickA protein of Rickettsia conorii activates the Arp2/3 complex. Nature 427, 457-461.[CrossRef][Medline]

Edited by Cindy Zhang,student of Rachel Larsen and Kit Pogliano