Rickettsia conorii: Difference between revisions

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[[Image:JCS01382F1.jpg|frame|none|Preincubation of Vero cells with cytochalasin D diminished the ability of R. conorii to invade. Bar, 2 µm.]]




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==Description and Significance==
==Description and Significance==


''Rickettsia'' bacteria are well known pathogens. ''Rickettsia conorii'' have been described as the causative agents 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. These rickettsioses are transmitted to humans by Rhipicephalus ticks [1]. Furthermore, most of their clinical features overlap and are characterized by a febrile illness and a generalized maculopapular rash. However, an inoculation eschar is seldom present in Astrakhan fever and Israeli spotted fever but common in Mediterranean spotted fever and is contracted by contact with infected brown dog ticks.
''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.
 


==Genome Structure==
==Genome Structure==
The genome of ''Rickettsia conorii'' is 1,268,755 base pairs in length and contains 1374 protein-coding genes.There are no genes for anaerobic glycolysis and also the biosynthesis and regulation of amino acids and nucleosides in free-living bacteria.''Rickettsia'' are obligate intracellular small gram-negative proteobacteria of the -subdivision associated with different arthropod hosts.  The genomes of ''Rickettsia'' as well as the mitochondria are small, highly derived, "products of several types of reductive evolution" (Andersson et al. 1998).
The genome of ''Rickettsia conorii'' is 1,268,755 base pairs in length and contains 1374 protein-coding genes.(2)  ''Rickettsia'' are intracellular small gram-negative proteobacteria in a subdivision associated with different arthropod hosts.  The genomes of ''Rickettsia'' are small, highly derived, "products of several types of reductive evolution" (Andersson et al. 1998).
The comparison of the ''R. conorii'' genome sequence with its close relative ''Rickettsia prowazekii'' revealed a new type of "coding" mobile element (Rickettsia-specific palindromic element, RPE) frequently found inserted in frame within open reading frames (ORFs), whereas all previously described bacterial palindromic repeats appeared exclusively located within noncoding regions.  We identified 656 interspersed repeated sequences classified into 10 distinct families. Of the 10 families, three palindromic sequence families showed clear cases of insertions into open reading frames (ORFs). The location of those in-frame insertions appears to be always compatible with the encoded protein three-dimensional (3-D) fold and function.
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).  


==Cell Structure and Metabolism==
==Cell Structure and Metabolism==
Subsequent to adherence, rickettsiae, like some other pathogenic bacteria, enter into non-phagocytic host cells and then quickly lyse the phagocytic vacuole (Hackstadt, 1996). Within the cytoplasm, rickettsiae begin to divide and in some cases are able to polymerize host actin filaments to propel themselves intra- and intercellularly (Gouin et al., 2004; Gouin et al., 1999; Heinzen et al., 1993; Teysseire et al., 1992).  
''Rickettsiae'' enter into non-phagocytic host cells and adhere to it's vacuole(Hackstadt, 1996). Within the cytoplasm, ''rickettsiae'' begin to divide and are 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).  
 
Internalized 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 revealing 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 signal from these pathways may be coordinated to activate the Arp2/3 complex.  Various signaling pathways by activating one signal are able to either suppress or further activate the Arp2/3 complex . Internalization of ''R. conorii'' most likely involves R. conorii surface protein(s) with an unidentified host cell receptor(s)


Interactions of TG and SFG rickettsiae with various cultured cells show that internalization is associated with a phospholipase A2 activity and host actin polymerization (Silverman et al., 1992; Walker et al., 2001; Walker, 1984). However, little more is known about the interactions between SFG rickettsiae and cultured cells, in particular the mechanism(s) by which R. conorii invades non-phagocytic cells. An initial investigation of proteins that could control actin dynamics during R. conorii invasion revealed that the Arp2/3 complex is recruited to the entry site. We then utilized various approaches to disrupt signaling pathways that have been previously demonstrated to activate the Arp2/3 complex directly or indirectly. We found that 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 ultimately activate the Arp2/3 complex.
[[Image:JCS01382F8.gif|frame|none|Model of putative interactions involved in the uptake of Rickettsia conorii in non-phagocytic mammalian cells.Various signaling pathways can activate the Arp2/3 complex independently or in synergy. Internalization of R. conorii most likely involves the interaction of R. conorii surface protein(s) with an unidentified host cell receptor(s) (black rectangle with question mark), which serves to activate multiple pathways involving Cdc42, PI 3-kinase, Src, FAK and cortactin, ultimately leading to Arp2/3-dependent actin cytoskeletal changes that drive bacterial entry (see Discussion). Putative associations of proteins during bacterial entry are indicated by question marks and dotted arrows.]]
==Ecology==
==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).
''R. conorii'' is a boutonneus fever disease and it is spread in Mediterranean countries.  It is divided into two groups, the spotted fever group and the typhus group(Vishwanath, 1991). It's mostly carried by ticks or fleas on animals.  These diseases are distributed in a lot of different areas around the world.  If it is infected with this disease, it will result with a dermal rash (Hand et al., 1970; Walker et al., 1988). Bacteria can spread via lymphatic vessels to the lymph nodes and by bloodstream to other tissues like the lungs, spleen, liver, etc. (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==
==Pathology==
''R. conorii'' can cause boutonneuse fever.  It came from an African origin. Eliza tests to examine specimens, the results show in the early stage of a high percentage of the symptoms and it lasted a  long time after the acute attack.
Spotted fever group of ''rickettsiae'' are maintained in nature through transovarial transmission.  In the tick, it is very critical that the ovaries transmit rickettsiae from one generation to the next. Ticks can usually maintain several species of rickettsiae, but only a single species is tranferred transovarily.  Phages are found over 100 in bacterial genera and also rickettsiae. 
Below are tables of different groups of ''Ricketsia'' along with the diseases that each species cause and their general geological distribution. From [http://www.med.sc.edu:85/mayer/ricketsia.htm The University of South Carolina.]
Below are tables of different groups of ''Ricketsia'' along with the diseases that each species cause and their general geological distribution. From [http://www.med.sc.edu:85/mayer/ricketsia.htm The University of South Carolina.]


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| width="339" | Asia, northern Australia, Pacific Islands
| width="339" | Asia, northern Australia, Pacific Islands
|}
|}
==Application to Biotechnology==
''Rickettsia conorii'' revealed under microsope some pathologic features and presence of rickettsiae in the endothelium of infected tissues.  Some key antioxidant enzymes involved 
"namely glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase, and superoxide dismutase, at these times exhibited a pattern of differential and selective modulation in brain, lungs, and testes of mice infected with viable organisms, whereas heat-inactivated or sonically disrupted rickettsiae had no effect" [4 under current research in reference]. The involvement of these enzymes of glutathione redox and superoxide scavenging systems in the antioxidant response depends on the viable rickettsiae in different organs of the host.
==Current Research==
1)A case of acute quadriplegia complicating Mediterranean spotted fever
''Rickettsia conorii'' caused mediterranean spotted fever and this was considered to be a benign disease. However, about 10% of the patients with severe symptom are neurologic involved.  A case of a 80 year old man was studied with ''R. conorii'' infection.  A characterisitic of tache noire was diagnosed on the lateral region of the thigh.  After running a immunofluorescence test, elevated IgM antibody was detected against ''R conorii'' and it was talked about it in this research paper.
2)Serological and molecular evidence of exposure to arthropod-borne organisms in cats from northeastern Spain
This research paper talks about tests from cats for IgG antibodies to "Rickettsia conorii (Rc), Ehrlichia canis (Ec), Anaplasma phagocytophilum (Ap) and Bartonella henselae (Bh) antigens using IFA and for FeLV antigen and FIV antibody by ELISA"[2 under current research column of reference]. PCR testing was performed and Bh antibodies were detected with seroreactivity to both Ec and Rc antigens and FIV antibodies were involve with illness and cats older than 2 years.
3)Characterisation of rickettsial diseases in a hospital-based population in Malta
The aim of the paper was to find out the causative agents of rickettsial disease in Malta and epidemiology of cases related to the disease. Thirty-three cases were studied.  One patient was diagnosed of ''Rickettsia conorii'' but none of the sera showed any activity with ''Rickettsia typhi''. Spotted fever rickettsiosis is endemic in Malta. None of the cases were due to murine typhus. The  causative agent of rickettsial disease in Malta should be ''R. conorii''.


==References==
==References==
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* Hackstadt, T. (1996). The biology of rickettsiae. Infect. Agents Dis. 5, 127-143.[Medline]  
* 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]
* 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]
===current research===
*Santo Caroleo, Chiara Longo, Domenico Pirritano, Rita Nisticò, Paola Valentino, Maurizio Iocco, Ermenegildo Santangelo and Bruno Amantea. 2007. A case of acute quadriplegia complicating Mediterranean spotted fever. Clinical Neurology and Neurosurgery.
*Laia Solano-Gallego, Barbara Hegarty, Yvonne Espada, Joan Llull and Edward Breitschwerdt. 2006.
Serological and molecular evidence of exposure to arthropod-borne organisms in cats from northeastern Spain. Veterinary Microbiology.
*I. Tonna, C. Mallia Azzopardi, T. Piscopo, P. Cuschieri, F. Fenollar and D. Raoult. 2006. Characterisation of rickettsial diseases in a hospital-based population in Malta. Journal of Infection.
*Elena Rydkinaa, Sanjeev K. Sahni, , a, Lisa A. Santuccib, Loel C. Turpina, Raymond B. Baggsc and David J. Silvermanb. 2003. Selective modulation of antioxidant enzyme activities in host tissues during Rickettsia conorii infection. University of Maryland School of Medicine.
Edited by Cindy Zhang,student of [mailto:ralarsen@ucsd.edu Rachel Larsen] and Kit Pogliano
Edited by Cindy Zhang,student of [mailto:ralarsen@ucsd.edu Rachel Larsen] and Kit Pogliano
KMG

Latest revision as of 18:44, 22 April 2011

This is a curated page. Report corrections to Microbewiki.

A Microbial Biorealm page on the genus Rickettsia conorii


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.

Genome Structure

The genome of Rickettsia conorii is 1,268,755 base pairs in length and contains 1374 protein-coding genes.(2) Rickettsia are intracellular small gram-negative proteobacteria in a subdivision associated with different arthropod hosts. The genomes 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).

Cell Structure and Metabolism

Rickettsiae enter into non-phagocytic host cells and adhere to it's vacuole(Hackstadt, 1996). Within the cytoplasm, rickettsiae begin to divide and are 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).

Internalized 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 revealing 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 signal from these pathways may be coordinated to activate the Arp2/3 complex. Various signaling pathways by activating one signal are able to either suppress or further activate the Arp2/3 complex . Internalization of R. conorii most likely involves R. conorii surface protein(s) with an unidentified host cell receptor(s)

Ecology

R. conorii is a boutonneus fever disease and it is spread in Mediterranean countries. It is divided into two groups, the spotted fever group and the typhus group(Vishwanath, 1991). It's mostly carried by ticks or fleas on animals. These diseases are distributed in a lot of different areas around the world. If it is infected with this disease, it will result with a dermal rash (Hand et al., 1970; Walker et al., 1988). Bacteria can spread via lymphatic vessels to the lymph nodes and by bloodstream to other tissues like the lungs, spleen, liver, etc. (Walker and Gear, 1985).

Pathology

R. conorii can cause boutonneuse fever. It came from an African origin. Eliza tests to examine specimens, the results show in the early stage of a high percentage of the symptoms and it lasted a long time after the acute attack. Spotted fever group of rickettsiae are maintained in nature through transovarial transmission. In the tick, it is very critical that the ovaries transmit rickettsiae from one generation to the next. Ticks can usually maintain several species of rickettsiae, but only a single species is tranferred transovarily. Phages are found over 100 in bacterial genera and also rickettsiae.

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


Application to Biotechnology

Rickettsia conorii revealed under microsope some pathologic features and presence of rickettsiae in the endothelium of infected tissues. Some key antioxidant enzymes involved "namely glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase, and superoxide dismutase, at these times exhibited a pattern of differential and selective modulation in brain, lungs, and testes of mice infected with viable organisms, whereas heat-inactivated or sonically disrupted rickettsiae had no effect" [4 under current research in reference]. The involvement of these enzymes of glutathione redox and superoxide scavenging systems in the antioxidant response depends on the viable rickettsiae in different organs of the host.

Current Research

1)A case of acute quadriplegia complicating Mediterranean spotted fever

Rickettsia conorii caused mediterranean spotted fever and this was considered to be a benign disease. However, about 10% of the patients with severe symptom are neurologic involved. A case of a 80 year old man was studied with R. conorii infection. A characterisitic of tache noire was diagnosed on the lateral region of the thigh. After running a immunofluorescence test, elevated IgM antibody was detected against R conorii and it was talked about it in this research paper.

2)Serological and molecular evidence of exposure to arthropod-borne organisms in cats from northeastern Spain

This research paper talks about tests from cats for IgG antibodies to "Rickettsia conorii (Rc), Ehrlichia canis (Ec), Anaplasma phagocytophilum (Ap) and Bartonella henselae (Bh) antigens using IFA and for FeLV antigen and FIV antibody by ELISA"[2 under current research column of reference]. PCR testing was performed and Bh antibodies were detected with seroreactivity to both Ec and Rc antigens and FIV antibodies were involve with illness and cats older than 2 years.

3)Characterisation of rickettsial diseases in a hospital-based population in Malta

The aim of the paper was to find out the causative agents of rickettsial disease in Malta and epidemiology of cases related to the disease. Thirty-three cases were studied. One patient was diagnosed of Rickettsia conorii but none of the sera showed any activity with Rickettsia typhi. Spotted fever rickettsiosis is endemic in Malta. None of the cases were due to murine typhus. The causative agent of rickettsial disease in Malta should be R. conorii.

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]

current research

  • Santo Caroleo, Chiara Longo, Domenico Pirritano, Rita Nisticò, Paola Valentino, Maurizio Iocco, Ermenegildo Santangelo and Bruno Amantea. 2007. A case of acute quadriplegia complicating Mediterranean spotted fever. Clinical Neurology and Neurosurgery.
  • Laia Solano-Gallego, Barbara Hegarty, Yvonne Espada, Joan Llull and Edward Breitschwerdt. 2006.

Serological and molecular evidence of exposure to arthropod-borne organisms in cats from northeastern Spain. Veterinary Microbiology.

  • I. Tonna, C. Mallia Azzopardi, T. Piscopo, P. Cuschieri, F. Fenollar and D. Raoult. 2006. Characterisation of rickettsial diseases in a hospital-based population in Malta. Journal of Infection.
  • Elena Rydkinaa, Sanjeev K. Sahni, , a, Lisa A. Santuccib, Loel C. Turpina, Raymond B. Baggsc and David J. Silvermanb. 2003. Selective modulation of antioxidant enzyme activities in host tissues during Rickettsia conorii infection. University of Maryland School of Medicine.



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

KMG

Retrieved from "https://microbewiki.kenyon.edu/index.php?title=Rickettsia_conorii&oldid=61366"