Simkania negevensis: Difference between revisions
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==Classification== | ==Classification== | ||
Domain: Bacteria | Domain: Bacteria | ||
Kingdom: Bacteria | Kingdom: Bacteria | ||
Phylum: Chlamydiae | Phylum: Chlamydiae | ||
Class: Chlamydiae | Class: Chlamydiae | ||
Order: Chlamydiales | Order: Chlamydiales | ||
Family: Simkaniaceae | Family: Simkaniaceae | ||
Genus: Simkania | |||
Species: negevensis | Genus: ''Simkania'' | ||
Species: ''negevensis'' | |||
==Discovery== | ==Discovery== | ||
S. negevensis was first discovered in 1993 as a contaminant of human and simian cell cultures of unknown origin in an Israeli laboratory by Kahane and colleagues, who originally characterized it as a chlamydia-like microorganism called ‘Z’ (1). | ''S. negevensis'' was first discovered in 1993 as a contaminant of human and simian cell cultures of unknown origin in an Israeli laboratory by Kahane and colleagues, who originally characterized it as a chlamydia-like microorganism called ‘Z’ (1). | ||
==Characteristics & Growth== | ==Characteristics & Growth== | ||
Simkania negevensis is an obligate intracellular gram-negative bacterium that has been implicated in various respiratory diseases. Its growth cycle includes two distinct phases, the elementary and reticulate bodies, which are typical of | ''Simkania negevensis'' is an obligate intracellular gram-negative bacterium that has been implicated in various respiratory diseases. Its growth cycle includes two distinct phases, the elementary and reticulate bodies, which are typical of the Chlamydiales. The main function of reticulate bodies (RBs) is to replicate through binary fission and are usually not infectious. Unlike ''C. trachomatis'', the RBs of ''S. negevensis'' may also be infectious. The elementary bodies (EBs) do not replicate and are specialized for transmitting infection to other cells upon host cell lysis, so their electron-dense forms appear later during infection, after about 3 days (2). Mature EBs of ''S. negevensis'' are distinguishable from other Chlamydiales by their quadrangular or dumbbell shapes (2,3). | ||
After infection, S. negevensis undergoes rapid growth for 2-3 days, during which time reticulate bodies become abundant, and then enters a stationary phase for about 8 days . This cycle is much longer than most Chlamydiales, which typically lyse their host cells 2 to 3 days after infection. | After infection, ''S. negevensis'' undergoes rapid growth for 2-3 days, during which time reticulate bodies become abundant, and then enters a stationary phase for about 8 days (2). This cycle is much longer than most Chlamydiales, which typically lyse their host cells 2 to 3 days after infection. | ||
The intracellular lifestyle of S. negevensis is supported by four nucleotide transport proteins that allow it to exploit the host cell’s energy and nucleotide pools by importing ATP, GDP, GTP, and RNA nucleotides. Since S. negevensis seems unable to make its own nucleotides from scratch, these proteins are vital to the biosynthesis of RNA and DNA. | The intracellular lifestyle of ''S. negevensis'' is supported by four nucleotide transport proteins that allow it to exploit the host cell’s energy and nucleotide pools by importing ATP, GDP, GTP, and RNA nucleotides (4). Since ''S. negevensis'' seems unable to make its own nucleotides from scratch, these proteins are vital to the biosynthesis of RNA and DNA. | ||
==Genome== | ==Genome== | ||
The full-length 16S and 23S rRNA sequences are 80-87% identical with Chlamydiaceae, and the genome length is 1.7 Mbp, which is 2-3 times larger than the genome of Chlamydiaceae ( | The full-length 16S and 23S rRNA sequences are 80-87% identical with Chlamydiaceae, and the genome length is 1.7 Mbp, which is 2-3 times larger than the genome of Chlamydiaceae (5). The G + C content of ''S. negevensis'' and other Chlamydiae is about 40% despite the smaller genome size of Chlamydia (5,6). ''Simkania'' contains a 132-kb conjugative plasmid that is ten times larger than that found in Chlamydiaceae and encodes for proteins involved in metabolic processes, the maintenance and propagation of the plasmid, and virulence (6). | ||
==Pathogenicity== | ==Pathogenicity== | ||
Infants with bronchiolitis and adults with community-acquired pneumonia (CAP) or chronic obstructive pulmonary disease (COPD) have been linked to infection with S. negevensis ( | Infants with bronchiolitis and adults with community-acquired pneumonia (CAP) or chronic obstructive pulmonary disease (COPD) have been linked to infection with ''S. negevensis'' (7,8). Evidence of ''S. negevensis'' infection has been supported with culture, serological tests, and PCR. Despite a lack of reports concerning widespread infection in humans, a high seroprevalence (46-80%) of ''S. negevensis'' antibodies has been identified in healthy adults from all over the world (8). This may be due to the bacteria’s ability to survive and replicate within amoeba, thus supporting a broad distribution of ''S. negevensis'', particularly through aquatic environments (3). | ||
Similar to Chlamydia-infected cells, S. negevensis-infected cells display anti-apoptotic mechanisms to ensure host cell survival, allowing the bacteria to continue replication. The apoptotic resistance of cells infected with S. negevensis reaches a peak during the rapid growth phase (2-3 days), and the cells become slightly more susceptible to apoptosis after this phase ( | Similar to Chlamydia-infected cells, ''S. negevensis''-infected cells display anti-apoptotic mechanisms to ensure host cell survival, allowing the bacteria to continue replication. The apoptotic resistance of cells infected with ''S. negevensis'' reaches a peak during the rapid growth phase (2-3 days), and the cells become slightly more susceptible to apoptosis after this phase (6). | ||
Patients with CAP made quick recoveries after treatment with erythromycin ( | Patients with CAP made quick recoveries after treatment with erythromycin (8). ''S. negevensis'' is sensitive to tetracyclines and macrolides, but its growth is unaffected by sulfadiazine (1,5,9). ''S. negevensis'' is distinguished from Chlamydiaceae by its resistance to ampicillin, penicillin G, and cyclosporine (1). | ||
Because ''S. negevensis'' is able to thrive in both amoeba and human host cells and contains a conjugative plasmid, it has considerable potential as a model organism (3,6). | |||
==References== | ==References== | ||
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3. Michel R, Muller K-D, Zoller L, Walochnik J, Hartmann M, Schmid E-N. Free-living Amoebae Serve as a Host for the Chlamydia-like Bacterium Simkania negevensis. Acta Protozool. 2005;44:113–21. | 3. Michel R, Muller K-D, Zoller L, Walochnik J, Hartmann M, Schmid E-N. Free-living Amoebae Serve as a Host for the Chlamydia-like Bacterium Simkania negevensis. Acta Protozool. 2005;44:113–21. | ||
4. Kahane S, Everett KDE, Kimmel N, Friedman MG. Simkania negevensis strain ZT: growth, antigenic and genome characteristics. Int J Syst Bacteriol. 1999 Apr 1;49(2):815–20. | 4. Knab S, Mushak TM, Schmitz-Esser S, Horn M, Haferkamp I. Nucleotide parasitism by Simkania negevensis (Chlamydiae). J Bacteriol. 2011 Jan;193(1):225–35. | ||
5. Kahane S, Everett KDE, Kimmel N, Friedman MG. Simkania negevensis strain ZT: growth, antigenic and genome characteristics. Int J Syst Bacteriol. 1999 Apr 1;49(2):815–20. | |||
6. Collingro A, Tischler P, Weinmaier T, Penz T, Heinz E, Brunham RC, et al. Unity in variety--the pan-genome of the Chlamydiae. Mol Biol Evol. 2011 Dec;28(12):3253–70. | |||
7. Karunakaran K, Mehlitz A, Rudel T. Evolutionary conservation of infection-induced cell death inhibition among Chlamydiales. PloS One. 2011;6(7):e22528. | |||
8. Lieberman D, Kahane S, Lieberman D, Friedman MG. Pneumonia with serological evidence of acute infection with the Chlamydia-like microorganism “Z.”Am J Respir Crit Care Med. 1997 Aug;156(2 Pt 1):578–82. | |||
9. Donati M, Di Paolo M, Avanzi S, Di Francesco A, Fiani N, Favaroni A, et al. Detection of Simkania negevensis in cell culture by using a monoclonal antibody. New Microbiol. 2013 Jan;36(1):85–8. |
Revision as of 05:13, 12 December 2013
Classification
Domain: Bacteria
Kingdom: Bacteria
Phylum: Chlamydiae
Class: Chlamydiae
Order: Chlamydiales
Family: Simkaniaceae
Genus: Simkania
Species: negevensis
Discovery
S. negevensis was first discovered in 1993 as a contaminant of human and simian cell cultures of unknown origin in an Israeli laboratory by Kahane and colleagues, who originally characterized it as a chlamydia-like microorganism called ‘Z’ (1).
Characteristics & Growth
Simkania negevensis is an obligate intracellular gram-negative bacterium that has been implicated in various respiratory diseases. Its growth cycle includes two distinct phases, the elementary and reticulate bodies, which are typical of the Chlamydiales. The main function of reticulate bodies (RBs) is to replicate through binary fission and are usually not infectious. Unlike C. trachomatis, the RBs of S. negevensis may also be infectious. The elementary bodies (EBs) do not replicate and are specialized for transmitting infection to other cells upon host cell lysis, so their electron-dense forms appear later during infection, after about 3 days (2). Mature EBs of S. negevensis are distinguishable from other Chlamydiales by their quadrangular or dumbbell shapes (2,3). After infection, S. negevensis undergoes rapid growth for 2-3 days, during which time reticulate bodies become abundant, and then enters a stationary phase for about 8 days (2). This cycle is much longer than most Chlamydiales, which typically lyse their host cells 2 to 3 days after infection.
The intracellular lifestyle of S. negevensis is supported by four nucleotide transport proteins that allow it to exploit the host cell’s energy and nucleotide pools by importing ATP, GDP, GTP, and RNA nucleotides (4). Since S. negevensis seems unable to make its own nucleotides from scratch, these proteins are vital to the biosynthesis of RNA and DNA.
Genome
The full-length 16S and 23S rRNA sequences are 80-87% identical with Chlamydiaceae, and the genome length is 1.7 Mbp, which is 2-3 times larger than the genome of Chlamydiaceae (5). The G + C content of S. negevensis and other Chlamydiae is about 40% despite the smaller genome size of Chlamydia (5,6). Simkania contains a 132-kb conjugative plasmid that is ten times larger than that found in Chlamydiaceae and encodes for proteins involved in metabolic processes, the maintenance and propagation of the plasmid, and virulence (6).
Pathogenicity
Infants with bronchiolitis and adults with community-acquired pneumonia (CAP) or chronic obstructive pulmonary disease (COPD) have been linked to infection with S. negevensis (7,8). Evidence of S. negevensis infection has been supported with culture, serological tests, and PCR. Despite a lack of reports concerning widespread infection in humans, a high seroprevalence (46-80%) of S. negevensis antibodies has been identified in healthy adults from all over the world (8). This may be due to the bacteria’s ability to survive and replicate within amoeba, thus supporting a broad distribution of S. negevensis, particularly through aquatic environments (3).
Similar to Chlamydia-infected cells, S. negevensis-infected cells display anti-apoptotic mechanisms to ensure host cell survival, allowing the bacteria to continue replication. The apoptotic resistance of cells infected with S. negevensis reaches a peak during the rapid growth phase (2-3 days), and the cells become slightly more susceptible to apoptosis after this phase (6).
Patients with CAP made quick recoveries after treatment with erythromycin (8). S. negevensis is sensitive to tetracyclines and macrolides, but its growth is unaffected by sulfadiazine (1,5,9). S. negevensis is distinguished from Chlamydiaceae by its resistance to ampicillin, penicillin G, and cyclosporine (1).
Because S. negevensis is able to thrive in both amoeba and human host cells and contains a conjugative plasmid, it has considerable potential as a model organism (3,6).
References
1. Kahane S, Gonen R, Sayada C, Elion J, Friedman MG. Description and partial characterization of a new chlamydia-like microorganism. FEMS Microbiol Lett. 1993;109(2):329–33.
2. Kahane S, Kimmel N, Friedman MG. The growth cycle of Simkania negevensis. Microbiol Read Engl. 2002 Mar;148(Pt 3):735–42.
3. Michel R, Muller K-D, Zoller L, Walochnik J, Hartmann M, Schmid E-N. Free-living Amoebae Serve as a Host for the Chlamydia-like Bacterium Simkania negevensis. Acta Protozool. 2005;44:113–21.
4. Knab S, Mushak TM, Schmitz-Esser S, Horn M, Haferkamp I. Nucleotide parasitism by Simkania negevensis (Chlamydiae). J Bacteriol. 2011 Jan;193(1):225–35.
5. Kahane S, Everett KDE, Kimmel N, Friedman MG. Simkania negevensis strain ZT: growth, antigenic and genome characteristics. Int J Syst Bacteriol. 1999 Apr 1;49(2):815–20.
6. Collingro A, Tischler P, Weinmaier T, Penz T, Heinz E, Brunham RC, et al. Unity in variety--the pan-genome of the Chlamydiae. Mol Biol Evol. 2011 Dec;28(12):3253–70.
7. Karunakaran K, Mehlitz A, Rudel T. Evolutionary conservation of infection-induced cell death inhibition among Chlamydiales. PloS One. 2011;6(7):e22528.
8. Lieberman D, Kahane S, Lieberman D, Friedman MG. Pneumonia with serological evidence of acute infection with the Chlamydia-like microorganism “Z.”Am J Respir Crit Care Med. 1997 Aug;156(2 Pt 1):578–82.
9. Donati M, Di Paolo M, Avanzi S, Di Francesco A, Fiani N, Favaroni A, et al. Detection of Simkania negevensis in cell culture by using a monoclonal antibody. New Microbiol. 2013 Jan;36(1):85–8.