C. trachomatis: Difference between revisions

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==References==
==References==
[Sample reference] [http://ijs.sgmjournals.org/cgi/reprint/50/2/489 Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "''Palaeococcus ferrophilus'' gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". ''International Journal of Systematic and Evolutionary Microbiology''. 2000. Volume 50. p. 489-500.]
[1]Kalman, Sue et al. 1999. "Comparative genomes of Chlamydia pnuemoniae and C.trachomatis." Nature, 21: 385-389.
[2]Stephens, Richard S. et al. "Genome sequence of an obligate intracellular pathogen of humans: Chlamydia trachomatis." Science, 282: 754-759.  
[3]Byrne, Gerald I. 2003. "Chlamydia uncloaked." PNSA 100:14. 2003
[4]Brunham RC, MacLean IW, Binns B, Peeling RW. Chlamydia trachomatis: its role in tubal infertility. J. Infect. Dis. 1985;152:1275.
[5]Mohit Singla & Bikram Bal: "Infectivity Assays For Chlamydia trachomatis". The Internet Journal of Microbiology. 2006; Volume 2, Number 2.
[6]Wang, Y. 1999. "Etiology of trachoma: a great success in isolating and cultivating Chlamydia trachomatis." Chinese Medical Journal 112, 938 - 941.
[7] Hess, S. et al. 2007. "Expression of Inflammatory Host Genes in Chlamydia trachomatis Infected Human Monocytes." Arthritis Research & Therapy. 24;9(3):R54.  
[8] Donnellan NM, et al. 2007. "Inflammation on liquid-based cervical cytology: can leukocytes be used to triage for Chlamydia trachomatis testing?" American Journal of Obstetric Gynecology. 196(5):e33-5.
[9]Ananaba GA, et al. 2007. "Live-attenuated influenza viruses as delivery vectors for Chlamydia vaccines." Immunology (epub ahead of print).  
[10] Brunham, Robert, et al. 2000. "Priming with Chlamydia trachomatis Major Outer Membrane Protein (MOMP) DNA followed by MOMP ISCOM Boosting Enhances Protection and Is Associated with Increased Immunoglobulin A and Th1 Cellular Immune Responses." Infection and Immunity. 3074-3078.
[11]Grayston JT. Infections caused by Chlamydia pneumoniae strain TWAR. Clin. Infect. Dis. 1992;15:757.
[12]Brunham RC, MacLean IW, Binns B, Peeling RW. Chlamydia trachomatis: its role in tubal infertility. J. Infect. Dis. 1985;152:1275.


==Author==
==Author==

Latest revision as of 04:10, 19 April 2011

This student page has not been curated.

Classification

• Kingdom - Bacteria • Phylum - Firmicutes • Class - Clostridia • Order - Clostridiales • Family - Clostridiaceae • Genus - Clostridium


Species

Chlamydia muridarum, Chlamydia trachomatis, Chlamydia pneumoniae (also known as Chlamydophila pnemoniae)

Description and Significance

C. trachomatis is an obligate, aerobic, intracellular parasite of eukaryotic cells. It is a Gram-negative bacteria and has a cocci or rod shape. It has a cytoplasmic membrane and outer membrane like to Gram-negative bacteria but, it deficiencies of a peptidoglycan cell wall. C. trachomatis require growing cells in order to stay possible since it cannot create its own ATP. If there is no host organism, C. trachomatis cannot survive on alone [3]. C. trachomatis is the major cause of all sexually transmitted disease in the world; in the United States, its self, more than 4 million cases are diagnosed each year. It is also the chief cause of preventable blindness (affected by a chlamydia infection called trachoma) in the world [5]. C. trachomatis is one of the main causes of pelvic inflammatory disease (PID) and infertility in women [3]. It is very significant to understand and sequence the genome of C. trachomatis because it would aid us in better understanding its functions as a pathogen; the assets that allow it to survive within its human host and its virulence and biological capabilities as a pathogen. Therefore, an effort has been put forth to sequence a lot of the C. trachomatis genome [2].

Genome Structure

Chlamydia trachomatis has a genome that comprises of 1,042,519 nucleotide base pairs and has roughly 894 likely protein coding sequences. [2] C. trachomatis strains have an extrachromosomal plasmid, which was sequenced to be a 7493-base pair plasmid. Because there is a smaller amount than 1% nucleotide sequence variation, ll plasmids from human C. trachomatis isolates are reflected to be very comparable. All the isolates "are about 7,500 nucleotides long and has eight open reading frames computer-predicted to code for proteins comprised of more than 100 amino acids, along with short non-coding sequences amongst some of them." [1] Stimulatingly, in their nucleotide sequence, chlamydial plasmids are extra closely related than is the matching chromosomal DNA. The plasmid of C. trachomatis is a likely target for DNA-based diagnosis of C. trachomatis simply because there are give or take 7-10 copies of the plasmid existing per chlamydial particle. Its sequence is exceedingly conserved among different isolates of C. trachomatis. Some C. trachomatis strains are absent in these plasmids, and the concerns aid in recognition of the C. trachomatis strain. Plaque purified C. trachomatis that do not comprise the plasmids have uncommon inclusion morphology, have no glycogen, and show no change in antibiotic sensitivity. Nevertheless, the fact that such strains are present displays that the plasmid is not a must for C. trachomatis survival [1].

Cell Structure, Metabolism and Life Cycle

The life phase of Chlamydia trachomatis comprises of two steps: elementary body and reticulate body. The elementary body is the spreading form, which is analogous to a spore. The spreading form is about 0.3 um in diameter and makes its own endocytosis upon contact to target cells. It is this form that averts phagolysosomal fusion, which then permits for intracellular survival of the bacteria. Once inside the endosome, the elementary body develops into the reticulate body as a result of the glycogen that is created. The reticulate body splits through binary fission at approximately 2-3 hours per generation. The cell body has a maturation period of 7-21 days in the host. It has no cell wall and is identified as an inclusion in the cell. After division, the reticulate body converts back to the elementary form and is released by the cell by exocytosis. One phagolysosome generally make bout 100-1000 elementary bodies [2]. For metabolism, Chlamydia trachomatis has a glycolytic pathway and a linked tricarboxylic acid cycle. Glycogen production and use of glucose derivatives plays a supportive role in chlamydial metabolism. The occurrence of metabloic precursors and products, such as pyruvate, succinate, glycerol-3-phosphate and NADH dehydrogenases, NADH-ubiquinone oxidoreductase and cytochrome oxidase specify that Chlamydia trachomatis uses a form of electron transport in order to yield energy [2].

Ecology and Pathogenesis

Chlamydia trachomatis is a pathogenic bacteria. It cannot stay alive outside of a eukaryotic host. In fact, humans are the only recognized usual host for C. trachomatis. The bacterium is transmitted by sexual contact with an infected individual.[3] Usually, C. trachomatis is asymptomatic in its hosts, but can produce discharge from the penis, pain and burning through urination, infection or inflammation in the ducts of testicles, and sensitivity or pain in the testicles. [3]

References

[1]Kalman, Sue et al. 1999. "Comparative genomes of Chlamydia pnuemoniae and C.trachomatis." Nature, 21: 385-389. [2]Stephens, Richard S. et al. "Genome sequence of an obligate intracellular pathogen of humans: Chlamydia trachomatis." Science, 282: 754-759. [3]Byrne, Gerald I. 2003. "Chlamydia uncloaked." PNSA 100:14. 2003 [4]Brunham RC, MacLean IW, Binns B, Peeling RW. Chlamydia trachomatis: its role in tubal infertility. J. Infect. Dis. 1985;152:1275. [5]Mohit Singla & Bikram Bal: "Infectivity Assays For Chlamydia trachomatis". The Internet Journal of Microbiology. 2006; Volume 2, Number 2. [6]Wang, Y. 1999. "Etiology of trachoma: a great success in isolating and cultivating Chlamydia trachomatis." Chinese Medical Journal 112, 938 - 941. [7] Hess, S. et al. 2007. "Expression of Inflammatory Host Genes in Chlamydia trachomatis Infected Human Monocytes." Arthritis Research & Therapy. 24;9(3):R54. [8] Donnellan NM, et al. 2007. "Inflammation on liquid-based cervical cytology: can leukocytes be used to triage for Chlamydia trachomatis testing?" American Journal of Obstetric Gynecology. 196(5):e33-5. [9]Ananaba GA, et al. 2007. "Live-attenuated influenza viruses as delivery vectors for Chlamydia vaccines." Immunology (epub ahead of print). [10] Brunham, Robert, et al. 2000. "Priming with Chlamydia trachomatis Major Outer Membrane Protein (MOMP) DNA followed by MOMP ISCOM Boosting Enhances Protection and Is Associated with Increased Immunoglobulin A and Th1 Cellular Immune Responses." Infection and Immunity. 3074-3078. [11]Grayston JT. Infections caused by Chlamydia pneumoniae strain TWAR. Clin. Infect. Dis. 1992;15:757. [12]Brunham RC, MacLean IW, Binns B, Peeling RW. Chlamydia trachomatis: its role in tubal infertility. J. Infect. Dis. 1985;152:1275.

Author

Page authored by Alicia Smith, student of Prof. Doreen Cunningham at Saint Augustine's College.