Chlamydophila caviae
A Microbial Biorealm page on the genus Chlamydophila caviae
Classification
Higher order taxa
Domain: Bacteria; Phylum: Chlamydiae; Order: Chlamydiales; Family: Chlamydiaceae; Genus: Chlamydophila; Species: caviae (1)
Species
Chlamydophila caviae
Description and significance
Chlamydophila caviae is a rod-shaped organism that causes inclusion conjunctivitis in guinea pigs; inflammation of the eyelid is a result of infection. (2) The diameter of this Chlamydiae organism is approximately 0.25 to 0.8 micrometers long. It was isolated from infected guinea pigs. (5) Chlamydophila caviae is a Gram-negative strain (5) with an outer membrane that lacks peptidoglycan. (6) These organisms are intracellular parasites that inhabit eukaryotic cells. (2) These organisms also rely on their hosts for energy and nutrients; (5) they receive nucleotides, lipids, and amino acids from their hosts. (7)
Genome structure
In the Chlamydophila caviae GPIC genome, there is one circular chromosome and one plasmid with an unknown function. The chromosome is 1,173,390 base pairs long and it has a 39.2 percent GC content. The chromosome codes for 998 proteins and 41 RNAs. The plasmid, pCpGP1, is 7,966 base pairs long. The plasmid has a 33.7 percent GC content and it codes for seven proteins. (2) In the entire genome, there are a total of 1061 genes. Thirty-eight of these genes code for tRNAs and three genes code for rRNAs. There are 462,922 total GC base pairs, 3 rRNA genes and 1020 genes for proteins. (8)
Cell structure and metabolism
The metabolism of Chlamydophila caviae is simple compared to most bacteria. The organisms of Chlamydiae contain OmpA and OmpB porins and do not contain siderophores for iron transport. The organisms contain dnaK and groE, genes induced by stress. In Chlamydiae organisms, the enzymes: citrate synthase, aconitase, and isocitrase dehydrogenase are missing from the Krebs Cycle. The surface of the elementary bodies is hydrophobic and negatively charged. (7) Chlamydia trachomatis is capable of producing energy by glycolysis, but it is missing hexokinase and fructose 1,6 bisphosphate aldolase. (6) Little is known about the specific metabolism of Chlamydophila caviae. Its close relative, Chlamydophila psittaci does not have cytochrome and flavoprotein carriers in its electron transport chain. Generally, it relies on the host cell for ATP, (9) but it can produce some ATP from glycolysis. (5) Chlamydophila psittaci produces RNA, DNA, proteins, lipids, glycogen, amino acids and coenzymes. It has the cellular machinery for the electron transport chain, substrate-level phosphorylation, and oxidative phosphorylation. (9)
Chlamydia trachomatis contains genes for amino acid transporters and several genes for amino acid biosynthesis. It also contains TrpA, TrpB, TrpC, enzymes for the biosynthesis of tryptophan and a TrpR aporepressor. Chlamydia trachomatis can synthesize long chain fatty acids. (5)
Ecology
Two organisms that are close relatives, Chlamydophila pneumoniae and Chlamydia trachomatis, cause disease in humans. Chlamydophila pneumoniae is the agent of pneumonia and asthma. Every year, approximately ninety-million people in the world are infected with Chlamydia trachomatis. The number of infections by Chlamydia trachomatis is second only to papillomavirus. Also, it is the major cause of sexually transmitted disease and pelvic inflammatory disease. Chlamydia trachomatis is the agent of trachoma, which causes ocular disease. This infection is common among children and it is one of the leading cases of blindness. Trachoma is common in India, the Middle East, Africa and Latin America. (5)
Pathology
Chlamydophila caviae causes ocular disease and conjunctivitis in guinea pigs. (10) The following cycle describes the infection and replication of Chlamydophila caviae and Chlamydia organisms within its hosts. The two major components of this cycle are the elementary body and the reticulate body. The elementary body infects the cell and the reticulate body initiates metabolic processes inside the cell. During the infection cycle, the elementary bodies attach to the surface of the epithelial cells. The elementary bodies enter the host via endocytosis and fuse with each other to form inclusions in the infected cell. Inside the host cell, the elementary bodies are converted into the reticulate bodies and replicate by binary fission. The reticulate bodies insert proteins into the inclusion membrane in order to obtain nutrients from the host cell. The projections from the surface of Chlamydia enter the inclusion membrane of the host cell. Chlamydia do not have to leave the vacuole in order to obtain nutrients from their eukaryotic hosts. Then, the reticulate bodies are converted into elementary bodies before leaving the host cells. (5)
In addition, Chlamydophila psittaci, a close relative of Chlamydophila caviae, infects birds and causes infection of the respiratory system. This disease is rare in the United States and in many cases, it is undiagnosed. Psittacne birds are usually infected, along with parrots and parakeets. In bird factories, humans can be infected via the respiratory tract. Common symptoms of infection by Chlamydophila psittaci are coughing, fevers, and headaches; this disease is often fatal. (7)
Application to Biotechnology
Chlamydia organisms produce proteins that may have potential applications to biotechnology. MOMP, which is located in the elementary bodies and the reticulate bodies, is produced by the OmpA gene. In the elementary bodies, MOMP is linked by disulfide bonds. MOMP is a porin in the outer membrane of Chlamydia organisms. Also, OmcA and OmcB are located in elementary bodies. They are proteins in the outer membrane and they contain cysteine. These proteins may be utilized for cellular processes. (7)
Current Research
Current research regarding Chlamydophila caviae focuses on the infections in guinea pigs, causing ocular disease. This research focuses on the identification and pathogenesis of Chlamydial infections. Tests are used to determine whether or not the Acanthamoebae species is present in the guinea pigs’ eyes and possible use as vectors in the Chlamydiae organisms. The following methods were used in this experiment: gross pathology, histology, cytology, immunohistochemistry, PCR, sequencing, DNA sampling, and bacteriological staining. The basic conclusion of this experiment is that it has a zoonotic potential regarding the guinea pig inclusion conjunctivitis; Chlamydophila caviae is capable of infecting guinea pigs. Also, its infection is prevalent mainly in young guinea pigs. (10)
Another current study investigates a gene derived from ArgR that is encoded in many of the Chlamydia species. In bacteria, ArgR regulates arginine anabolism and degradation based on intracellular levels. Chlamydia does not contain arginine synthesis genes. These organisms contain artJ, glnQ and glnP, which encode a transport system for arginine. ArgR binds to operator sequences adjacent to the glnPQ operon. ArgR operators are located upstream of glnPQ. Based on this research, some Chlamydiaceae organisms have genetic mechanisms that control the uptake of arginine into the cell. One finding is that Chlamydophila trachomatis does not have the ability to control the intracellular arginine concentrations. (11)
The following current study is based on the fact that asthma is caused by Chlamydophila pneumoniae infection. Also, its cell wall inhibits the production of IgE. The IgE response from asthmatics is inhibited by tetracyclines. The goal of this experiment is to examine the Chlamydophila pneumoniae infection in asthmatics. The production of IgE in mononuclear cells is also a main focus in this experiment. Based on this research, Chlamydophila pneumoniae causes a switch from Th1 to Th2 in asthmatics. Therefore, Chlamydophila pneumoniae modulates IgE in asthmatics. (12)
References
1. KEGG. Chlamydophila caviae GPIC. 2007. http://www.genome.jp/kegg-bin/show_organism?org=cca
2. Entrez Genome Project. 2007. Chlamydophila caviae GPIC. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=genomeprj&cmd=Retrieve&dopt=Overview&list_uids=228
3. Wishart, D. Chlamydophila caviae. BacMap Genome Atlas. University of Alberta. http://wishart.biology.ualberta.ca/BacMap/cgi/getSpeciesCard.cgi?accession=NC_003361&ref=index_2.html
4. Singla, M., and B. Bikram. “Infectivity Assays for Chlamydia Trachomatis.” The Internet Journal of Microbiology. 2006. Volume 2. http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ijmb/vol2n2/chlamydia.xml
5. Engleberg, N.C., DiRita, V., and T.S. Dermody. Schaechter’s Mechanisms of Microbial Disease. 4th Ed. Lippincott Williams & Wilkins. 2007. Chapter 27. p. 284-291.
6. Barton, L.L. Structural and Functional Relationships in Prokaryotes. Springer. 2005. p. 96, 596.
7. Stephens, R.S. Chlamydia: Intracellular Biology, Pathogenesis and Immunity. American Society for Microbiology. 1999. p. 16-19, 54, 78-79, 81, 89, 104-108, 140, 143-144.
8. TIGR Comprehensive Microbial Resource. Chlamydophila caviae GPIC Genome Page. http://cmr.tigr.org/tigr-scripts/CMR/GenomePage.cgi?org=gcp
9. Prescott, L.M., Harley, J.P. and D.A. Klein. Microbiology. 6th Ed. McGraw-Hill. 2005. Chapter 21. p. 464-466.
10. Lutz- Wohlgroth, L., Becker, A., Brugnera, E., Huat, Z.L., Zimmermann, D., Grimm, F., Haessig, M., Greub, G., Kaps, S., Spiess, B., Pospischil, A., and L. Vaughan. “Chlamydiales in guinea-pigs and their zoonotic potential.” J Vet Med A Physiology Pathology Clinical Medicine. 2006. Volume 53 p.185-193. http://www.blackwell-synergy.com/links/doi/10.1111/j.1439-0442.2006.00819.x
11. Schaumburg, C.S., and M. Tan. “Arginine-Dependent Gene Regulation via the ArgR Repressor Is Species Specific in Chlamydia.” J. Bacteriology. 2006. Volume 188. p. 919-927. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16428395
12. Kohlhoff, S.A., Joks, R., Kamath, T., Kutlin, A., Smith-Norowitz, T., Nowakowski, M., Bluth, M., Durkin, H., and M.R. Hammerschlag. “Chlamydophila pneumoniae (Cpn) Mediated IgE Production by Peripheral Blood Mononuclear Cells (PBMCs) of Allergic Asthmatics is Suppressed by Doxycycline.” Journal of Allergy and Clinical Immunology. 2007. Volume 119. p. 525. http://linkinghub.elsevier.com/retrieve/pii/S0091674906038255
Edited by Katherine Kaushal, student of Rachel Larsen and Kit Pogliano
