Chlamydia (genus)(Redirected from Chlamydia (bacterium))
Chlamydia is a genus of pathogenic bacteria that are obligate intracellular parasites. Chlamydia infections are the most common bacterial sexually transmitted diseases in humans and are the leading cause of infectious blindness worldwide.
|C. trachomatis inclusion bodies (brown) in a McCoy cell culture.|
Chlamydia avium Sachse et al. 2015
The three Chlamydia species include Chlamydia trachomatis (a human pathogen), Chlamydia suis (affects only swine), and Chlamydia muridarum (affects only mice and hamsters). Additionally, three species that were previously classified as Chlamydia have since 1999 been reclassified into the then newly created Chlamydophila genus: Chlamydophila psittaci, Chlamydophila pneumoniae, and Chlamydophila pecorum.
Because of Chlamydia's unique developmental cycle, it was taxonomically classified in a separate order. Chlamydia is part of the Chlamydiales order, Chlamydiaceae family. As of March 2008, a new chlamydial agent has been proposed to be introduced into the Chlamidiaceae family, namely "Candidatus Clavochlamydia salmonicola".
Chlamydia species have genomes around 1.0 to 1.3 megabases in length. Most encode ~900 to 1050 proteins. Some species also contain a DNA plasmids or phage genomes (see Table). The elementary body contains an RNA polymerase responsible for the transcription of the DNA genome after entry into the host cell cytoplasm and the initiation of the growth cycle. Ribosomes and ribosomal subunits are found in these bodies.
|C. trachomatis MoPn||C. trachomatis D||C. pneumoniae AR39||C. pneumoniae CWL029|
|plasmids||1 (7m501 nt)||1 (7,493 nt)||1 ssDNA phage||none|
Table 1. Genome features of selected Chlamydia species and strains. MoPn is a mouse pathogen while strain "D" is a human pathogen. About 80% of the genes in C. trachomatis and C. pneumoniae are orthologs. Adapted after Read et al. 2000
Chlamydia may be found in the form of an elementary body and a reticulate body. The elementary body is the nonreplicating infectious particle that is released when infected cells rupture. It is responsible for the bacteria's ability to spread from person to person and is analogous to a spore. The elementary body may be 0.25 to 0.30 μm in diameter, and it mainly consists of C. trachomatis, C. pneumoniae, and C. psittaci. This form is covered by a rigid cell wall (hence the combining form chlamyd- in the genus name). The elementary body induces its own endocytosis upon exposure to target cells. One phagolysosome usually produces an estimated 100–1000 elementary bodies.
Chlamydia may also take the form of a reticulate body, which is in fact an intracytoplasmic form, highly involved in the process of replication and growth of these bacteria. The reticulate body is slightly larger than the elementary body and may reach up to 0.6 μm in diameter with a minimum of 0.5 μm. It does not present a cell wall. When stained with iodine, reticulate bodies appear as inclusions in the cell. The DNA genome, proteins, and ribosomes are retained in the reticulate body. This occurs as a result of the development cycle of the bacteria. The reticular body is basically the structure in which the chlamydial genome is transcribed into RNA, proteins are synthesized, and the DNA is replicated. The reticulate body divides by binary fission to form particles which, after synthesis of the outer cell wall, develop into new infectious elementary body progeny. The fusion lasts about three hours and the incubation period may be up to 21 days. After division, the reticulate body transforms back to the elementary form and is released by the cell by exocytosis.
Studies on the growth cycle of C. trachomatis and C. psittaci in cell cultures in vitro reveal that the infectious elementary body (EB) develops into a noninfectious reticulate body (RB) within a cytoplasmic vacuole in the infected cell. After the elementary body enters the infected cell, an eclipse phase of 20 hours occurs while the infectious particle develops into a reticulate body. The yield of chlamydial elementary bodies is maximal 36 to 50 hours after infection.
A histone like protein HctA and HctB play role in controlling the differentiation between the two cell types. The expression of HctA is tightly regulated and repressed by small non-coding RNA, IhtA until the late RB to EB re-differentiation. The IhtA RNA is conserved across Chlamydia species.
Most commonly, chlamydial infections do not cause symptoms. However, for men, a burning sensation when urinating is often probable. For women, odor and itching are possible symptoms. Both sexes may notice more sebum production as the infection escalates, all which produces greasy sweat, more oily complexion, and can be misdiagnosed as acne eruptions rather than the whole body's hidden fight to defend itself from an STD. All people who have engaged in sexual activity with potentially infected individuals may be offered one of several tests to diagnose the condition.
Chlamydia can be detected through culture tests or nonculture tests. The main nonculture tests include fluorescent monoclonal antibody test, enzyme immunoassay, DNA probes, rapid Chlamydia tests and leukocyte esterase tests. Whereas the first test can detect the major outer membrane protein (MOMP), the second detects a colored product converted by an enzyme linked to an antibody. The rapid Chlamydia tests use antibodies against the MOMP, the leukocyte esterase tests detect enzymes produced by leukocytes containing the bacteria in urine.
Recent phylogenetic studies have revealed that Chlamydia likely shares a common ancestor with cyanobacteria, the group containing the endosymbiont ancestor to the chloroplasts of modern plants, hence, Chlamydia retains unusual plant-like traits, both genetically and physiologically. In particular, the enzyme L,L-diaminopimelate aminotransferase, which is related to lysine production in plants, is also linked with the construction of chlamydial cell walls. The genetic encoding for the enzymes is remarkably similar in plants, cyanobacteria, and Chlamydia, demonstrating a close common ancestry.
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- Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 463–70. ISBN 0-8385-8529-9.
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