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Chlamydia pneumoniae

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Chlamydia pneumoniae
Scientific classification
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C. pneumoniae

Chlamydophila pneumoniae is a species of Chlamydophila, an obligate intracellular bacterium[1] that infects humans and is a major cause of pneumonia. It was known as the Taiwan acute respiratory agent (TWAR) from the names of the two original isolates - Taiwan (TW-183) and an acute respiratory isolate designated AR-39.[2] Until recently, it was known as Chlamydia pneumoniae, and that name is used as an alternate in some sources.[3] In some cases, to avoid confusion, both names are given.[4]

C. pneumoniae has a complex life cycle and must infect another cell to reproduce; thus, it is classified as an obligate intracellular pathogen. The full genome sequence for C. pneumoniae was published in 1999. It also infects and causes disease in koalas, emerald tree boas (Corallus caninus), iguanas, chameleons, frogs, and turtles.

The first known case of infection with C. pneumoniae was a case of sinusitis in Taiwan. This atypical bacterium commonly causes pharyngitis, bronchitis and atypical pneumonia,[5] mainly in elderly and debilitated patients, but in healthy adults, also.[6]

Micrograph ofChlamydophila (Chlamydia) pneumoniae in an epithelial cell in acute bronchitis: 1 - infected epitheliocyte, 2 - uninfected epitheliocytes, 3 - chlamydial inclusion bodies in cell, 4 - cell nuclei


Life cycle and method of infection

Life cycle of Chlamydophila pneumoniae

Chlamydophila pneumoniae is a small bacterium (0.2 to 1 μm) that undergoes several transformations during its life cycle. It exists as an elementary body (EB) between hosts. The EB is not biologically active, but is resistant to environmental stresses and can survive outside a host for a limited time. The EB travels from an infected person to the lungs of an uninfected person in small droplets and is responsible for infection. Once in the lungs, the EB is taken up by cells in a pouch called an endosome by a process called phagocytosis. However, the EB is not destroyed by fusion with lysosomes, as is typical for phagocytosed material. Instead, it transforms into a reticulate body and begins to replicate within the endosome. The reticulate bodies must use some of the host's cellular metabolism to complete its replication. The reticulate bodies then convert back to elementary bodies and are released back into the lung, often after causing the death of the host cell. The EBs are thereafter able to infect new cells, either in the same organism or in a new host. Thus, the life cycle of C. pneumoniae is divided between the elementary body, which is able to infect new hosts but can not replicate, and the reticulate body, which replicates but is not able to cause new infection.

Diseases

C. pneumoniae is a common cause of pneumonia around the world; it is typically acquired by otherwise healthy people and is a form of community-acquired pneumonia. Because its treatment and diagnosis are different from historically recognized causes, such as Streptococcus pneumoniae, pneumonia caused by C. pneumoniae is categorized as an "atypical pneumonia".

In addition to pneumonia, C. pneumoniae less commonly causes several other illnesses. Among these are meningoencephalitis (infection and inflammation of the brain and meninges), arthritis, myocarditis (inflammation of the heart), and Guillain-Barré syndrome.[who?][citation needed]

Multiple studies have evaluated prior C. pneumoniae infection and a possible connection to lung cancer. One meta-analysis of serological data comparing prior C. pneumoniae infection in patients with and without lung cancer found results suggesting prior infection was associated with a slightly increased risk of developing lung cancer.[7]

In research into the association between C. pneumoniae infection and atherosclerosis and coronary artery disease, serological testing, direct pathologic analysis of plaques and in vitro testing suggest chronic infection with C. pneumoniae may be a risk factor for development of atherosclerotic plaques. C. pneumoniae infection increases adherence of macrophages to endothelial cells in vitro and aortas ex vivo.[8] However, the current data do not define how often C. pneumoniae is found in atherosclerotic or normal vascular tissue, nor does it allow for determining whether C. pneumoniae infection has a causative effect on atheroma formation or is merely an "innocent passenger" in these plaques. The largest trials that studied the use of antibiotics as a prevention for diseases associated with atherosclerosis, such as heart attacks and strokes, did not show any significant difference between antibiotics and placebo.[9]

C. pneumoniae has also been found in the cerebrospinal fluid of some patients diagnosed with multiple sclerosis.[10]

References

  1. ^ Chlamydophila+pneumoniae at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
  2. ^ http://pathmicro.med.sc.edu/mayer/chlamyd.htm
  3. ^ "www.ncbi.nlm.nih.gov". Retrieved 2009-01-27.
  4. ^ Appelt DM, Roupas MR, Way DS; et al. (2008). "Inhibition of apoptosis in neuronal cells infected with Chlamydophila (Chlamydia) pneumoniae". BMC Neurosci. 9: 13. doi:10.1186/1471-2202-9-13. PMC 2266938. PMID 18218130. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  5. ^ Lang, B. R., Chlamydia pneumonia as a differential diagnosis? Follow-up to a case report on progressive pneumonitis in an adolescent, Patient Care, Sept. 15, 1991
  6. ^ Little, Linda, Elusive pneumonia strain frustrates many clinicians, Medical Tribune, p. 6, September 19, 1991
  7. ^ Zhan P, Suo LJ, Qian Q; et al. (2011). "Chlamydia pneumoniae infection and lung cancer risk: A meta-analysis". Eur. J. Cancer. 47 (5): 742–7. doi:10.1016/j.ejca.2010.11.003. PMID 21194924. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  8. ^ Takaoka N, Campbell LA, Lee A, Rosenfeld ME, Kuo CC (2008). "Chlamydia pneumoniae infection increases adherence of mouse macrophages to mouse endothelial cells in vitro and to aortas ex vivo". Infect Immun. 76 (2): 510–4. doi:10.1128/IAI.01267-07. PMID 18070891. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  9. ^ Mussa FF, Chai H, Wang X, Yao Q, Lumsden AB, Chen C (2006). "Chlamydia pneumoniae and vascular disease: an update". J. Vasc. Surg. 43 (6): 1301–7. doi:10.1016/j.jvs.2006.02.050. PMID 16765261. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  10. ^ Sriram S, Stratton CW, Yao S; et al. (1999). "Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis". Ann. Neurol. 46 (1): 6–14. doi:10.1002/1531-8249(199907)46:1<6::AID-ANA4>3.0.CO;2-M. PMID 10401775. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)