Chlamydia Pneumoniae

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Etiology/Bacteriology

Taxonomy

| Order = Chlamydiales | Family = Chlamydiaceae | Genus = Chlamydia | Species = Chlamydia pneumoniae
|NCBI: Taxonomy Genome: Genome|}

Description

Chlamydophila pneumonia (TWAR) is a recently recognized third species of the genus Chlamydia that causes acute respiratory disease. The strain name TWAR was derived from the first conjunctival isolates of the species (TW-183 and AR-39), although the pathogen initially colonizes the reparatory tract. [1]

Pathogenesis

Incubation and Colonization

The incubation period of C pneumoniae is approximately 3-4 weeks, with a usually gradual onset.[6] If upper respiratory tract symptoms (eg. rhinitis, laryngitis, pharyngitis, sinusitis) increase in severity to bronchitis or pneumonia, symptoms can present in an additional 1-4 weeks.[6] The symptoms are not always biphasic, however, and many hosts do not show symptoms beyond a mild initial respiratory infection. As C. pneumoniae is a respiratory pathogen, its initial sites of colonization are the oral and nasal mucosa. Once it colonizes the lungs, it is distributed by monocytes through blood circulation to other areas of the body.

Epidemiology

The estimated number of cases of pneumonia caused by C pneumoniae in the United States is 300,000 cases per year, and the pathogen is estimated to cause 10-20% of community-acquired pneumonia (CAP) cases among adults.[6] While all ages are at risk, C. Pneumoniae infection is most common in children between 5 and 14 years old. In the United States, about 50% of adults have evidence of past infection by age 20, and reinfection throughout life is common.[7] C. pneumoniae appears to have a worldwide distribution, although the prevalence of infection varies by region.[7] Studies of adults from 10 areas of the world have shown a higher population prevalence in tropical, less developed countries.[7]

Most of the fatalities associated with C. pneumoniae infection have been in persons with underlying illness and complications [7]. C. pneumonia has been known to contribute to serious morbidity and mortality among populations with weakened immune responses such as residents of nursing homes who suffer respiratory disease outbreaks.[17]

References

1. Grayston, J. T., C.-C. Kuo, L. A. Campbell, and S.-P. Wang. 1989. Chlamydia pneumoniae sp. nov. for Chlamydia sp. strain TWAR. Int. J. Syst. Bacteriol. 39:88–90.
2. Kuo, C., & Grayston, J. (n.d.). Chlaymydia spp. strain TWAR A newly recognized organism associated with atypical pneumonia and other respiratory infections. Clinical Microbiology Newsletter, 137-140.
3. "Chlamydophila Pneumoniae Infection." Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 7 Feb. 2014. Available at: http://www.cdc.gov/pneumonia/atypical/chlamydophila.html
4. Humphrey, Nancy. "Chlamydia Pneumoniae Not Caught like You Thought (04/23/99)." Reporter: Vanderbilt University Medical Center. Available at: http://www.mc.vanderbilt.edu:8080/reporter/index.html?ID=779.
5. Oba, Yuji. "Chlamydial Pneumonias." : Overview, Pathophysiology, Epidemiology. 2 Nov. 2013. Available at: http://emedicine.medscape.com/article/297351-overview#a1.
6. Kuo CC, Jackson LA, Campbell LA, Grayston JT. Chlamydia pneumoniae (TWAR). Clinical Microbiology Reviews. 1995;8(4):451-461.
7. Casadevall A, Pirofski L. 2003. The Damage Response Framework of Microbial Pathogenesis. Nat Rev 1:17-24.
8. Hudson, MAP. What is the evidence for a relationship between Chlamydia pneumoniae and late-onset Alzheimer's disease? Laboratory Medicine. 2001:680–685.
9. Gérard, H. C., Dreses-Werringloer, U., Wildt, K. S., Deka, S., Oszust, C., Balin, B. J., Frey, W. H., Bordayo, E. Z., Whittum-Hudson, J. A. and Hudson, A. P. (2006), Chlamydophila (Chlamydia) pneumoniae in the Alzheimer's brain. FEMS Immunology & Medical Microbiology, 48: 355–366. doi: 10.1111/j.1574-695X.2006.00154.x
10. Mahony JB, Coombes BK. Chlamydia pneumoniae and atherosclerosis: does the evidence support a causal or contributory role? FEMS Microbiol Lett. 2001;197:1-9.
11. Farb A, Tang AL, Burke AP, Sessums L, Liang Y, et al. Sudden coronary death. Frequency of active coronary lesions, inactive coronary lesions, and myocardial infarction. Circulation. 1995;92:1701–1709.
12. Kalayoglu, M. V., & Byrne, G. I. (1998). A Chlamydia pneumoniae Component That Induces Macrophage Foam Cell Formation Is Chlamydial Lipopolysaccharide. Infection and Immunity, 66(11), 5067–5072.
13. Layh-Schmitt G, Bendl C, Hildt U, Dong-Si T, Juttler E, Schnitzler P, Grond-Ginsbach C, Grau AJ: Evidence for infectionwithChlamydiapneumoniaeina subgroupofpatientswithmultiplesclerosis.AnnNeurol47,652-655 (2000).
14. Hahn DL, Schure A, Patel K et al. (2012). "Chlamydia pneumoniae-specific IgE is prevalent in asthma and is associated with disease severity". PLoS ONE 7 (4): e35945. doi:10.1371/journal.pone.0035945. PMC 3335830. PMID 22545149.
15. Bailey, Leslie. "Infection Biology of Chlamydia Pneumoniae." Department of Molecular Biology: Laboratory for Molecular Infection Medicine Sweden (MIMS), 2008. <http://www.diva-portal.org/smash/record.jsf?pid=2:141442>.
16. Troy CJ, Peeling RW, Ellis AG, et al. Chlamydia pneumoniae as a New Source of Infectious Outbreaks in Nursing Homes. JAMA. 1997;277(15):1214-1218. doi:10.1001/jama.1997.03540390044033.

Created by Erika Cummings, a student of Tyrrell Conway at the University of Oklahoma.