Lymphogranuloma venereum pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
*''C. trachomatis'' primarily infects lymphatic tissue and lymph nodes. | |||
*''C. trachomatis'' enters the body through skin abrasions, microabrasions incurred during sexual intercourse or by crossing epithelial cells of mucous membranes. | |||
==References== | ==References== | ||
Revision as of 16:24, 9 February 2016
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Nate Michalak, B.A.
Overview
Pathophysiology
Lymphogranuloma venereum (LGV) is a chronic (long-term) infection of the lymphatic system caused by three different types of the bacteria Chlamydia trachomatis. The bacteria spread through sexual contact. The infection is caused by a different bacteria than that which causes genital chlamydia.
Transmission
- Lyphogranuloma venereum (LGV) may develop after transmission of servars L1, L2, or L3 of the bacterium Chlamydia trachomatis.
- C. trachomatis can be transmitted through vaginal, anal, or oral sexual contact.[1]
- C. trachomatis is an obligate intracellular pathogen.[2]
Pathogenesis
- C. trachomatis primarily infects lymphatic tissue and lymph nodes.
- C. trachomatis enters the body through skin abrasions, microabrasions incurred during sexual intercourse or by crossing epithelial cells of mucous membranes.
References
- ↑ Ceovic R, Gulin SJ (2015). "Lymphogranuloma venereum: diagnostic and treatment challenges". Infect Drug Resist. 8: 39–47. doi:10.2147/IDR.S57540. PMC 4381887. PMID 25870512.
- ↑ Datta B, Njau F, Thalmann J, Haller H, Wagner AD (2014). "Differential infection outcome of Chlamydia trachomatis in human blood monocytes and monocyte-derived dendritic cells". BMC Microbiol. 14: 209. doi:10.1186/s12866-014-0209-3. PMC 4236547. PMID 25123797.