Lymphogranuloma venereum pathophysiology: Difference between revisions
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*After necrosis, EBs and RBs travel via [[lymphatics]] to regional [[lymph nodes]], primarily to [[inguinal lymph nodes]]. | *After necrosis, EBs and RBs travel via [[lymphatics]] to regional [[lymph nodes]], primarily to [[inguinal lymph nodes]]. | ||
*Systemic infection occurs when this process repeats as ''C. trachomatis'' is phagocytized by and continues to replicate in [[monocytes]], causing [[lymphadenopathy]] and eventually the formation of inguinal [[buboes]].<ref name="pmid25870512" /> | *Systemic infection occurs when this process repeats as ''C. trachomatis'' is phagocytized by and continues to replicate in [[monocytes]], causing [[lymphadenopathy]] and eventually the formation of inguinal [[buboes]].<ref name="pmid25870512" /> | ||
====Virulence Factors==== | |||
*''C. trachomatis'' produces major outer membrane protein (MOMP), which is responsible for attachment of ''C. trachomatis'' EBs to mucous membrane epithelial cells | |||
*Functional MOMP is required for ''C. trachomatis'' infection.<ref name="pmid2318528">{{cite journal| author=Su H, Watkins NG, Zhang YX, Caldwell HD| title=Chlamydia trachomatis-host cell interactions: role of the chlamydial major outer membrane protein as an adhesin. | journal=Infect Immun | year= 1990 | volume= 58 | issue= 4 | pages= 1017-25 | pmid=2318528 | doi= | pmc=PMC258576 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2318528 }} </ref> | |||
====Adhesion==== | |||
*MOMP is 40 kDa ligand composed of 4 symmetrically spaced variable domains (VDs) I to IV. | |||
*VD II and IV have been identified as the domains responsible for attachment:<ref name="pmid2318528"></ref> | |||
:*VD II structure promotes electrostatic interactions | |||
:*VD IV structure promotes hydrophobic interactions | |||
==References== | ==References== | ||
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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
- Inoculation and replication of C. trachomatis serovars L1, L2, or L3 depends on alternation between two forms of the bacterium: the infectious elementary body (EB) and noninfectious, replicating reticulate body (RB).[3]
- The EB form is responsible for inoculation with C. trachomatis.
- The C. trachomatis EB enters the body through skin abrasions, microabrasions incurred during sexual intercourse or by crossing epithelial cells of mucous membranes.[4]
- C. trachomatis produces the extracellular ligand major outer membrane protein (MOMP), which is presumed to bind with heparan sulfate host epithelial cells.[3]
- Once bound, the EB is engulfed by receptor-mediated endocytosis creating vacuoles termed "inclusions".[5]
- EB inclusions are able to avoid lysosomal fusion, thus preventing their destruction.
- Once inside the host cell, EBs immediately start differentiating into reticulate bodies (RBs) that undergo replication.
- The process of endocytosis and accumulation of RBs within host epithelial cells causes host cell destruction (necrosis) which leads to the formation of a papule at the site of inoculation which may ulcerate, depending on the extent of infection and number or EBs transmitted.[5]
- After necrosis, EBs and RBs travel via lymphatics to regional lymph nodes, primarily to inguinal lymph nodes.
- Systemic infection occurs when this process repeats as C. trachomatis is phagocytized by and continues to replicate in monocytes, causing lymphadenopathy and eventually the formation of inguinal buboes.[1]
Virulence Factors
- C. trachomatis produces major outer membrane protein (MOMP), which is responsible for attachment of C. trachomatis EBs to mucous membrane epithelial cells
- Functional MOMP is required for C. trachomatis infection.[6]
Adhesion
- MOMP is 40 kDa ligand composed of 4 symmetrically spaced variable domains (VDs) I to IV.
- VD II and IV have been identified as the domains responsible for attachment:[6]
- VD II structure promotes electrostatic interactions
- VD IV structure promotes hydrophobic interactions
References
- ↑ 1.0 1.1 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.
- ↑ 3.0 3.1 Taraktchoglou M, Pacey AA, Turnbull JE, Eley A (2001). "Infectivity of Chlamydia trachomatis serovar LGV but not E is dependent on host cell heparan sulfate". Infect Immun. 69 (2): 968–76. doi:10.1128/IAI.69.2.968-976.2001. PMC 97976. PMID 11159992.
- ↑ Mabey D, Peeling RW (2002). "Lymphogranuloma venereum". Sex Transm Infect. 78 (2): 90–2. PMC 1744436. PMID 12081191.
- ↑ 5.0 5.1 Moulder JW (1991). "Interaction of chlamydiae and host cells in vitro". Microbiol Rev. 55 (1): 143–90. PMC 372804. PMID 2030670.
- ↑ 6.0 6.1 Su H, Watkins NG, Zhang YX, Caldwell HD (1990). "Chlamydia trachomatis-host cell interactions: role of the chlamydial major outer membrane protein as an adhesin". Infect Immun. 58 (4): 1017–25. PMC 258576. PMID 2318528.