Lymphogranuloma venereum pathophysiology: Difference between revisions
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===Pathogenesis=== | ===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).<ref name="pmid11159992">{{cite journal| author=Taraktchoglou M, Pacey AA, Turnbull JE, Eley A| title=Infectivity of Chlamydia trachomatis serovar LGV but not E is dependent on host cell heparan sulfate. | journal=Infect Immun | year= 2001 | volume= 69 | issue= 2 | pages= 968-76 | pmid=11159992 | doi=10.1128/IAI.69.2.968-976.2001 | pmc=PMC97976 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11159992 }} </ref> | *Inoculation and replication of ''C. trachomatis'' [[Serovar|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).<ref name="pmid11159992">{{cite journal| author=Taraktchoglou M, Pacey AA, Turnbull JE, Eley A| title=Infectivity of Chlamydia trachomatis serovar LGV but not E is dependent on host cell heparan sulfate. | journal=Infect Immun | year= 2001 | volume= 69 | issue= 2 | pages= 968-76 | pmid=11159992 | doi=10.1128/IAI.69.2.968-976.2001 | pmc=PMC97976 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11159992 }} </ref> | ||
*The EB form is responsible for inoculation with ''C. trachomatis''. | *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.<ref name="pmid12081191">{{cite journal| author=Mabey D, Peeling RW| title=Lymphogranuloma venereum. | journal=Sex Transm Infect | year= 2002 | volume= 78 | issue= 2 | pages= 90-2 | pmid=12081191 | doi= | pmc=PMC1744436 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12081191 }} </ref> | :*The ''C. trachomatis'' EB enters the body through skin abrasions, microabrasions incurred during sexual intercourse or by crossing [[epithelial cells]] of [[mucous membranes]].<ref name="pmid12081191">{{cite journal| author=Mabey D, Peeling RW| title=Lymphogranuloma venereum. | journal=Sex Transm Infect | year= 2002 | volume= 78 | issue= 2 | pages= 90-2 | pmid=12081191 | doi= | pmc=PMC1744436 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12081191 }} </ref> | ||
:*''C. trachomatis'' produces the extracellular ligand major outer membrane protein (MOMP), which is presumed to bind with heparan sulfate host epithelial cells.<ref name="pmid11159992" | :*''C. trachomatis'' produces the extracellular ligand major outer membrane protein (MOMP), which is presumed to bind with heparan sulfate host epithelial cells.<ref name="pmid11159992" /> | ||
:*Once bound, the EB is engulfed by receptor-mediated endocytosis creating vacuoles termed "inclusions".<ref name="pmid2030670">{{cite journal| author=Moulder JW| title=Interaction of chlamydiae and host cells in vitro. | journal=Microbiol Rev | year= 1991 | volume= 55 | issue= 1 | pages= 143-90 | pmid=2030670 | doi= | pmc=PMC372804 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2030670 }} </ref> | :*Once bound, the EB is engulfed by receptor-mediated [[endocytosis]] creating vacuoles termed "inclusions".<ref name="pmid2030670">{{cite journal| author=Moulder JW| title=Interaction of chlamydiae and host cells in vitro. | journal=Microbiol Rev | year= 1991 | volume= 55 | issue= 1 | pages= 143-90 | pmid=2030670 | doi= | pmc=PMC372804 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2030670 }} </ref> | ||
*EB inclusions are able to avoid lysosomal fusion, thus preventing their destruction. | *EB inclusions are able to avoid [[Lysosome|lysosomal]] fusion, thus preventing their destruction. | ||
*Once inside the host cell, EBs immediately start differentiating into reticulate bodies (RBs) that undergo replication. | *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.<ref name="pmid2030670" | *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.<ref name="pmid2030670" /> | ||
*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" /> | ||
==References== | ==References== | ||
Revision as of 17:00, 11 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
- 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]
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.