Urethritis pathophysiology: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Urethritis}} | {{Urethritis}} | ||
{{CMG}}; {{AE}}{{MehdiP}} | {{CMG}}; {{AE}}{{MehdiP}} {{ZMalik}} | ||
==Overview== | ==Overview== | ||
Urethritis is an inflammation of the genital tract that is mostly due to infectious causes. Its pathogenesis depends on the causative pathogen. | Urethritis is an [[inflammation]] of the [[Sex organ|genital tract]] that is mostly due to infectious causes. Its pathogenesis depends on the causative pathogen. ''[[Neisseria gonorrhoeae|N. gonorrhea]]'' is usually transmitted via the [[Sex organ|genital tract]] to the human host. Following attachment to host cell, which is mediated by [[pili]], [[Gonorrhea|''gonococci'']] become engulfed in a process known as parasite-directed [[endocytosis]]. This [[organism]] will survive inside the [[Vacuole|vacuoles]] and replicate. Among non-gonorrheal causes, ''[[Chlamydiae|Chlamydia trachomatis]]'' is the most common. The infectious process begins with cell surface attachment and [[phagocytosis]] by the host cell. The [[pathogen]] survives inside the [[Cell (biology)|cell]] by debilitating the cellular [[lysosomes]] and replicating as elementary bodies which is considered as the infective form of the [[pathogen]]. | ||
==Pathophysiology== | ==Pathophysiology== | ||
Urethritis is divided into gonorrheal and non-gonorrheal | Urethritis is divided into gonorrheal and non-gonorrheal causes. The [[pathophysiology]] of each one of them is different. | ||
=== | ===Gonorrheal=== | ||
*[[Neisseria gonorrhoeae|N. | *''[[Neisseria gonorrhoeae|N. gonorrhea]]'' is usually transmitted via the [[Sex organ|genital tract]] to the human host. | ||
*Following attachment to host cell, which is mediated by pili, gonococci become engulfed in a process known as parasite-directed endocytosis. This organism will survive inside the vacuoles and replicate.<ref name="pmid9916098">{{cite journal |vauthors=Scheuerpflug I, Rudel T, Ryll R, Pandit J, Meyer TF |title=Roles of PilC and PilE proteins in pilus-mediated adherence of Neisseria gonorrhoeae and Neisseria meningitidis to human erythrocytes and endothelial and epithelial cells |journal=Infect. Immun. |volume=67 |issue=2 |pages=834–43 |year=1999 |pmid=9916098 |pmc=96394 |doi= |url=}}</ref> | *Following attachment to host cell, which is mediated by [[pili]], [[Gonorrhea|''gonococci'']] become engulfed in a process known as parasite-directed [[endocytosis]]. This [[organism]] will survive inside the [[Vacuole|vacuoles]] and replicate.<ref name="pmid9916098">{{cite journal |vauthors=Scheuerpflug I, Rudel T, Ryll R, Pandit J, Meyer TF |title=Roles of PilC and PilE proteins in pilus-mediated adherence of Neisseria gonorrhoeae and Neisseria meningitidis to human erythrocytes and endothelial and epithelial cells |journal=Infect. Immun. |volume=67 |issue=2 |pages=834–43 |year=1999 |pmid=9916098 |pmc=96394 |doi= |url=}}</ref> | ||
*Gonococcal [[virulence factors]] include:<ref name="pmid4958881">{{cite journal| author=Sparling PF| title=Genetic transformation of Neisseria gonorrhoeae to streptomycin resistance. | journal=J Bacteriol | year= 1966 | volume= 92 | issue= 5 | pages= 1364-71 | pmid=4958881 | doi= | pmc=276432 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4958881 }} </ref><ref name="pmid4631989">{{cite journal| author=Swanson J| title=Studies on gonococcus infection. IV. Pili: their role in attachment of gonococci to tissue culture cells. | journal=J Exp Med | year= 1973 | volume= 137 | issue= 3 | pages= 571-89 | pmid=4631989 | doi= | pmc=2139381 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4631989 }} </ref><ref name="pmid9701824">{{cite journal| author=Wolfgang M, Lauer P, Park HS, Brossay L, Hébert J, Koomey M| title=PilT mutations lead to simultaneous defects in competence for natural transformation and twitching motility in piliated Neisseria gonorrhoeae. | journal=Mol Microbiol | year= 1998 | volume= 29 | issue= 1 | pages= 321-30 | pmid=9701824 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9701824 }} </ref> | *Gonococcal [[virulence factors]] include:<ref name="pmid4958881">{{cite journal| author=Sparling PF| title=Genetic transformation of Neisseria gonorrhoeae to streptomycin resistance. | journal=J Bacteriol | year= 1966 | volume= 92 | issue= 5 | pages= 1364-71 | pmid=4958881 | doi= | pmc=276432 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4958881 }} </ref><ref name="pmid4631989">{{cite journal| author=Swanson J| title=Studies on gonococcus infection. IV. Pili: their role in attachment of gonococci to tissue culture cells. | journal=J Exp Med | year= 1973 | volume= 137 | issue= 3 | pages= 571-89 | pmid=4631989 | doi= | pmc=2139381 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4631989 }} </ref><ref name="pmid9701824">{{cite journal| author=Wolfgang M, Lauer P, Park HS, Brossay L, Hébert J, Koomey M| title=PilT mutations lead to simultaneous defects in competence for natural transformation and twitching motility in piliated Neisseria gonorrhoeae. | journal=Mol Microbiol | year= 1998 | volume= 29 | issue= 1 | pages= 321-30 | pmid=9701824 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9701824 }} </ref> | ||
** | **[[Pilus|Pili]] | ||
**The ability to attach to urethral [[epithelial cells]] | **The ability to attach to urethral [[epithelial cells]] | ||
**Production of extracellular [[proteases]] that cleave [[IgA]] | **Production of extracellular [[proteases]] that cleave [[IgA]] | ||
===Non-Gonorrheal=== | ===Non-Gonorrheal=== | ||
*Among non-gonorrheal causes, ''[[Chlamydiae|Chlamydia trachomatis]]'' is most common. | *Among non-gonorrheal causes, ''[[Chlamydiae|Chlamydia trachomatis]]'' is the most common. | ||
*The infectious process begins with cell surface attachment and [[phagocytosis]] by the host cell. The pathogen survives inside the cell by debilitating the cellular [[lysosomes]] and replicating as | *The infectious process begins with cell surface attachment and [[phagocytosis]] by the host cell. The [[pathogen]] survives inside the [[Cell (biology)|cell]] by debilitating the cellular [[lysosomes]] and replicating as elementary bodies which is considered as the infective form of the [[pathogen]].<ref>Beatty, Wandy L., Richard P. Morrison, and Gerald I. Byrne. "Persistent chlamydiae: from cell culture to a paradigm for chlamydial pathogenesis." Microbiological reviews 58.4 (1994): 686-699.</ref><ref>Baron, Samuel. Medical microbiology. Galveston, Tex: University of Texas Medical Branch at Galveston, 1996. Print.</ref> | ||
==Genetics== | |||
Urethritis does not follow any [[genetic]] pattern. | |||
==Associated Conditions== | |||
*[[Stevens-Johnson syndrome]] | |||
*Nongonococcal urethritis (NGU) due to [[C. trachomatis]] may be associated with: | |||
**[[Epididymitis]] | |||
**[[Prostatitis]] | |||
**[[Reactive arthritis]] | |||
*[[HIV]] transmission is facilitated by co-existing [[non-gonococcal urethritis|non-gonococcal urethritis]], however [[treatment]] of NGU is the same in [[HIV]] negative or positive [[patients]]. | |||
==Gross Pathology== | |||
On [[gross pathology]], [[mucoid]], [[mucopurulent]], or [[purulent]] [[discharge]] can be observed. | |||
==Microscopy== | ==Microscopy== | ||
===Gonorrheal=== | |||
Characteristic findings include:<ref name="pmid8627027">{{cite journal |vauthors=Apicella MA, Ketterer M, Lee FK, Zhou D, Rice PA, Blake MS |title=The pathogenesis of gonococcal urethritis in men: confocal and immunoelectron microscopic analysis of urethral exudates from men infected with Neisseria gonorrhoeae |journal=J. Infect. Dis. |volume=173 |issue=3 |pages=636–46 |year=1996 |pmid=8627027 |doi= |url=}}</ref> | |||
*[[Gram-negative]] [[intracellular]] [[diplococci]] ([[GNID]]) or purple [[intracellular]] [[diplococci]] on [[methylene blue]], or [[gentian violet]] stain. | |||
*Invaded [[epithelial cells]] | |||
*[[Vacuoles]] that contain multiple [[organisms]] | |||
*[[Polymorphic nuclear cells]]s | |||
===Non-Gonorrheal=== | |||
*Absence of [[gram-negative]] [[intracellular]] [[diplococci]] ([[GNID]]) | |||
*[[Signs]] of [[inflammation]] present | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
[[Category:Medicine]] | |||
[[Category:Emergency medicine]] | |||
[[Category:Up-To-Date]] | |||
[[Category:Infectious disease]] | |||
[[Category:Urology]] | |||
[[Category:Nephrology]] | |||
Latest revision as of 14:59, 23 August 2021
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2] Zehra Malik, M.B.B.S[3]
Overview
Urethritis is an inflammation of the genital tract that is mostly due to infectious causes. Its pathogenesis depends on the causative pathogen. N. gonorrhea is usually transmitted via the genital tract to the human host. Following attachment to host cell, which is mediated by pili, gonococci become engulfed in a process known as parasite-directed endocytosis. This organism will survive inside the vacuoles and replicate. Among non-gonorrheal causes, Chlamydia trachomatis is the most common. The infectious process begins with cell surface attachment and phagocytosis by the host cell. The pathogen survives inside the cell by debilitating the cellular lysosomes and replicating as elementary bodies which is considered as the infective form of the pathogen.
Pathophysiology
Urethritis is divided into gonorrheal and non-gonorrheal causes. The pathophysiology of each one of them is different.
Gonorrheal
- N. gonorrhea is usually transmitted via the genital tract to the human host.
- Following attachment to host cell, which is mediated by pili, gonococci become engulfed in a process known as parasite-directed endocytosis. This organism will survive inside the vacuoles and replicate.[1]
- Gonococcal virulence factors include:[2][3][4]
- Pili
- The ability to attach to urethral epithelial cells
- Production of extracellular proteases that cleave IgA
Non-Gonorrheal
- Among non-gonorrheal causes, Chlamydia trachomatis is the most common.
- The infectious process begins with cell surface attachment and phagocytosis by the host cell. The pathogen survives inside the cell by debilitating the cellular lysosomes and replicating as elementary bodies which is considered as the infective form of the pathogen.[5][6]
Genetics
Urethritis does not follow any genetic pattern.
Associated Conditions
- Stevens-Johnson syndrome
- Nongonococcal urethritis (NGU) due to C. trachomatis may be associated with:
- HIV transmission is facilitated by co-existing non-gonococcal urethritis, however treatment of NGU is the same in HIV negative or positive patients.
Gross Pathology
On gross pathology, mucoid, mucopurulent, or purulent discharge can be observed.
Microscopy
Gonorrheal
Characteristic findings include:[7]
- Gram-negative intracellular diplococci (GNID) or purple intracellular diplococci on methylene blue, or gentian violet stain.
- Invaded epithelial cells
- Vacuoles that contain multiple organisms
- Polymorphic nuclear cellss
Non-Gonorrheal
- Absence of gram-negative intracellular diplococci (GNID)
- Signs of inflammation present
References
- ↑ Scheuerpflug I, Rudel T, Ryll R, Pandit J, Meyer TF (1999). "Roles of PilC and PilE proteins in pilus-mediated adherence of Neisseria gonorrhoeae and Neisseria meningitidis to human erythrocytes and endothelial and epithelial cells". Infect. Immun. 67 (2): 834–43. PMC 96394. PMID 9916098.
- ↑ Sparling PF (1966). "Genetic transformation of Neisseria gonorrhoeae to streptomycin resistance". J Bacteriol. 92 (5): 1364–71. PMC 276432. PMID 4958881.
- ↑ Swanson J (1973). "Studies on gonococcus infection. IV. Pili: their role in attachment of gonococci to tissue culture cells". J Exp Med. 137 (3): 571–89. PMC 2139381. PMID 4631989.
- ↑ Wolfgang M, Lauer P, Park HS, Brossay L, Hébert J, Koomey M (1998). "PilT mutations lead to simultaneous defects in competence for natural transformation and twitching motility in piliated Neisseria gonorrhoeae". Mol Microbiol. 29 (1): 321–30. PMID 9701824.
- ↑ Beatty, Wandy L., Richard P. Morrison, and Gerald I. Byrne. "Persistent chlamydiae: from cell culture to a paradigm for chlamydial pathogenesis." Microbiological reviews 58.4 (1994): 686-699.
- ↑ Baron, Samuel. Medical microbiology. Galveston, Tex: University of Texas Medical Branch at Galveston, 1996. Print.
- ↑ Apicella MA, Ketterer M, Lee FK, Zhou D, Rice PA, Blake MS (1996). "The pathogenesis of gonococcal urethritis in men: confocal and immunoelectron microscopic analysis of urethral exudates from men infected with Neisseria gonorrhoeae". J. Infect. Dis. 173 (3): 636–46. PMID 8627027.