Gonorrhea pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Mehrsefat, M.D. [2]
Overview
Pathophysiology
Gonorrhea is a sexually transmitted disease (STD) that is caused by Neisseria gonorrhea. Neisseria gonorrhea is gram-negative intracellular diplococcus, oxidase-positive, utilizes glucose, but not sucrose, maltose, or lactose. It can infectmucus-secreting epithelial cells both in men and women.
Transmission
The recognized routes of transmission of the Neisseria gonorrhoeae include:
- Male to female via semen. The transmission rate is estimated to be 50%-70% per episode of vaginal intercourse
- Female vagina to male urethra. The transmission rate is estimated to be 20% per episode of vaginal intercourse and increases to 60%-80% after 4 or more exposures.
- Rectal intercourse
- Fellatio and less commonly cunnilingus can result in pharyngeal gonorrhea
- Perinatal transmission
Virulence factors
The recognized virulence factors of the Neisseria gonorrhoeae include:
- The main pathogenicity of the Neisseria gonorrhea obtains from the surface pili by following mechanisms:[1][2][3]
- Mediate attachment to on the surface of the urethra, fallopian tubes and endocervix
- Preventing phagocytosis by neutrophils
- Opa proteins (opacity-associated protein) is a surface proteins that helps gonococcus binds to receptors on immune cells[4][5][6]
- Down-regulate activated CD4 cells (prevent an Immune response)
- Inhibit B-cell antibody production (unable immunological memory against gonorrhea)
- Porin, two main serotypes have been identified:[7][8][9]
- PorB.1A strains
- Have ability to bind to complement inhibitory molecules and resulting in a diminished inflammatory response (disseminated gonococcal infection)
- PorB.1B strains
- Cause local genital infections only
- PorB.1A strains
- Lipooligosaccharides (LOS)
- LOS binds to human asialoglycoprotein receptor (ASGP-R) expressed on sperm cells and urethral epithelial cells
- Gonococcal ribosomal protein L12
- allows attachment to and invasion of an endometrial cell line via interaction with the lutropin receptor (LHr) which lead to pelvic inflammatory disease (PID) or disseminated gonococcal infection (DGI) in women
- Release of IgA1 proteases[10][11]
- The exact pathogenesis is not fully understood. It is though that IgA protease may play a role gonococcal infection in women
In pregnancy, gonococcus can be transmitted to the fetus at the time of delivery. This results in infection of the conjuctiva. This appears 1 to 4 days after birth as severe discharge with marked swelling and redness of the eyelids and conjunctiva.
Associated Conditions
HIVinfection
Gonorrhea is associated with increased susceptibility to the transmission of HIV infection. It is thought, gonorrhea infections can result in the increase HIV shedding in individuals.
References
- ↑ 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.
- ↑ Jerse AE, Cohen MS, Drown PM, Whicker LG, Isbey SF, Seifert HS; et al. (1994). "Multiple gonococcal opacity proteins are expressed during experimental urethral infection in the male". J Exp Med. 179 (3): 911–20. PMC 2191399. PMID 8113683.
- ↑ Boulton IC, Gray-Owen SD (2002). "Neisserial binding to CEACAM1 arrests the activation and proliferation of CD4+ T lymphocytes". Nat Immunol. 3 (3): 229–36. doi:10.1038/ni769. PMID 11850628.
- ↑ Pantelic M, Kim YJ, Bolland S, Chen I, Shively J, Chen T (2005). "Neisseria gonorrhoeae kills carcinoembryonic antigen-related cellular adhesion molecule 1 (CD66a)-expressing human B cells and inhibits antibody production". Infect Immun. 73 (7): 4171–9. doi:10.1128/IAI.73.7.4171-4179.2005. PMC 1168567. PMID 15972507.
- ↑ Young JD, Blake M, Mauro A, Cohn ZA (1983). "Properties of the major outer membrane protein from Neisseria gonorrhoeae incorporated into model lipid membranes". Proc Natl Acad Sci U S A. 80 (12): 3831–5. PMC 394146. PMID 6407021.
- ↑ Ram S, Cullinane M, Blom AM, Gulati S, McQuillen DP, Monks BG; et al. (2001). "Binding of C4b-binding protein to porin: a molecular mechanism of serum resistance of Neisseria gonorrhoeae". J Exp Med. 193 (3): 281–95. PMC 2195916. PMID 11157049.
- ↑ Ram S, McQuillen DP, Gulati S, Elkins C, Pangburn MK, Rice PA (1998). "Binding of complement factor H to loop 5 of porin protein 1A: a molecular mechanism of serum resistance of nonsialylated Neisseria gonorrhoeae". J Exp Med. 188 (4): 671–80. PMC 2213355. PMID 9705949.
- ↑ Lin L, Ayala P, Larson J, Mulks M, Fukuda M, Carlsson SR; et al. (1997). "The Neisseria type 2 IgA1 protease cleaves LAMP1 and promotes survival of bacteria within epithelial cells". Mol Microbiol. 24 (5): 1083–94. PMID 9220014.
- ↑ Hobbs MM, Sparling PF, Cohen MS, Shafer WM, Deal CD, Jerse AE (2011). "Experimental Gonococcal Infection in Male Volunteers: Cumulative Experience with Neisseria gonorrhoeae Strains FA1090 and MS11mkC". Front Microbiol. 2: 123. doi:10.3389/fmicb.2011.00123. PMC 3119411. PMID 21734909.