Chancroid pathophysiology
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Chancroid pathophysiology On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.; Nate Michalak, B.A.; Serge Korjian M.D.
Overview
Pathophysiology
Transmission
Chancroid may develop after transmission of the bacterium Haemophilus ducreyi through sexual contact.[1]
Pathogenesis
- H. ducreyi enters skin through microabrasions incurred during sexual intercourse.
- H. ducreyi is thought to bind with epithelial cells and then colonize in the subcutaneous tissue.[2]
- H. ducreyi is then presumed to react predominantly with B cell and some T cell markers, which may lead to development of 1 or more erythematous papules. The papule(s) may progress into pustule(s) after further bacterial growth.[2][3]
- Ulcers develop after pustules undergo necrosis.[3] The pathogenesis of ulceration is not fully understood but may involve release of toxic products by H. ducreyi on bacterial-induced inflamation.[2]
- Potential H. ducreyi by-products include:
- Phospholipase C
- Protease
- Elastase
- Lecithinase
- Lipase
- Collagenase
- Potential H. ducreyi by-products include:
- It is presumed that iron plays an essential role in chancroid pathogenesis.[2]
References
- ↑ Chancroid. MedlinePlus (Decemner 2, 2015). https://www.nlm.nih.gov/medlineplus/ency/article/000635.htm Accessed January 6, 2015.
- ↑ 2.0 2.1 2.2 2.3 Abeck D, Johnson AP (1992). "Pathophysiological concept of Haemophilus ducreyi infection (chancroid)". Int J STD AIDS. 3 (5): 319–23. PMID 1391058.
- ↑ 3.0 3.1 Chancroid. Wikipedia (July 16, 2015). https://en.wikipedia.org/wiki/Chancroid Accessed on January 6, 2016.