Dermatophytosis pathophysiology: Difference between revisions
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*Fungal arthroconidia attach to keratinocytes via long and sparse microprojections (fibrils).<ref name="pmid18478361">{{cite journal |vauthors=Vermout S, Tabart J, Baldo A, Mathy A, Losson B, Mignon B |title=Pathogenesis of dermatophytosis |journal=Mycopathologia |volume=166 |issue=5-6 |pages=267–75 |year=2008 |pmid=18478361 |doi=10.1007/s11046-008-9104-5 |url=}}</ref> | *Fungal arthroconidia attach to keratinocytes via long and sparse microprojections (fibrils).<ref name="pmid18478361">{{cite journal |vauthors=Vermout S, Tabart J, Baldo A, Mathy A, Losson B, Mignon B |title=Pathogenesis of dermatophytosis |journal=Mycopathologia |volume=166 |issue=5-6 |pages=267–75 |year=2008 |pmid=18478361 |doi=10.1007/s11046-008-9104-5 |url=}}</ref> | ||
====Penetration==== | ====Penetration==== | ||
*Penetration by dermatophytes is achieved by secreting multiple serine-subtilisins and metallo-endoproteases (fungalysins) formerly called keratinases that are found only in the dermatophytes.<ref name="pmid8077506">{{cite journal |vauthors=Dahl MV |title=Dermatophytosis and the immune response |journal=J. Am. Acad. Dermatol. |volume=31 |issue=3 Pt 2 |pages=S34–41 |year=1994 |pmid=8077506 |doi= |url=}}</ref> | |||
*Fungal mannans in the dermatophyte cell wall have immunosupressive ability and inhibit the action of T cells. T. rubrum cell wall mannans (TRM) may lead to inhibition of lymphoproliferative response of mononuclear leukocytes. This leads to fungal growth and proliferation on the host skin. | |||
====Host response==== | |||
*Fungal metabolic products diffuse through the stratum basale and stratum spinosum to cause erythema, vesicle or even pustule formation and pruritus. | |||
*Acutely, the host responds to fungal invasion by | |||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]
Overview
Pathophysiology
Pathogenesis
- Dermatophytes survive on the outer layer of skin called stratum corneum.
- Stratum corneum has been known to be not only source of nutrition for the dermatophytes, but also the growing fungal mycelia.[1]
- After the inoculation in the host skin, suitable conditions favor the infection to progress through the following stages:
Adherence
- Dermatophyte-secreted proteases not only are mediate adherence to the host skin but also help in germination of arthroconidia and hyphal growth leading to growth of the fungi in multiple directions.[2][3]
- Fungal arthroconidia attach to keratinocytes via long and sparse microprojections (fibrils).[3]
Penetration
- Penetration by dermatophytes is achieved by secreting multiple serine-subtilisins and metallo-endoproteases (fungalysins) formerly called keratinases that are found only in the dermatophytes.[4]
- Fungal mannans in the dermatophyte cell wall have immunosupressive ability and inhibit the action of T cells. T. rubrum cell wall mannans (TRM) may lead to inhibition of lymphoproliferative response of mononuclear leukocytes. This leads to fungal growth and proliferation on the host skin.
Host response
- Fungal metabolic products diffuse through the stratum basale and stratum spinosum to cause erythema, vesicle or even pustule formation and pruritus.
- Acutely, the host responds to fungal invasion by
References
- ↑ Samdani AJ (2005). "Dermatophyte growth and degradation of human stratum corneum in vitro (pathogenesis of dermatophytosis)". J Ayub Med Coll Abbottabad. 17 (4): 19–21. PMID 16599028.
- ↑ Aljabre SH, Richardson MD, Scott EM, Rashid A, Shankland GS (1993). "Adherence of arthroconidia and germlings of anthropophilic and zoophilic varieties of Trichophyton mentagrophytes to human corneocytes as an early event in the pathogenesis of dermatophytosis". Clin. Exp. Dermatol. 18 (3): 231–5. PMID 8348716.
- ↑ 3.0 3.1 Vermout S, Tabart J, Baldo A, Mathy A, Losson B, Mignon B (2008). "Pathogenesis of dermatophytosis". Mycopathologia. 166 (5–6): 267–75. doi:10.1007/s11046-008-9104-5. PMID 18478361.
- ↑ Dahl MV (1994). "Dermatophytosis and the immune response". J. Am. Acad. Dermatol. 31 (3 Pt 2): S34–41. PMID 8077506.