Dermatophytosis pathophysiology
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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 Type IV delayed type hypersensitivity reaction (also known as "Trichophytin reaction) leading to a cell mediated response.[5]
- Interferon-α secretion from type 1 T-helper lymphocytes, cytokines like interferon-γ (IFN-γ), IL-8 and macrophages are the effector mechanisms involved in defense against dermatophytes acutely.[6]
- IL-8 mediated chemotaxis allows polymorphonuclear leukocytes adhere to opsonized and unopsonized hyphae to inhibit growth of the dermatophyte.[4]
- The dermatophyte antigen is thought to be processed by epidermal Langerhans cells and presented in local lymph nodes to T lymphocytes which proliferate, migrate to the infected site, and produce inflammation.[7]
- The immune response, and especially the level of inflammation, is different for different dermatophyte species, the host species and the pathophysiological status of the host. In general, the zoophilic species cause more inflammatory infections, which may heal spontaneously and result in relative resistance to re-infection. The anthropophilic species usually cause more chronic, less circumscribed infections, which consequently lead to a poor resistance to re-infection.
- Cell-associated as well as secreted factors contribute to the dermatophyte's ability to exaggerate or suppress an inflammatory response.
- Many host factors for example, number and activity of sebaceous glands (due to inhibitory effect of sebum on dermatophytes) in a particular body region, breaks in the integrity of skin barrier, moisturized and macerated skin can promote invasion of dermatophytes.
- Fungus secreted proteases are one of the most important virulence factors of dermatophytes and are thought to be responsible for evasion from host defense mechanisms.[7]
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.
- ↑ 4.0 4.1 Dahl MV (1994). "Dermatophytosis and the immune response". J. Am. Acad. Dermatol. 31 (3 Pt 2): S34–41. PMID 8077506.
- ↑ Almeida SR (2008). "Immunology of dermatophytosis". Mycopathologia. 166 (5–6): 277–83. doi:10.1007/s11046-008-9103-6. PMID 18478362.
- ↑ Brasch J (2009). "Current knowledge of host response in human tinea". Mycoses. 52 (4): 304–12. doi:10.1111/j.1439-0507.2008.01667.x. PMID 19207841.
- ↑ 7.0 7.1 Tainwala R, Sharma Y (2011). "Pathogenesis of dermatophytoses". Indian J Dermatol. 56 (3): 259–61. doi:10.4103/0019-5154.82476. PMC 3132899. PMID 21772583.