Dermatophytosis pathogenesis
Dermatophytosis pathophysiologyJump to navigation Jump to search
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2] OverviewDermatophytes mode of transmission is direct (or)indirect contact with skin (or) scalp lesions of infected people,animals (or) fomites. Following transmission, the dermatophytes use proteases to adhere to the stratum corneum of the skin. Penetration by dermatophytes is achieved by secreting multiple serine-subtilisins and metallo-endoproteases (fungalysins) formerly called keratinases that are found only in the dermatophytes. 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. 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. Secreted subtilisin proteases expressed in the dermatophytes could play a role in keratin degradation. Dermatophyte infections of the skin surface (tinea corporis and tinea faciei) mostly present as erythematous, scaly papules that gradually progress to annular or circular red patches or plaques, with central clearing and scaling at the periphery. On microscopic examination of the skin, there may be neutrophils retained in the stratum corneum, parakeratosis, spongiosis and dermal edema. Pathophysiology
PathogenesisAfter the inoculation in the host skin, suitable conditions favor the infection to progress through the following stages: Adherence
Penetration
Host response
Genetics
Gross Pathology
Microscopic PathologyThe following features may be seen on microscopic examination of the skin in dermatophytosis:[12]
References
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