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Pathogenesis of tinea
Author(s) -
Brasch Jochen
Publication year - 2010
Publication title -
jddg: journal der deutschen dermatologischen gesellschaft
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.463
H-Index - 60
eISSN - 1610-0387
pISSN - 1610-0379
DOI - 10.1111/j.1610-0387.2010.07481.x
Subject(s) - dermis , pathogenesis , keratin , epidermis (zoology) , immune system , immunology , biology , innate immune system , microbiology and biotechnology , dermatophyte , nail (fastener) , materials science , anatomy , metallurgy , paleontology
Summary Dermatophytes are hyphomycetes that can degrade keratin. This puts them in a position to cause infections of the keratin‐containing superficial skin. The resulting clinical picture is called tinea. The pathogenesis and course of tinea is decisively determined by pathogen‐related factors and by the defense mechanisms of the host. An infection starts with an adherence of fungal propagules, followed by the formation of hyphae that can spread within the tissue. This process is accompanied by a release of fungal enzymes and other pathogenic factors. Next keratinocytes are activated, the epidermal barrier is destroyed, epidermal proliferation is enhanced and defensins are expressed within the epidermis. In addition, innate and specific immune responses are initiated, involving neutrophilic granulocytes, macrophages, antibodies and T cells. The cellular mechanisms are thought to be crucial for healing. Special conditions apply to nail infections, because within nail plates the fungi are not accessible to effective defense mechanisms, as well as to infections of hair follicles that contain specific concentrations of steroid hormones. Dermatophytes that penetrate into the dermis can cause granulomatous inflammatory reactions and systemic immune reactions are supposed to be a trigger of so‐called id reactions.