Answer of Dermatopathology Case 69

Dermatophyte Infection (Dermatophytoses) - Superficial filamentous Infection (Tinea - ringworm)

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Abstract:

Current knowledge of host response in human tinea.Mycoses.2009 Jan 21.
Summary Skin infection caused by dermatophytes is called tinea. In this short review, the known mechanisms and factors involved in human tinea and important for the host response are briefly delineated. To establish tinea, fungal propagules must attach to the skin, germinate and overcome the epidermal barrier. Keratinases and other enzymes are released in this process and host keratinocytes are activated. This is followed by an inflammatory response mediated by a plentitude of cytokines and receptors, comprising innate as well as acquired immunity, including neutrophilic granulocytes, macrophages, antibodies and T cells. Cellular defence mechanisms appear to be decisive for clearing of infection. Nails and hair follicles are the particular sites often invaded by dermatophytes that show distinctive patterns of infection. Nails are largely excluded from defence mechanisms and steroid hormones of the pilosebaceous units may have a particular effect on follicular infection. Fungal invasion of the dermis can cause granulomatous reactions. Immune reactions to dermatophytes may lead to sterile eruptions distant from the infected skin areas.

Pathogenesis of dermatophytosis and tinea versicolor. Clin Dermatol. 2010 Mar 4;28(2):185-9.
Dermatophytoses are infections caused by keratinophilic fungi known as dermatophytes. Several steps are required for infection to take place: contact, adherence, and invasion of keratin layers. The severity of the infection depends on the type of agent, environmental factors, and the host immunologic status. Tinea versicolor is caused by the Malassezia spp yeasts, which are microorganisms that belong to normal biota in seborrheic areas, but some contributing factors, such as the application of oily preparations, creams, an increase in ambient humidity, corticosteroid abuse, or genetic predisposition can induce its overgrowth in both filamentous and yeast structures. Exposure to sunlight stimulates the production of azelaic acid, which causes the appearance of hypopigmented spots. Currently, there is no scientific explanation for hyperpigmented lesions.

Evaluation of a modified microscopic direct diagnosis of dermatophytosis. J Microbiol Methods. 2010 May;81(2):205-7. Epub 2010 Mar 6.
Here we present a modified protocol for dematophyte diagnosis, utilizing a simple centrifugation step to significantly decrease false-negative results of the original KOH direct microscopy-based technique. Although culture constitutes the gold-standard diagnosis, the time spent for results is a limit. Fast and low-cost techniques are important for infection screening in underdeveloped countries.

The dermatophytes. Clin Microbiol Rev.1995 Apr;8(2):240-59.
The etiologic agents of the dermatophytoses (ringworm) are classified in three anamorphic (asexual or imperfect) genera, Epidermophyton, Microsporum, and Trichophyton. Species capable of reproducing sexually belong in the teleomorphic genus, Arthroderma, of the Ascomycota. On the basis of primary habitat association, they may be grouped as geophilic (soil associated), zoophilic, and anthropophilic. Adaptation to growth on humans by most geophilic species resulted in diminished loss of sporulation, sexuality, and other soil-associated characteristics. The dermatophytes have the ability to invade keratinized tissue (skin, hair, and nails) but are usually restricted to the nonliving cornified layer of the epidermis because of their inability to penetrate viable tissue of an immunocompetent host. However, invasion does elicit a host response ranging from mild to severe. Acid proteinases, elastase, keratinases, and other proteinases reportedly act as virulence factors. The development of cell-mediated immunity correlated with delayed hypersensitivity and an inflammatory response is associated with clinical cure, whereas the lack of or a defective cell-mediated immunity predisposes the host to chronic or recurrent dermatophyte infection. Chronic dermatophytosis is mostly caused by Trichophyton rubrum, and there is some evidence that mannan produced by this fungus suppresses or diminishes the inflammatory response. Since dermatophytes cause a communicable disease, modes of transmission and control are discussed as well as a survey of recent trends in therapy. Collection of specimens, culture media, and tests for identification are also presented. Genetic studies have led to an understanding of incompatibility mechanisms, pleomorphism and variation, resistance to griseofulvin, and virulence. Molecular biology has contributed to our knowledge of the taxonomy and phylogenetic relationships of dermatophytes.