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      Dermatology for the practicing allergist: Tinea pedis and its complications

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          Abstract

          Tinea pedis is a chronic fungal infection of the feet, very often observed in patients who are immuno-suppressed or have diabetes mellitus. The practicing allergist may be called upon to treat this disease for various reasons. Sometimes tinea infection may be mistaken for atopic dermatitis or allergic eczema. In other patients, tinea pedis may complicate allergy and asthma and may contribute to refractory atopic disease. Patients with recurrent cellulitis may be referred to the allergist/immunologist for an immune evaluation and discovered to have tinea pedis as a predisposing factor. From a molecular standpoint, superficial fungal infections may induce a type2 T helper cell response (Th2) that can aggravate atopy. Th2 cytokines may induce eosinophil recruitment and immunoglobulin E (IgE) class switching by B cells, thereby leading to exacerbation of atopic conditions. Three groups of fungal pathogens, referred to as dermatophytes, have been shown to cause tinea pedis: Trychophyton sp, Epidermophyton sp, and Microsporum sp. The disease manifests as a pruritic, erythematous, scaly eruption on the foot and depending on its location, three variants have been described: interdigital type, moccasin type, and vesiculobullous type. Tinea pedis may be associated with recurrent cellulitis, as the fungal pathogens provide a portal for bacterial invasion of subcutaneous tissues. In some cases of refractory asthma, treatment of the associated tinea pedis infection may induce remission in airway disease. Very often, protracted topical and/or oral antifungal agents are required to treat this often frustrating and morbid disease. An evaluation for underlying immuno-suppression or diabetes may be indicated in patients with refractory disease.

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          Most cited references43

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          Dermatophyte infections.

          B L Hainer (2003)
          Dermatophytes are fungi that require keratin for growth. These fungi can cause superficial infections of the skin, hair, and nails. Dermatophytes are spread by direct contact from other people (anthropophilic organisms), animals (zoophilic organisms), and soil (geophilic organisms), as well as indirectly from fomites. Dermatophyte infections can be readily diagnosed based on the history, physical examination, and potassium hydroxide (KOH) microscopy. Diagnosis occasionally requires Wood's lamp examination and fungal culture or histologic examination. Topical therapy is used for most dermatophyte infections. Cure rates are higher and treatment courses are shorter with topical fungicidal allylamines than with fungistatic azoles. Oral therapy is preferred for tinea capitis, tinea barbae, and onychomycosis. Orally administered griseofulvin remains the standard treatment for tinea capitis. Topical treatment of onychomycosis with ciclopirox nail lacquer has a low cure rate. For onychomycosis, "pulse" oral therapy with the newer imidazoles (itraconazole or fluconazole) or allylamines (terbinafine) is considerably less expensive than continuous treatment but has a somewhat lower mycologic cure rate. The diagnosis of onychomycosis should be confirmed by KOH microscopy, culture, or histologic examination before therapy is initiated, because of the expense, duration, and potential adverse effects of treatment.
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            Molecular analysis of Malassezia microflora on the skin of atopic dermatitis patients and healthy subjects.

            Members of the genus Malassezia, lipophilic yeasts, are considered to be one of the exacerbating factors in atopic dermatitis (AD). We examined variation in cutaneous colonization by Malassezia species in AD patients and compared it with variation in healthy subjects. Samples were collected by applying transparent dressings to the skin lesions of AD patients. DNA was extracted directly from the dressings and amplified in a specific nested PCR assay. Malassezia-specific DNA was detected in all samples obtained from 32 AD patients. In particular, Malassezia globosa and M. restricta were detected in approximately 90% of the AD patients and M. furfur and M. sympodialis were detected in approximately 40% of the cases. The detection rate was not dependent on the type of skin lesion. In healthy subjects, Malassezia DNA was detected in 78% of the samples, among which M. globosa, M. restricta, and M. sympodialis were detected at frequencies ranging from 44 to 61%, with M. furfur at 11%. The diversity of Malassezia species found in AD patients was greater (2.7 species detected in each individual) than that found in healthy subjects (1.8 species per individual). Our results suggest that M. furfur, M. globosa, M. restricta, and M. sympodialis are common inhabitants of the skin of both AD patients and healthy subjects, while the skin microflora of AD patients shows more diversity than that of healthy subjects. To our knowledge, this is the first report of the use of a nested PCR as an alternative to fungal culture for analysis of the distribution of cutaneous Malassezia spp.
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              New yeast species, Malassezia dermatis, isolated from patients with atopic dermatitis.

              Malassezia species are considered to be one of the exacerbating factors in atopic dermatitis (AD). During examination of the cutaneous colonization of Malassezia species in AD patients, we found a new species on the surface of the patients' skin. Analysis of ribosomal DNA sequences suggested that the isolates belonged to the genus MALASSEZIA: They did not grow in Sabouraud dextrose agar but utilized specific concentrations of Tween 20, 40, 60, and 80 as a lipid source. Thus, we concluded that our isolates were new members of the genus Malassezia and propose the name Malassezia dermatis sp. nov. for these isolates.
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                Author and article information

                Journal
                Clin Mol Allergy
                Clinical and molecular allergy : CMA
                BioMed Central (London )
                1476-7961
                2004
                29 March 2004
                : 2
                : 5
                Affiliations
                [1 ]Department of Internal Medicine, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, USA
                [2 ]James H. Quillen V.A. Medical Center Mountain Home, Tennessee, USA
                Article
                1476-7961-2-5
                10.1186/1476-7961-2-5
                419368
                15050029
                a7fae07f-509c-4973-bd74-46a94dc9db1d
                Copyright © 2004 Al Hasan et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
                History
                : 25 November 2003
                : 29 March 2004
                Categories
                Review

                Immunology
                trichophyton mentagrophytes,cellulitis,asthma,trichophyton rubrum,immunity,epidermophyton floccosum,antifungal agents,allergy,tinea pedis,dermatitis,type 2 t helper cytokines,ige

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