A new minimal medium consisting only of L-tryptophan (L-Trp) and a lipid source induced formation of brown pigmentation only in the species Malassezia furfur, which diffuses into the agar. Strains of the species M. sympodialis and M. pachydermatis failed to grow on this medium. On mDixon medium, however, after replacement of peptone by L-Trp, growth of all three Malassezia species was achieved. Under these conditions pigment production was observed with all M. furfur strains tested, although the results for M. pachydermatis strains were inconsistent. M. sympodialis strains showed no pigment production. On the minimal medium pigmentogenesis was induced in M. furfur by only 0.01 g% tryptophan; the pH optimum was pH 5. In all M. furfur strains, alternative amino nitrogen sources given concurrently with Trp suppressed pigmentogenesis. Furthermore, there were differences in the optimal temperature among the individual M. furfur strains. CBS 7019, CBS 6000 and CBS 6001 failed to produce pigment at 37 degrees C. The extract of the culture exhibited remarkable fluorescence, and several indole derivatives with a broad spectrum of colours were detected. This finding may have an impact on the clinical appearance of pityriasis versicolor, a very common skin disease caused by lipophilic yeasts of the genus Malassezia. We hypothesize that in pityriasis versicolor metabolic adaptation of Malassezia yeasts to altered nitrogen conditions on superficial skin might be of patho-physiological importance. Tryptophan as an inducer of pigmentogenesis probably accumulates during excessive sweating, a well-known manifestation of pityriasis versicolor.
Pityriasis versicolor is the most common skin mycosis in humans worldwide. Yeasts of the genus Malassezia, particularly M. furfur, a saprophyte occurring widely on human skin, are generally regarded as the causative agents. Pityriasis versicolor is often accompanied by a long-lasting depigmentation that persists even after successful antimycotic therapy. M. furfur is able to convert tryptophan into a variety of indole alkaloids, some of them showing biological properties that correlate well with certain clinical features of pityriasis versicolor. This suggests a possible role for these compounds in the depigmentation process. We now report that human melanocytes undergo apoptosis when exposed to the crude mixture of tryptophan metabolites from M. furfur. The active compound was identified as malassezin, previously isolated by us from the same source and characterized as an agonist of the aryl hydrocarbon (Ah) receptor. The compound could, therefore, contribute to the marked depigmentation observed during the course of pityriasis versicolor.
Pityriasis versicolor alba is a hypopigmented or depigmented variant of pityriasis versicolor characterized by maculous, partly pityriasiform, scaly depigmented lesions occurring particularly in seborrhoeic areas. Long-persisting hypopigmentation after healing of the pityriasis versicolor was first described by Gudden in 1853. Hypopigmentation and depigmentation were later differentiated as an independent variant of the disease. In 1848, Eichstedt recognized the pathogen-related character of pityriasis versicolor in its hyperpigmented form. Today it is generally accepted that the disease is caused by yeasts of the genus Malassezia, of which nine species are differentiated. It is controversial whether a single species is responsible for the disease. The pathogenesis of depigmentation has not been established. A screening effect by the scale layer as well as toxic effects on pigment synthesis by fungal metabolites have been discussed. With regard to the second mechanism, the newly discovered tryptophan-derived metabolites of M. furfur might be significant. Evidence-based data concerning the therapy of pityriasis versicolor alba do not exist. According to current recommendations, pityriasis versicolor should be rapidly treated with antimycotics, followed by ultraviolet therapy to induce maturation of existent melanosomes and accelerate repigmentation. However, depigmented lesions are difficult to improve by ultraviolet therapy.
In diabetic patients, mycotic infections may increase the risk of developing diabetic foot syndrome. However, few data are available on the prevalence of fungal foot infections in patients with diabetes. During a conference attended by patients with long-term diabetes, 95 individuals with type 1 diabetes mellitus (52 men, 43 women, mean disease duration 35.8 years) were examined for fungal infections of the feet. As well as frequency of infection and risk profiles, the level of patient awareness and preventive measures taken were assessed by means of a questionnaire. Clinically, 78 patients (82.1 %) showed probable pedal fungal infections, of which 84.6 % (66/78) were mycologically confirmed by direct microscopy and/or culture. Skin mycoses were found in 9 patients (toe webs 5, soles 4), onychomycosis in 29 patients and simultaneous infection of nails and skin in 28 patients (toe webs 8, soles 20). Thirty-seven (47.4 %) of these patients had positive cultures, particularly for the dermatophyte Trichophyton rubrum (69.2 % of isolates). A significant correlation was found between infection and gender (men more frequently affected) and the age of the patients. The actual frequency of mycoses was underestimated by the patients. This correlated with the assessment of their own knowledge level concerning fungal infections: 83.2 % of patients with skin mycoses and 88.4 % of those with onychomycosis of the feet felt that they needed more information about their disease. Marked mycoses on the soles were often considered to be dry skin by the patients. The high number of infections detected is especially remarkable in that this group of patients were highly motivated. It therefore appears that diabetics require more diagnostic, therapeutic and preventive care in terms of mycotic diseases than has been previously thought.
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