Pitiriasis versicolor por Malassezia pachydermatis: caso clínico / Pityriasis versicolor caused by Malassezia pachydermatis: clinical case

Se presenta un caso clínico de pitiriasis versicolor por M. pachydermatis en una paciente de 11 años de edad, diagnosticado mediante clínica, morfofisiología y biología molecular. Malassezia pachydermatis es parte de la microbiota común de diversos mamíferos domésticos y animales salvajes. En éstos se reconoce como agente causal de dermatitis y otitis externa. En humanos se han descrito escasas infecciones ya sea superficiales como invasoras, lo que puede atribuirse a la difícil transmisión y adaptación a partir de los animales domésticos. Se comentan los aspectos biológicos y epidemiológicos de esta infección zoonótica.

A clinical case of pityriasis versicolor caused by M. pachydermatis in an 11 year old patient which was diagnosed by means of clinic, morphophysiology and molecular biology is presented. Malassezia pachydermatis is part of regular microbiota in several domestic mammals as well as wild animals. It is recognized as the causing agent of dermatitis and external otitis in the latter. As to human beings, superficial infections have rarely been given an invasive character what can be explained by the difficult transmission and adaptation coming from domestic animals. Biological and epidemiological aspects of this zoonotic infection are described.

Historical aspects of dermatomycoses.

Physicians have been aware of superficial fungal infections for centuries, but the causal agents and treatments of fungal infections remained unknown until the mid-1800s, when numerous important findings were reported. Among the relevant researchers in the field of superficial mycoses were Remak, who found the fungal nature of favus in 1837; Berg, who reported oral candidosis in 1841; and Wilkinson, who described vaginal candidosis in 1849. Tinea versicolor was described clinically in 1846 by Eichstedt, and its etiologic agent was identified in 1853. Beigel reported white piedra in 1856, and Cerqueira, tinea nigra in 1891. The book Les Tiegnes was published by Sabouraud in 1910, and black piedra infection was described by Horta in 1911. In 1927, Nannizzi reported the description of the sexual state of Microsporum gypseum. The current classification of dermatophytes was published by Emmons in 1934, and the taxonomy of yeast fungi was described by Lodder and Kreger-van Rij in 1952. Finally, the successful treatment of tinea capitis with griseofulvin by Gentles in 1958 saved many patients with tinea capitis from permanent hair loss, a common side effect after treatment with thallium. (c) 2010 Elsevier Inc. All rights reserved.

Pityriasis versicolor alba.

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.