Pediatric Tinea Versicolor Clinical Presentation
- Author: Lyubomir A Dourmishev, MD, PhD; Chief Editor: Dirk M Elston, MD more...
Questioning the patient with tinea versicolor about skin or systemic diseases, current therapy, and drug allergies provides guidance in selecting an appropriate therapy. The following are factors that may be used to guide therapy:
Other diseases, including renal disease, hepatic disease, and endocrine disease (eg, diabetes mellitus)
History of HIV or other immunocompromising disorder, which can increase the severity of tinea versicolor
Other skin disorders, including personal or family history of atopy or other eczematous conditions
Current or recent topical or systemic therapy
Seasonal variations in skin color
Use of some body oils, which may supply additional nutrients to the M furfur
Sweat associated with exercise, which may contribute to disease development and recurrence
Skin lesions are either hypopigmented or hyperpigmented maculae in various shapes. Hyperpigmented maculae become hypopigmented after solar irradiation and subsequent tanning, as the name implies.
Lesions are either macules or very superficial plaques with fine scale that may not be evident except upon close examination. Even when scale is not apparent, when the skin is wiped with a wet cloth and scraped for examination, it yields a surprising amount of dirty-brown keratin. If not, the areas of dyschromia may represent residual effects of previously treated tinea versicolor. Occasionally, determining whether the lighter or darker skin is affected is difficult.
Lesions have relatively sharp margins and may be lighter or darker than the normal skin color. The lesions are frequently a light tan color in light-skinned individuals. The color of lesions varies from individual to individual, but each individual's lesions are approximately the same color. Lesions are evenly pigmented. The inflammatory border, relative central clearing, and erythema seen in most fungal infections are lacking.
Small lesions are usually circular or oval. Confluent patches with scattered circular or oval macules around the edges are common. Other lesions may be large enough to cover most of the trunk.
Lesions are usually asymptomatic but may be mildly pruritic. The pruritus is more intense when the patient is excessively warm.
Residual hypopigmentation, without overlying scale, may remain for many months following effective treatment. These areas may become more apparent following sun exposure, causing the patient to incorrectly suspect that the infection has recurred.
Examples of findings in tinea versicolor are shown in the images below.
The upper trunk is most commonly affected, but the lesions often spread to the upper arms, antecubital fossae, neck, abdomen, and popliteal fossae. Lesions in the axillae, groin, thighs, and genitalia are less common. Facial, scalp, and palmar lesions occur in the tropics but are rare in temperate zones
In some patients, tinea versicolor primarily affects the flexural regions, the face or isolated areas of the extremities. This unusual pattern of tinea versicolor is seen more often in immunocompromised hosts and can be confused with candidiasis, seborrheic dermatitis, psoriasis, erythrasma, and dermatophyte infections.
Lesions that are imperceptible or doubtful are more visible using a Wood lamp in a darkened room.
M furfur is now the most commonly accepted name for the etiologic agent of tinea versicolor. Thus, P orbiculare, P ovale, and Malassezia ovalis are synonyms .
M furfur is a dimorphic lipophilic organism that is cultured only in media enriched with C12-sized or C14-sized fatty acids. Malassezia is able to exist in both yeast and mycelial forms, with yeast most commonly associated with saprofital form (P ovale). Historically, the name M furfur was used to designate the fungal pathogen of tinea versicolor before it is grown in culture. M furfur is not a dermatophyte, does not grow on dermatophyte test media (DTM), and does not respond to griseofulvin therapy.
With the advent of DNA sequencing, numerous pathogenic and nonpathogenic species were found. Some of them appear to be more common in certain areas of the world, and some are more likely to be pathogenic in one area and not in another. Much of the confusion was resolved with the taxonomic revision in 1996, based on sequencing of the large-subunit rRNA and nuclear DNA of more than 100 isolates of Malassezia species. The genus Malassezia was revised to include 7 species: Malassezia globosa, Malassezia sympodialis, M furfur, Malassezia slooffiae, Malassezia pachydermatis, Malassezia restricta, and Malassezia obtusa. The clinical significance of each of these species is under investigation. A study of the epidemiology of Malassezia yeasts associated with pityriasis (tinea) versicolor in Canada revealed the most frequently isolated species included M sympodialis, M globosa, and M furfur.
One study found M globosa in 97% of patients with tinea versicolor; it was found alone in 60% of cases, was associated with M sympodialis in 29% of cases, and was associated with M slooffiae in 7% of cases. M sympodialis and M slooffiae were found in similar percentages on clinically uninvolved skin of the trunk, whereas M globosa was not isolated at other sites. Thus, some authors suggest that M globosa in its mycelial phase is the causative agent of tinea versicolor.[2, 3]
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