What is the pathophysiology of pediatric tinea versicolor?

Updated: Jan 27, 2020
  • Author: Lyubomir A Dourmishev, MD, PhD; Chief Editor: Dirk M Elston, MD  more...
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The nutritional requirement of M furfur is one of the most important factors that affect the growth of the organism on the skin. Studies show that lesion sites have a decrease in sebaceous gland secretions and water content, along with an increase in pH value compared with normal skin. M furfur is lipophilic, and the mycelial stage of M furfur can be induced in vitro by the addition of cholesterol and cholesterol esters to the appropriate medium. However, significantly more amino acids are extracted from the skin of infected patients, suggesting that amino acids, rather than lipids, are critical for the development of the disease. In vitro, the amino acid asparagine stimulates the growth of the organism, while glycine induces hyphal formation.

Patient immune response also affects infection. Studies suggest a reduced body response to the specific fungal elements that produce tinea versicolor. In various studies, defects in lymphokine production and natural killer T cells were found; phytohemagglutinin (PHA) and concanavalin A (Con A) stimulation was decreased; and interleukin (IL)–2, IL-10, and interferon (IFN)–g production by lymphocytes was decreased in affected patients. The exact pathophysiology of this disorder remains undefined, and additional studies are needed.

In patients with hypopigmentation, tyrosinase inhibitors competitively inhibit an enzyme necessary for melanocyte pigment formation. In hyperpigmented macules, the organism induces enlargement of melanosomes made by melanocytes in the basal layer of the epidermis.

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