Tinea Versicolor Workup

Updated: Jun 09, 2020
  • Author: Christopher Sayed, MD; Chief Editor: Dirk M Elston, MD  more...
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Laboratory Studies

The clinical presentation of tinea versicolor is distinctive, and the diagnosis is often made without any laboratory documentation.

The ultraviolet black light (Wood lamp) can be used to demonstrate the coppery-orange fluorescence of tinea versicolor. However, in some cases, the lesions appear darker than the unaffected skin under the Wood lamp, but they do not fluoresce.

The diagnosis is usually confirmed by potassium hydroxide (KOH) examination, which demonstrates the characteristic short, cigar-butt hyphae that are present in the diseased state. The KOH finding of spores with short mycelium has been referred to as the spaghetti and meatballs or the bacon and eggs sign of tinea versicolor. For better visualization, ink blue stain, Parker ink, methylene blue stain, or Swartz-Medrik stain can be added to the KOH preparation. Contrast stain containing 1% Chicago sky blue 6B and 8% KOH (as the clearing agent) achieves the greatest sensitivity and specificity. [34]

Special media are required for culture. Because the diagnosis is usually clinically suspected and can be confirmed with a KOH preparation, cultures are rarely obtained.

With blood examination, no definitive deficiencies of normal antibodies or complement are present in patients with tinea versicolor, but research continues in this area. For example, although individuals who are affected reveal no specific antibody levels above those of age-matched controls, M furfur antigens do elicit a specific immunoglobulin G response in patients with seborrheic dermatitis and tinea versicolor detected by enzyme-linked immunosorbent assay and Western blotting assays. M furfur does induce immunoglobulin A, immunoglobulin G, and immunoglobulin M antibodies, and it can activate complement via both the alternate pathway and the classical pathway.

Various studies have found defects in lymphokine production, natural killer T cells, decreased phytohemagglutinin and concanavalin A stimulation, interleukin 1, interleukin 10, and interferon gamma production by lymphocytes in patients.

Although these tests do not suggest an immunologic disorder, they do suggest a reduced body response to the specific fungal elements that produce tinea versicolor. Further assessment is warranted.


Histologic Findings

The organism that causes tinea versicolor is localized to the stratum corneum. M furfur can be detected by hematoxylin and eosin (H&E) alone, although periodic acid-Schiff (PAS) or methenamine silver staining are more confirmatory. On rare occurrences, the organism can approach the stratum granulosum, and it can even be found inside keratinocytes. [35] The epidermis reveals mild hyperkeratosis and acanthosis, and a mild perivascular infiltrate is present in the dermis. An acanthosis nigricans–like epidermal change is noted in the papular variety, with dilated blood vessels observed in erythematous lesions.