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Tinea Versicolor: Differential Diagnoses & Workup

Author: Craig G Burkhart, MD, MPH, Clinical Professor, Department of Medicine, Section of Dermatology, The University of Toledo College of Medicine; Clinical Assistant Professor, Department of Dermatology, Ohio State University College of Medicine
Coauthor(s): Lorie Gottwald, MD, Chief, Division of Dermatology, Associate Professor, Department of Internal Medicine, Medical College of Ohio at Toledo; Craig N Burkhart, MD, MSBS, Assistant Professor, Department of Dermatology, University of North Carolina at Chapel Hill
Contributor Information and Disclosures

Updated: Sep 25, 2009

Differential Diagnoses

Erythrasma
Pityriasis Alba
Psoriasis, Guttate
Seborrheic Dermatitis
Tinea Corporis
Vitiligo

Other Problems to Be Considered

Confluent and reticulated papillomatosis of Gougerot and Carteaud

Workup

Laboratory Studies

  • The clinical presentation of tinea versicolor is distinctive, and the diagnosis is often made without any laboratory documentation.
    • The ultraviolet black (Wood) light 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 light, 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.12
    • 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.13 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.

More on Tinea Versicolor

Overview: Tinea Versicolor
Differential Diagnoses & Workup: Tinea Versicolor
Treatment & Medication: Tinea Versicolor
Follow-up: Tinea Versicolor
References
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References

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Further Reading

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Keywords

tinea versicolor, pityriasis versicolor, chromophytosis, dermatomycosis furfuracea, tinea flava, aeromia parasitica, Kleinenflechte, Hodi-Potsy, cutaneous fungal infection, hypopigmented macules, hyperpigmented macules, Malassezia furfur, , Pityrosporon orbiculare, Pityrosporon ovale, Malassezia ovalis, Cushing disease

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Contributor Information and Disclosures

Author

Craig G Burkhart, MD, MPH, Clinical Professor, Department of Medicine, Section of Dermatology, The University of Toledo College of Medicine; Clinical Assistant Professor, Department of Dermatology, Ohio State University College of Medicine
Craig G Burkhart, MD, MPH is a member of the following medical societies: American Academy of Dermatology, Ohio State Medical Association, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Coauthor(s)

Lorie Gottwald, MD, Chief, Division of Dermatology, Associate Professor, Department of Internal Medicine, Medical College of Ohio at Toledo
Lorie Gottwald, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American Medical Association, American Medical Student Association/Foundation, and American Medical Women's Association
Disclosure: Nothing to disclose.

Craig N Burkhart, MD, MSBS, Assistant Professor, Department of Dermatology, University of North Carolina at Chapel Hill
Craig N Burkhart, MD, MSBS is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Kathryn Schwarzenberger, MD, Associate Professor of Medicine, Division of Dermatology, University of Vermont College of Medicine; Consulting Staff, Division of Dermatology, Fletcher Allen Health Care
Kathryn Schwarzenberger, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, American Dermatological Association, Dermatology Foundation, Medical Dermatology Society, and Women's Dermatologic Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Edward F Chan, MD, Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania School of Medicine
Edward F Chan, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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