Clinics in Dermatology (2010) 28, 137139

Tinea incognito
Roberto Arenas, MD a,, Gabriela Moreno-Coutio, MD a ,
Lucio Vera, DrSc b , Oliverio Welsh, MD b
Mycology Section, Department of Dermatology, Dr. Manuel Gea Gonzalez General Hospital,
Calzada de Tlalpan 4800, 14080 Mxico, DF, Mxico
b
Department of Dermatology, Dr. Jose Eleuterio Gonzalez University Hospital, Monterrey, Mxico
a

Abstract Tinea incognito was first described 50 years ago. It is a dermatophytic infection with a clinical
presentation modified by previous treatment with topical or systemic corticosteroids, as well as by the
topical application of immunomodulators such as pimecrolimus and tacrolimus. Tinea incognito usually
resembles neurodermatitis, atopic dermatitis, rosacea, seborrheic dermatitis, lupus erythematosus, or
contact dermatitis, and the diagnosis is frequently missed or delayed.
2010 Published by Elsevier Inc.

Introduction
Tinea corporis is clinically defined as patches of scaly
erythema with a slightly elevated border. This picture is
representative of most lesions affecting glabrous skin. One
of the diagnostic challenges in tinea corporis and tinea
capitis is identifying those cases that have been previously
mistreated by self-medication or secondary to the use of
topical and systemic immunosuppressants, such as steroids
and immunomodulators.
The term tinea incognito was originally described in 1968
by Ive and Marks in 14 patients with a dermatophytic
infection that had an atypical clinical presentation caused by
previous treatment with steroids. This occurred in the 1960s
after the introduction of these drugs for the topical treatment
of diverse dermatologic diseases. Since then, other cases have
been described with the topical application of pimecrolimus

Corresponding author. Tel.: + 55 4000 3058; fax: +55 4000 3058.

E-mail address: rarenas98@hotmail.com (R. Arenas).
0738-081X/$ see front matter 2010 Published by Elsevier Inc.
doi:10.1016/j.clindermatol.2009.12.011

and tacrolimus, although topical or systemic use of

corticosteroids continues to be the most common cause.
Over-the-counter access to steroids and other immunosuppressants in some countries, as well as the increase in
medications containing steroids, makes tinea incognito more
likely, and therefore, the diagnosis is frequently missed or
delayed. These drugs suppress the normal cutaneous immune
response to dermatophytes, thus enhancing the development
of fungal superficial infections.1-6
Some physicians, particularly nondermatologists, prescribe combinations of steroids and antifungals, such as
betamethasone and clotrimazole, in which the betamethasone
has a dominant effect over the antifungal agent, thus
exacerbating superficial dermatophytosis.7
As with other dermatophytosis, these infections may
involve patients of any age or sex. All areas may be affected,
but the face and arms are more prevalent; the feet are rarely
affected by this condition, because tinea pedis is an
exceptionally missed diagnosis.
Clinically, these lesions have a less raised margin and are
less scaly than common dermatophytosis. They tend to be

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R. Arenas et al.

Fig. 1

Tinea incognito on the upper part of the back.

pustular, pruritic, extensive, and erythematous and may

mimic other skin diseases (Figure 1). Another clinical form
that can be confused with bacterial infections or prurigo is
trichophytic granuloma (Majocchi granuloma), which is
more commonly found on the legs of women. The fungus
can be inoculated by shaving the legs, and a contributing
factor is the use of corticosteroid creams. It is common to
find tinea pedis or onychomycosis in these cases.
The main differential diagnosis depends on the affected
area. In the face, the lesions may resemble neurodermatitis,
atopic dermatitis, rosacea, seborrheic dermatitis, lupus
erythematosus, or contact dermatitis. A recent study
reported that facial tinea incognito is frequently associated
with tinea pedis or onychomycosis in toenails, or both.8 In
the glabrous skin, the main differential diagnosis is
impetigo, purpura, lichen planus, psoriasis, erythema
migrans, drug eruptions, Sweet neutrophilic dermatosis,
contact dermatitis, discoid lupus, and tuberculoid leprosy.
A 15-year survey from Italy reported 200 cases of tinea
incognito. Of these, 9% had folliculitis, and dermatophytids
were uncommon. The source of infection was human-tohuman transmission. Among elderly patients, the misdiagnosis of dermatitis in the legs associated with venous failure,
was reported as a common cause of tinea incognito. Up to
40% in this series required systemic steroids for treatment of
skin and nondermatologic diseases. For this reason, the
authors underlined the importance of looking for nail
alterations, which can indicate onychomycosis, especially
in chronic forms of tinea incognito.
The clinical history is fundamental, because the clinical
appearance may be confusing. The definitive diagnosis must
be attained in a mycology laboratory or by an expert in
dermatomycology using direct examination with potassium
hydroxide, which demonstrates fungal structures. The
species must be also identified by culture. Occasionally,
the diagnosis is made by histopathology with hematoxylin
and eosin and periodic acid-Schiff stains.9,10

The main etiologic agents reported are Trichophyton

rubrum, T mentagrophytes, Epidermophyton floccosum,
Microsporum canis, M. gypseum, T violaceum, and T erinacei.
The first two are most commonly isolated when the face is
involved.11-33 Fluorinated corticosteroids were implicated in a
hospital dermatophytosis outbreak by E floccosum.34
These dermatophytoses usually require systemic treatment with oral antifungal agents. Terbinafine, itraconazole,
and fluconazole have been shown to be superior to treatment
with griseofulvin, because they accumulate in the skin.
Therapy is generally indicated for 2 weeks, but the clinical
and mycologic responses will determine the definite duration
of treatment.35
In renal transplant patients, an uncommon presentation of
atypical tinea is dermatophytic granuloma. The lesions
evolve into chronic dermatophytosis that can clinically
resemble vasculitis.1

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