Optimizing Topical Antifungal Therapy for Superficial Cutaneous Fungal Infections: Focus on Topical Naftifine for Cutaneous Dermatophytosis

November 2013 | Volume 12 | Issue 11 | Supplement Individual Articles | 165 | Copyright © November 2013

James Q. Del Rosso DO FAOCDa and Leon H. Kircik MDb

aTouro University College of Osteopathic Medicine, Henderson, NV;
Las Vegas Skin and Cancer Clinics/West Dermatology Group, JDRx Dermatology LLC, Henderson, NV
bMount Sinai Medical Center, New York, NY; Indiana University School of Medicine, Indianapolis, IN;
Physicians Skin Care, PLLC, Louisville, KY

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will focus on CDIs in adult patients. These are caused by Trichophyton spp, Microsporum spp, and Epidermophyton floccosum, and they most often involve non-scalp skin and nails. Scalp infection (tinea capitis) is far less common in adults, but has been reported. Onychomycosis caused by a dermatophyte (tinea unguium) affecting the nail bed and nail plate, and sometimes also the nail matrix, is a very common SCFI that increases with age in adulthood, most often affects toenails with or without fingernail involvement, and is more refractory to therapy than CDIs involving glabrous or hair-bearing skin. Dermatophyte-induced onychomycosis frequently necessitates use of an oral antifungal agent to achieve clearance, is not fully responsive to therapy in many cases, is often recurrent even after complete clearance with antifungal therapy, and is rare in children and adolescents, including those presenting with nail dystrophy that is clinically suggestive of a fungal infection.13-15
A given CDI, which hereafter refers to those not involving scalp (skin, hair follicles, hair shaft) or nails, is categorized by the anatomic location affected, with the most common being tinea pedis (feet), tinea corporis (body except for scalp, face, hands, feet, and nails), and tinea cruris.16-19 Other CDIs include tinea faceii (face), tinea barbae (male beard area), tinea manus (hands), tinea profunda (deeper dermatophyte infection with follicular involvement), and tinea incognito.16,18,20 The latter refers to a CDI that is altered in appearance by application of a topical corticosteroid (TCS). Tinea profunda often presents as tinea incognito because of “local immunosuppression” from TCS application, or systemic immunosuppression, which leads to unchecked fungal proliferation with deeper skin penetration of organisms, including follicular involvement.21
Cutaneous dermatophyte infections such as tinea pedis, tinea corporis, and tinea cruris exhibit variable presentations that depend on host-related and/or exogenous factors, and sometimes the characteristics of the causative dermatophyte.6,16,17 The classic presentation is an annular patch or thin plaque with an accentuated scaly edge and a tendency for central clearing that corresponds to the magnitude of erythema intensity and is reflective of the host inflammatory response (Figure 2).6,16,17Host-related factors include genetic predisposition, general health status, and immune status. Exogenous factors include topically applied agents (ie, antifungal agents, TCS, calcineurin inhibitors, barrier repair) and/or systemic medications (ie, corticosteroids,immunosuppressants) that can alter appearance, disease progression,or therapeutic response. Even the application of barrier repair/moisturizer agents to tinea corporis, pedis, or cruris can reduce scaling and create a more homogenous rather than “annular edge” appearance. The altered appearance may cause the clinician to not consider a dermatophyte infection, leading to misdiagnosis and improper treatment. Similarly, moisture accumulation and maceration of the groin folds can alter the appearance of tinea cruris, thus simulating frictional intertrigo, again resulting in incorrect diagnosis and treatment. Three major presentations of tinea pedis are well recognized (Figure 3).6,16,18,19
In some cases, specific fungal organisms tend to produce certain clinical presentations such as the common association of T rubrum and dry plantar (“moccasin”) tinea pedis, or Trichophyton mentagrophytes and vesicular tinea pedis (Figure 3).6,16,18,19,22-24 Many adults with dermatophyte infections exhibit an “immunologic blind spot” against dermatophytes, especially T rubrum, which predisposes them to chronic dermatophyosis, presenting primarily as dry plantar tinea pedis and toenail +/- fingernail tinea unguium as the “pedal source,” with more diffuse involvement manifesting at other skin sites over time in some patients (Figure 4).23,24 These patients are prone to recurrence of dermatophyte infections after successful clearance with treatment. Children with tinea pedis and/or tinea unguium are almost always from families that are affected by the genetic predisposition of chronic dermatophytosis.14,15,23
In adults or children with tinea corporis and/or tinea faceii, with or without tinea capitis, especially with erythematous