Residency · Residency · Dermatology

Dermatophyte Infections: Diagnosis and Antifungal Therapy

Overview

Dermatophytoses (tinea infections) are superficial fungal infections of keratinized tissue (skin, hair, nails) caused by dermatophytes, a group of fungi that metabolize keratin. They are among the most common infections worldwide, affecting up to 20 to 25 percent of the global population. Accurate diagnosis using KOH preparation, culture, or histopathology, combined with appropriate antifungal selection, is fundamental to dermatologic practice.

Mycology

Dermatophyte Genera

Three genera cause virtually all dermatophyte infections. Trichophyton is the most common genus and infects skin, hair, and nails. Microsporum primarily infects skin and hair but rarely nails. Epidermophyton infects skin and nails only and does not involve hair.

Transmission Categories

Anthropophilic species (T. rubrum, T. tonsurans, E. floccosum) are transmitted human-to-human and tend to cause chronic, less inflammatory infections. Zoophilic species (M. canis from cats and dogs, T. mentagrophytes from rodents) are transmitted animal-to-human and produce more inflammatory disease. Geophilic species (M. gypseum) are acquired from soil and are highly inflammatory.

Pathogenesis

Dermatophytes produce keratinases that degrade keratin, and infection is limited to non-living keratinized tissue: the stratum corneum, hair shaft, and nail plate. The host immune response, specifically cell-mediated immunity, determines clinical severity. Strong CMI produces inflammatory tinea with clearing, as typically seen with zoophilic infections, while weak CMI leads to chronic, widespread, minimally inflammatory infection, as is typical with T. rubrum. Dermatophytes do not invade living tissue except in immunocompromised patients, where deep dermatophytosis can occur.

Clinical Presentations

Tinea Corporis (Body)

Tinea corporis presents as annular (ring-shaped) plaques with a raised, scaly, erythematous advancing border and central clearing. The lesions are pruritic and can be widespread in immunosuppressed patients. "Tinea incognito" is a modified, atypical presentation resulting from prior topical corticosteroid use, with reduced scale, loss of the annular configuration, and deeper follicular invasion. The differential includes granuloma annulare, nummular eczema, pityriasis rosea, psoriasis, and subacute cutaneous lupus.

Tinea Cruris (Groin)

Tinea cruris presents as well-demarcated, erythematous, scaly plaques on the inner thighs and inguinal folds with an advancing scaly border. A key distinguishing feature is that it spares the scrotum, unlike candidiasis which involves the scrotum. The most common causative organisms are T. rubrum and E. floccosum. Risk factors include obesity, sweating, tight clothing, and concurrent tinea pedis. The differential includes inverse psoriasis, candidal intertrigo, and erythrasma (caused by Corynebacterium minutissimum, which shows coral-red fluorescence under Wood lamp).

Tinea Pedis (Feet)

Tinea pedis is the most common dermatophyte infection, presenting in several patterns. The interdigital pattern shows macerated, fissured web spaces, especially in the fourth-to-fifth interdigital space. The moccasin type presents as chronic, diffuse hyperkeratosis and scaling of the soles and lateral feet, most commonly caused by T. rubrum, often bilateral, and is classically associated with the "two feet, one hand" syndrome (bilateral tinea pedis with unilateral tinea manuum). The vesiculobullous or inflammatory pattern features vesicles and bullae on the instep with acute onset, often from zoophilic species. Tinea pedis is an important portal of entry for bacterial cellulitis of the lower extremity, and its treatment reduces cellulitis recurrence.

Tinea Capitis (Scalp)

Tinea capitis primarily affects prepubertal children. The endothrix pattern (arthroconidia within the hair shaft), most commonly caused by T. tonsurans in North America, produces hair breakage at the scalp surface with "black dot" alopecia and is Wood lamp negative. The ectothrix pattern (arthroconidia on the outside of the hair shaft), caused by M. canis and M. audouinii, presents as a gray, scaly patch with broken hairs and is Wood lamp positive with bright green fluorescence for Microsporum species. Favus, caused by T. schoenleinii, produces yellow cup-shaped crusts (scutula) and scarring alopecia but is rare in developed nations. A kerion is an intense inflammatory response that presents as a boggy, tender, pustular mass with alopecia, usually from zoophilic organisms. Critically, a kerion is not an abscess and should not be incised and drained.

Diagnosis relies on KOH of plucked hairs and fungal culture on DTM or Sabouraud agar. Tinea capitis requires systemic antifungal therapy because topical agents cannot penetrate the hair shaft. Griseofulvin is the traditional first-line at 20 to 25 mg/kg/day microsize for 6 to 8 weeks, given with fatty food. Terbinafine is more effective for Trichophyton with a shorter course but less effective for Microsporum. Adjunctive antifungal shampoo (ketoconazole 2% or selenium sulfide) reduces spore shedding. A short course of oral corticosteroids may be added for kerion to reduce scarring.

Tinea Manuum (Hands)

Tinea manuum is usually unilateral, presenting as diffuse palmar scaling in the "one hand, two feet" syndrome. It often accompanies bilateral moccasin-type tinea pedis. KOH of palmar scale confirms the diagnosis. The differential includes hand eczema (typically bilateral), psoriasis, and contact dermatitis.

Tinea Faciei (Face)

Tinea faciei presents as erythematous, scaly patches on the face, often lacking the classic annular configuration, especially with prior steroid use. It is frequently misdiagnosed. The differential includes lupus, seborrheic dermatitis, rosacea, and contact dermatitis. KOH scraping is diagnostic.

Onychomycosis (Tinea Unguium)

Onychomycosis is a dermatophyte infection of the nail, most commonly caused by T. rubrum. | Pattern | Onset Site | Key Features | Associations |

Distal lateral subungual onychomycosis (DLSO), the most common pattern, begins at the distal or lateral nail edge with yellow-white discoloration, subungual hyperkeratosis, and onycholysis. Superficial white onychomycosis (SWO), caused by T. mentagrophytes, produces white, crumbly patches on the nail surface that are easily scraped. Proximal subungual onychomycosis (PSO) begins at the proximal nail fold, is rare, and is associated with immunosuppression, making it a potential marker for HIV. Total dystrophic onychomycosis is the end-stage of any pattern with complete nail destruction. Endonyx involves invasion within the nail plate without nail bed involvement and is rare.

Diagnosis must be confirmed before systemic treatment using KOH preparation of subungual debris, PAS stain of nail clipping (the most sensitive histologic method), fungal culture (gold standard for speciation but slow at 4 to 6 weeks), or PCR (increasingly available and rapid). Topical treatment is appropriate only for mild disease (SWO, less than 50 percent of nail, no matrix involvement) using efinaconazole 10% solution, tavaborole 5%, or ciclopirox 8% lacquer. Systemic therapy is the standard of care for most onychomycosis: terbinafine 250 mg/day for 6 weeks (fingernails) or 12 weeks (toenails) is most effective with approximately a 70 percent cure rate; itraconazole can be used as pulse dosing (200 mg twice daily for one week per month for 3 to 4 months) or continuously; fluconazole 150 to 300 mg/week for 6 to 12 months is an off-label option. LFTs should be monitored with terbinafine and itraconazole, and itraconazole drug interactions (CYP3A4 inhibitor) must be checked. Nail avulsion (chemical with urea or mechanical) is an adjunct for thick nails.

Majocchi Granuloma (Dermatophyte Folliculitis/Granuloma)

Majocchi granuloma is a deep follicular and perifollicular dermatophyte infection occurring when dermatophytes penetrate the follicle into the dermis. Risk factors include topical corticosteroid use (tinea incognito), leg shaving, and immunosuppression. It presents as perifollicular papules, pustules, and nodules, often on the lower legs. Histology shows follicular and perifollicular granulomatous inflammation with fungal elements in the dermis. Systemic antifungal therapy (terbinafine or itraconazole) is required, as topical therapy alone is inadequate.

Diagnostic Techniques

KOH Preparation

The active, scaling border (not the center) is scraped with a number 15 blade, placed on a glass slide with 10 to 20 percent KOH (adding DMSO accelerates clearing), gently heated, and examined under the microscope for septate, branching hyphae crossing cell borders. Sensitivity is approximately 60 to 80 percent depending on technique.

Fungal Culture

DTM (Dermatophyte Test Medium) turns red with dermatophyte growth due to a pH change from alkaline metabolites. Sabouraud dextrose agar with chloramphenicol and cycloheximide is the standard medium. Colony morphology and microscopic features (macroconidia, microconidia) enable speciation. Growth takes 1 to 4 weeks.

Wood Lamp Examination

Wood lamp is useful for Microsporum species, which show bright green fluorescence of infected hair. Trichophyton species do not fluoresce, meaning that T. tonsurans, the most common cause of tinea capitis in North America, is Wood lamp negative. Wood lamp is also useful for erythrasma (coral-red), Pseudomonas (green), and tinea versicolor (yellow-gold).

Histopathology with PAS Stain

PAS or GMS stain highlights fungal hyphae in the stratum corneum. This is most useful for onychomycosis, where PAS stain of a nail clipping has greater than 90 percent sensitivity. Histology also shows compact orthokeratosis, spongiosis, and inflammatory infiltrate.

<image>Clinical photograph panel of dermatophyte infections: (A) tinea corporis showing classic annular plaque with raised scaly border and central clearing, (B) tinea capitis with black dot alopecia on the scalp of a child, (C) moccasin-type tinea pedis with diffuse plantar scaling, (D) distal lateral subungual onychomycosis with yellow discoloration and subungual hyperkeratosis. Show on diverse skin tones.</image>

<image>Microscopy illustration showing: (A) KOH preparation with septate, branching dermatophyte hyphae crossing keratinocyte borders, (B) endothrix hair invasion pattern with arthroconidia packed within the hair shaft, (C) ectothrix pattern with arthroconidia coating the outside of the hair shaft. Include labels and magnification indicators for each panel.</image>

<image>Treatment algorithm for onychomycosis: starting with clinical suspicion, confirmation step (KOH, PAS nail clipping, culture), then branching based on severity -- mild/superficial (topical efinaconazole or ciclopirox) vs. moderate-severe (systemic terbinafine or itraconazole with LFT monitoring). Include expected cure rates and treatment durations.</image>

Key Clinical Pearls

Always confirm onychomycosis with laboratory testing before prescribing systemic antifungals, as only 50 percent of dystrophic nails are truly fungal (the differential includes psoriasis, lichen planus, and trauma). "Tinea incognito" results from treating a dermatophyte infection with topical corticosteroids, which suppresses inflammation and creates an atypical appearance while infection worsens with deeper follicular involvement leading to Majocchi granuloma. The "two feet, one hand" syndrome (bilateral tinea pedis with unilateral tinea manuum) is classic for T. rubrum infection. A kerion is an inflammatory immune response to fungal infection, not a bacterial abscess, and incision and drainage is contraindicated; treatment requires systemic antifungals with a short course of oral corticosteroids. T. tonsurans (endothrix) is Wood lamp negative, so the Wood lamp cannot be relied upon to exclude tinea capitis in North America. Tinea pedis is the most modifiable risk factor for lower extremity cellulitis, and interdigital tinea should be aggressively treated in patients with recurrent cellulitis.

References

• Gupta AK, Foley KA, Versteeg SG. New antifungal agents and new formulations against dermatophytes. Mycopathologia. 2017;182(1-2):127-141.
• Elewski BE, Hay RJ. Update on the management of onychomycosis: highlights of the third annual international summit on cutaneous antifungal therapy. Clin Infect Dis. 2014;47(8):1028-1033.
• Hay RJ. Tinea capitis: current status. Mycopathologia. 2017;182(1-2):87-93.
• Gupta AK, Stec N, Summerbell RC, et al. Onychomycosis: a review. J Eur Acad Dermatol Venereol. 2020;34(9):1972-1990.

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