Superficial Fungal Infections
Superficial fungal infections are the most common surface skin infections in dermatology practice, affecting 20–25% of the world's population. They are caused by three main groups of organisms: keratin-loving dermatophytes (the genera Trichophyton, Microsporum and Epidermophyton), lipid-dependent yeasts (Malassezia spp., responsible for tinea versicolor and seborrheic dermatitis) and opportunistic yeasts (Candida spp.). What sets these infections apart is that they stay confined to keratin-rich structures that have no blood supply: the stratum corneum, the hair shaft and the nail plate. Although not directly life-threatening, they cause persistent itch, changes in skin color and damage to nails and hair, with a serious impact on quality of life and appearance. At Haute-Derma, we follow a standardized microbiology workup: dermoscopy to spot characteristic signs, skin scrapings examined in KOH with a fluorescent stain, fungal culture to identify the species, and an individualized topical or systemic antifungal plan.
How the infection develops in the skin and how the immune system responds:
- Dermatophyte adhesion and keratinase enzymes:
- Fungal arthroconidia attach to skin keratinocytes through surface adhesins within 2–6 hours of contact.
- Once attached, the spores germinate and release a wide range of extracellular proteases, notably keratinases, endoproteases and metalloproteases. These enzymes break tough keratin fibers down into oligopeptides and amino acids that feed the fungus, while clearing a path for hyphae to spread sideways through the stratum corneum.
- The Th17 response and the IL-17/IL-22 pathway:
- Mannan and beta-glucan in the fungal cell wall are recognized by Dectin-1 and Dectin-2 receptors on dendritic cells in the skin.
- Activated dendritic cells steer the immune response toward T-helper 17 (Th17) cells, which release IL-17A, IL-17F and IL-22.
- IL-17 prompts keratinocytes to make natural antimicrobial peptides (such as beta-defensin 2 and S100A7/psoriasin) and draws in neutrophils to wall off the fungus. The balance between how fast the hyphae grow and how fast the epidermis sheds its keratinocytes explains the outward-spreading ring shape of the lesions.
- Shape-shifting and the roles of Malassezia and Candida:
- Malassezia spp. are lipid-dependent yeasts that normally live on the skin. With heat, high humidity and increased sebum, they switch from the yeast form to an invasive hyphal form.
- Malassezia produces azelaic acid, which inhibits tyrosinase in melanocytes and causes the pale patches typical of tinea versicolor.
- Candida albicans takes advantage of a disturbed microbiome or weakened local immunity to change from yeast to pseudohyphae. It releases the toxin candidalysin, which punches holes in keratinocyte membranes and triggers a superficial pustular inflammation.
Clinical Features of Superficial Fungal Infections
- Tinea Capitis (Scalp Ringworm): The infection involves the stratum corneum of the scalp and the hair shafts, and its appearance depends on how the fungus invades the hair. Ectothrix infection produces well-defined bald patches covered in fine gray scale, with hairs snapped off a few millimeters above the skin like a "mown meadow." Endothrix infection breaks the hairs right at the follicle opening, leaving scattered black dots on the scalp. Kerion celsi reflects an intense hypersensitivity reaction: a raised, boggy swelling riddled with pus-draining openings like a honeycomb, which can leave permanent scarring hair loss if not treated promptly.
- Tinea Corporis and Tinea Cruris: These affect the stratum corneum of smooth skin. The typical lesion is a round or oval red patch that clears in the center as it spreads outward. The border is raised and sharp, with small blisters, inflamed papules and crust. Itch is often marked, especially with sweating. In the groin, the rash usually starts in both groin creases and spreads down the thighs, perineum or buttocks, but typically spares the scrotum.
- Tinea Pedis and Onychomycosis: On the feet there are three main types: interdigital (scaling, cracking and erosion between the fourth and fifth toes), vesicular (deep, intensely itchy blisters on the arch) and "moccasin" (red, thickened soles with scattered dry, fine scale). In the nails, dermatophytes or Candida enter from the free or lateral edge of the plate. The nail loses its clarity, turns yellow-gray, thickens underneath, becomes brittle and crumbly, and separates from the nail bed.
- Tinea (Pityriasis) Versicolor: Caused by overgrowth of Malassezia yeast in the upper stratum corneum. Lesions are pale, darkened or faintly pink macules, from a few millimeters to several centimeters, that merge into larger patches. A fine scale lifts off easily with light scraping (Besnier's sign, or the "wood-shaving" sign). The chest, back, neck and forearms, which are rich in oil glands, are most often affected. It is usually painless, with mild itch when the body is hot or sweaty.
- Cutaneous and Mucosal Candidiasis: Usually affects skin folds such as under the breasts, abdominal folds, the gluteal cleft and between the fingers. The typical rash is bright red, moist and eroded with a sharp border, surrounded by satellite lesions: small pustules and red papules scattered around the main patch. In the mouth it forms white, curd-like pseudomembranes stuck to the tongue or inner cheeks; scraping them off leaves raw, red, bleeding mucosa.
Our Diagnostic Approach to Superficial Fungal Infections
At Haute-Derma, we diagnose superficial fungal infections with a rigorous microbiology workup to rule out other scaly skin conditions such as psoriasis, eczema and atopic dermatitis:
- Clinical History and Wood's Lamp Examination:
- A Wood's lamp shines 365 nm UV light on the lesion.
- Scalp ringworm caused by Microsporum glows bright green. Tinea versicolor (Malassezia) glows copper-yellow or pale yellow. Corynebacterium infection (erythrasma, a key differential) glows coral pink-red.
- Sampling and Same-Day KOH Microscopy:
- The doctor gently scrapes scale from the active edge of the lesion with a sterile scalpel blade, collects debris from under the nail, or plucks broken hairs.
- The sample is placed on a slide with 1–2 drops of 10–20% KOH, sometimes combined with Parker ink or calcofluor white to highlight the fungal walls.
- The slide is warmed briefly over a spirit lamp so the KOH dissolves the keratinocytes quickly, then examined under a light microscope at ×10 and ×40:
| Dermatophytes | Clear, branching, septate hyphae running between the keratinocytes. |
|---|---|
| Malassezia | The classic "spaghetti and meatballs" picture: short hyphal fragments mixed with clusters of round yeast cells. |
| Candida | Oval budding yeast cells together with chains of pseudohyphae. |
- Fungal Culture and Antifungal Susceptibility Testing: Samples are cultured on Sabouraud dextrose agar (SDA) with cycloheximide and chloramphenicol to suppress contaminating bacteria and molds, then incubated at 25–30°C for 1–3 weeks to identify the exact species and, when treatment fails, to test antifungal susceptibility.
Treatment Options at Haute-Derma
Treatment aims to eliminate the fungus, remove the conditions that favor it (moisture, friction) and restore the skin barrier:
- Topical Antifungal Therapy:
- Used for limited tinea corporis, tinea cruris, tinea versicolor or tinea pedis (for 2–4 weeks, continuing for 1 week after the rash has completely cleared).
- Topical azoles: clotrimazole 1%, ketoconazole 2% or sertaconazole 2%, applied once or twice daily.
- Topical allylamines: terbinafine 1% cream once daily, which kills the fungus quickly because it concentrates in the stratum corneum.
- Ketoconazole 2% or selenium sulfide 2.5% shampoo 2–3 times a week for widespread tinea versicolor and scalp seborrheic dermatitis.
- Systemic Antifungal Therapy:
- Indicated for extensive disease, tinea capitis, onychomycosis, kerion celsi, or when topical treatment has failed.
- Oral terbinafine: First choice for dermatophyte skin and nail infections. Adult dose 250 mg/day for 2–4 weeks for body or foot infections, 6 weeks for fingernails and 12 weeks for toenails.
- Oral itraconazole: Preferred for tinea versicolor, Candida and onychomycosis. 200 mg/day for 7 days (or pulse dosing of 400 mg/day for 7 days each month).
- Oral fluconazole: 150 mg once weekly for 2–4 weeks for tinea corporis or cruris, or 150 mg/day for mucosal candidiasis.
- Supportive Care and Relapse Prevention at Haute-Derma:
- Keep skin folds dry and wear breathable cotton clothing.
- Sprinkle clotrimazole antifungal powder into shoes and socks every day.
- Wash clothing and bedding in water above 60°C to kill fungal arthroconidia.