Superficial fungal infections
Superficial mycoses are infections of keratinised tissues—skin, hair and nails—or the moist mucosal folds. They range from cosmetically disturbing but mild colour changes to inflammatory dermatophyte infection, scalp disease with permanent alopecia, and extensive disease in diabetes or immunosuppression. The key clinical skill is to identify the anatomic site, distinguish dermatophytes from yeast and non-fungal mimics, and choose topical or systemic therapy based on depth and extent.
Do not treat every itchy rash as “ringworm”: confirm the morphology, site and likely organism.
Learning objectives
- Classify dermatophyte, yeast and other superficial infections.
- Explain transmission, keratin digestion and inflammatory patterns.
- Recognise tinea of the body, groin, foot, scalp and nail, pityriasis versicolor, piedra, tinea nigra and cutaneous candidiasis.
- Perform and interpret KOH microscopy, culture, Wood-lamp examination and dermoscopy where available.
- Select topical versus oral treatment and prevent recurrence, reinfection and steroid-modified tinea.
Classification
| Group | Examples | Typical tissue |
|---|---|---|
| Dermatophytes | Trichophyton, Microsporum, Epidermophyton | Stratum corneum, hair and nails; named tinea/ringworm. |
| Yeasts | Candida, Malassezia | Moist folds, mucosa, skin surface and sebaceous areas. |
| Other superficial fungi | Hortaea werneckii, Piedraia, Trichosporon | Palms/soles or hair shafts, usually limited disease. |
Transmission and risk factors
Dermatophytes spread by direct contact, infected humans or animals, contaminated floors, combs, clothing and towels. Warm humid climates, occlusive footwear, communal bathing, contact sports, obesity, diabetes, peripheral vascular disease, HIV, corticosteroids and immunosuppressive medicines increase risk. Auto-inoculation from the feet to groin, nails or hands is common. Chronic steroid-containing combination creams suppress inflammation while allowing fungal growth, producing tinea incognito.
Pathophysiology
Dermatophytes digest keratin using proteases and remain mainly in the stratum corneum. The advancing edge of active infection contains more fungus and inflammation, producing an annular plaque with central clearing. Host cell-mediated immunity determines inflammation: strong response causes vesicles and pustules, while impaired immunity allows extensive or atypical lesions. Malassezia alters melanocyte function and produces azelaic-acid-like metabolites, leading to hypo- or hyperpigmented macules. Candida overgrowth follows moisture, maceration and altered local immunity.
Clinical syndromes
Tinea corporis
Annular scaly plaques with a raised active border, central clearing and peripheral vesicles. Lesions may be multiple or confluent. Examine feet, nails and household contacts as reservoirs.
Tinea cruris
Itchy erythematous plaques begin in the groin and spread onto the upper thigh, usually sparing the scrotum. Bilateral scrotal involvement or satellite pustules suggests candidiasis instead.
Tinea pedis
- Interdigital maceration and fissuring (“athlete’s foot”).
- Moccasin-type diffuse scale on soles and lateral feet.
- Inflammatory vesiculobullous type after an immune response.
- Complications: bacterial cellulitis through fissures and onychomycosis.
Tinea capitis
Common in children: scaling, broken hairs, black dots, alopecia, kerion (boggy inflammatory plaque) or favus. Kerion can scar and cause permanent hair loss; treat systemically and assess contacts.
Tinea unguium/onychomycosis
Thickened, discoloured, brittle or separated nails. Distal-lateral, white superficial and proximal patterns occur. Psoriasis, trauma and lichen planus mimic fungal nails; confirm before prolonged oral therapy.
Pityriasis versicolor
Fine-scaling hypo- or hyperpigmented macules on trunk, neck and upper arms. More obvious after sun exposure. KOH shows short curved hyphae and round yeast (“spaghetti and meatballs”). Pigment normalisation may take months after cure.
Candidal intertrigo
Beefy-red macerated plaques in folds with satellite papules/pustules. Risk factors include obesity, diabetes, antibiotics, pregnancy and immunosuppression.
Piedra and tinea nigra
White/soft or black/hard nodules attached to hair shafts occur in piedra. Tinea nigra produces a slowly enlarging brown-black palm/sole macule without inflammation and can mimic melanoma.
History and examination
Ask duration, itch/pain, spread, contacts, animal exposure, footwear, shared showers, prior steroid creams, diabetes, HIV, medicines and previous treatment. Examine the entire skin, scalp, nails, interdigital spaces, groin, mouth and mucosal sites; a local lesion may coexist with an untreated reservoir elsewhere. Look for bacterial infection, lymphadenopathy, fever, kerion and scarring.
Diagnosis
| Test | Use | Limitations |
|---|---|---|
| KOH preparation | Skin scale, nail scrapings or hair; demonstrates branching septate hyphae or yeast | Operator-dependent; negative test does not exclude disease if sampling is poor. |
| Fungal culture | Species identification, scalp/nail/refractory infection | Slow; prior antifungal use can cause false negatives. |
| Wood lamp | Some Microsporum hair infections and erythrasma comparison | Many dermatophytes do not fluoresce; not a rule-out test. |
| Nail clipping/PAS | Confirms onychomycosis before oral therapy | Requires laboratory processing; nail dystrophy has many mimics. |
Sample the active scaly edge after cleaning off creams. For scalp, pluck broken hairs and scrape scale. In steroid-modified lesions stop unnecessary steroid and sample multiple sites.
Differential diagnosis
Atopic or contact dermatitis, psoriasis, seborrhoeic dermatitis, pityriasis rosea, erythrasma, intertrigo, bacterial impetigo, scabies, lichen planus, vitiligo, post-inflammatory pigment change and cutaneous lymphoma. A changing pigmented acral lesion requires melanoma assessment, not empirical antifungal therapy alone.
Management
General measures
- Keep folds and feet dry; change socks and underwear daily.
- Do not share towels, combs, hats, shoes or nail instruments.
- Treat infected pets or close contacts when indicated.
- Control diabetes, reduce occlusion and stop non-prescribed steroid combinations.
Topical therapy
For limited tinea corporis/cruris/pedis use a topical allylamine or azole for the recommended duration, extending slightly beyond clinical clearing. For pityriasis versicolor use topical selenium sulfide, ketoconazole or another UCG-approved agent.
Oral therapy
Use oral terbinafine, itraconazole, griseofulvin or another guideline-recommended agent for tinea capitis, extensive disease, nail infection, recurrent disease or treatment failure. Check liver disease, pregnancy, interactions and local formulary before prescribing.
Inflammatory disease
Kerion, severe vesicular tinea or bacterial superinfection needs prompt systemic antifungal treatment and sometimes antibacterial therapy. Avoid steroid monotherapy; specialist-directed short anti-inflammatory treatment may be considered after antifungal coverage.
Special syndromes
- Tinea capitis: topical therapy alone is inadequate. Examine household members and avoid sharing combs; oral treatment and shampoo to reduce spores are usually required.
- Onychomycosis: confirm fungus before months of systemic therapy; assess liver function and interactions.
- Diabetes/HIV: search for extensive disease, bacterial cellulitis and recurrent infection.
- Pregnancy/children: choose agents with UCG/obstetric guidance; avoid unnecessary systemic exposure.
Complications and referral
- Permanent scarring alopecia after untreated kerion/favus.
- Bacterial cellulitis or lymphangitis through fissured feet.
- Disseminated or atypical disease in immunosuppression.
- Drug hepatotoxicity and interactions from prolonged oral treatment.
- Refer uncertain pigmented lesions, severe scalp inflammation, nail disease requiring systemic therapy, recurrent disease and immunocompromised patients.
Exam pearls
- Sample the active edge, not the quiet centre.
- Tinea cruris usually spares the scrotum; candidiasis produces satellite pustules.
- Kerion is inflammatory tinea capitis and can scar.
- Pigment can remain abnormal for months after pityriasis versicolor is cured.
- Never give a steroid–antifungal combination without a clear indication and follow-up.
References
- SlideShare: Superficial fungal infections.
- SlideShare: Superficial fungal infections—clinical review.
- Current Uganda Clinical Guidelines and dermatology/antifungal treatment guidance.
Safety note: Confirm diagnosis and drug selection before prolonged oral antifungal treatment, especially in pregnancy, children, liver disease and polypharmacy.
