Tinea Capitis

Tinea capitis is a dermatophyte infection of the scalp skin and hair shafts. It is the commonest dermatophytosis of childhood, mostly affecting children aged 3 to 14 years, and is uncommon after puberty. Prevalence in school children in parts of sub-Saharan Africa reaches 10 to 30 percent or more, and outbreaks occur in schools and households.

The pubertal decline is attributed to a rise in sebum medium chain fatty acids with fungistatic action. Adult disease occurs in postmenopausal women, in immunosuppressed patients and in household contacts of affected children. An adult with tinea capitis should prompt a search for immunosuppression.

Causative organisms vary by region.

Species distribution shifts with migration and should be confirmed by culture.

Transmission is by direct contact with an infected person or animal, and by fomites: combs, brushes, hats, pillows, headrests, barber tools and head coverings. Asymptomatic carriers sustain household and school transmission.

Arthroconidia attach to scalp skin and hair, germinate, and hyphae enter the hair at the cuticle and grow down the shaft to Adamson fringe, the keratinising zone above the bulb. Further growth is stopped by living cells, so the hair is infected only in its dead keratin.

The pattern of arthroconidia determines the clinical form:

• Ectothrix: arthroconidia coat the outside of the shaft, and the cuticle is destroyed. Hairs break a few millimetres above the scalp, leaving stubs.
• Endothrix: arthroconidia fill the inside of the shaft with the cuticle intact. Hairs break at the surface, leaving black dots.
• Favus: hyphae and air bubbles inside the shaft, and scutula formed from hyphae, keratin and cellular debris. Hairs are not broken but become dull and are lost with scarring.

Inflammation depends on the source. Anthropophilic species cause little inflammation, but zoophilic and geophilic species cause marked inflammation, culminating in kerion, a delayed type hypersensitivity response to a high fungal load.

Complications:

• Scarring alopecia from kerion and favus.
• Secondary bacterial infection, usually Staphylococcus aureus.
• Id reaction (a sterile, symmetrical papular or vesicular eruption).
• Posterior cervical and occipital lymphadenopathy, sometimes tender and large, mistaken for lymphoma or infection.
• Rarely, spread to adjacent skin, or deep disease in the immunodeficient.

Microscopy and culture are obtained before any oral treatment, because treatment lasts weeks and carries drug risks.

• Specimens: plucked hairs with roots (the most infected portions are the broken and black dot hairs), scale scraped with a blade, and a moistened swab, cytobrush or sterile toothbrush for sparse or carrier disease. In kerion, hairs and pus are sampled, and cultures are often negative because the fungal load has fallen, so several samples are taken.
• Potassium hydroxide preparation: endothrix shows chains of arthroconidia inside the hair, which appears swollen and filled with spores, and ectothrix shows a mosaic sheath of spores on the surface. Small spored (2 to 3 micrometres) or large spored (5 to 8 micrometres) pattern narrows the species.
• Culture: Sabouraud dextrose agar with chloramphenicol and cycloheximide at 25 to 30 degrees Celsius, held for 3 to 4 weeks.
• Wood lamp: examine in a dark room. Yellow green fluorescence indicates Microsporum infection, and pale blue green fluorescence indicates favus. Absence of fluorescence does not exclude disease.
• Trichoscopy: comma hairs, corkscrew hairs, zigzag hairs, Morse code hairs, black dots and bar code hairs support the diagnosis and the invasion pattern.
• Histopathology: rarely needed. It demonstrates hyphae and arthroconidia in hair shafts and a follicular and perifollicular inflammatory infiltrate.

Oral therapy is required, because topical agents do not reach the hair follicle. Topical agents are used only as adjuncts.

First line oral agents

Alternative oral agents

Adult doses: griseofulvin microsize 500 mg to 1 g daily for 6 to 8 weeks; terbinafine 250 mg daily for 4 weeks for Trichophyton and for longer where Microsporum is the cause; itraconazole 200 mg daily for 4 to 6 weeks.

Choice of agent: terbinafine for Trichophyton disease (Trichophyton tonsurans, Trichophyton violaceum, Trichophyton soudanense) because the course is shorter. Griseofulvin for Microsporum disease, unless unavailable. When the organism is unknown, griseofulvin covers both groups, and terbinafine is used if the local flora is Trichophyton. Itraconazole and fluconazole are used when first line drugs fail, are not tolerated, or are unavailable.

Adjunctive and supportive measures

• Ketoconazole 2 percent shampoo or selenium sulphide 1 to 2.5 percent shampoo, applied to the scalp and hair for 5 to 10 minutes, twice weekly for the first 2 to 4 weeks. This reduces viable arthroconidia shed into the environment, and it does not cure the infection.
• Kerion: treat with the same oral antifungal. Antibacterial therapy is added only for secondary bacterial infection. Surgical drainage and incision are avoided. A short course of oral prednisolone (1 mg per kg daily for 1 to 2 weeks) is used by some clinicians in painful, extensive kerion to reduce inflammation and scarring, but a benefit has not been proven.
• Favus: oral griseofulvin or terbinafine, usually for a longer period, and scarring that has occurred is permanent.
• Household members and close contacts are examined. Culture positive carriers receive antifungal shampoo, with oral therapy where disease is evident.
• Children can return to school once treatment has started, and sharing of hats, combs and brushes is stopped. Combs, brushes and bedding are cleaned, and infected household pets are treated.
• Response: improvement is expected at 2 to 4 weeks, and hair regrows over months. Treatment continues until clinical resolution, and mycological cure is confirmed by repeat culture in persistent or recurrent disease.

Drug safety

• Griseofulvin: photosensitivity, headache, gastrointestinal upset, rash; rare hepatotoxicity. It induces CYP enzymes, lowering levels of warfarin and reducing the efficacy of oral contraceptives. Contraindicated in porphyria, hepatocellular failure and pregnancy. Conception is avoided during treatment and for 1 month afterwards in women and 6 months in men.
• Terbinafine: taste disturbance, gastrointestinal upset, rash, rare hepatotoxicity including liver failure, and rare severe cutaneous reactions. Baseline liver tests are considered with prolonged courses or a history of liver disease. Avoided in chronic or active liver disease and when creatinine clearance is below 50 mL per minute. It inhibits CYP2D6.
• Itraconazole: strong CYP3A4 inhibition, and avoided with simvastatin, lovastatin, oral midazolam and triazolam, among others. Hepatotoxicity, negative inotropy.
• Fluconazole: hepatotoxicity, QT prolongation; dose reduced by half when creatinine clearance is below 50 mL per minute.