Tinea capitis: scalp ringworm needs oral antifungal tablets, not cream

Scalp ringworm in children — the basics

Tinea capitis is a fungal infection of the scalp skin and hair shafts. Despite being called “ringworm,” no worm is involved — it is entirely caused by dermatophyte fungi, the same family of organisms responsible for tinea corporis (body ringworm), tinea pedis (athlete’s foot), and tinea unguium (nail fungus). In Australia, it almost exclusively affects children between the ages of three and ten.

The single most important fact about tinea capitis is that antifungal cream and shampoo alone do not cure it. The fungus invades the interior of the hair shaft and burrows down to the hair bulb at skin level — a location entirely unreachable by topical products. Oral antifungal medication taken by mouth for four to eight weeks is always required.

A. Core clinical — the AU general-practice framework

Patterns and how they look

Per Therapeutic Guidelines (eTG) and the Royal Children’s Hospital Melbourne clinical practice guidelines, tinea capitis presents in several patterns:

Gray-patch (non-inflammatory). The classic pattern with Microsporum canis from cat or dog exposure. One or more discrete scaly patches with hair breakage a few millimetres above the scalp. The patch often looks dusted with ash or grey scale. Using a Wood’s lamp (UV light) in the clinic causes ectothrix Microsporum species to fluoresce bright blue-green — a useful bedside clue.

Black-dot. Caused by Trichophyton tonsurans — the species responsible for urban outbreaks in schools and contact sports. The fungus grows inside the hair shaft (endothrix), causing hairs to break off at scalp level, leaving black dots visible in the patch. The Wood’s lamp is negative for Trichophyton species, so a negative scan does not exclude tinea capitis — it just says Microsporum is unlikely.

Kerion. An intensely inflammatory, boggy, tender, weeping pustular mass on the scalp, often accompanied by enlarged lymph glands in the neck. A kerion is caused by a strong immune reaction to the fungus — it is not a bacterial abscess and should not be incised, drained, or shaved. Opening a kerion surgically destroys hair follicles and leaves permanent bald patches (cicatricial alopecia) that proper antifungal treatment alone would largely have prevented.

Diffuse scaly (seborrhoeic-like). A presentation that looks like persistent dandruff, with diffuse scaling and minimal hair loss. This pattern is easily missed and may be written off as seborrhoeic dermatitis; tinea capitis should be considered in any child with scalp scale that does not respond to standard dandruff management.

Investigations

Always send a fungal culture before or at the same time as starting treatment. KOH microscopy (wet preparation of plucked hairs and skin scrapings) confirms dermatophyte infection quickly; fungal culture on Sabouraud agar identifies the specific species and takes two to four weeks. Species identification matters because it determines which antifungal to use and for how long.

To collect samples: pluck (do not cut) affected hairs from the edge of the patch using forceps, because the fungal load is highest at the root. Combine with skin scrapings from the patch. Send to a microbiology laboratory with a request for fungal culture and KOH microscopy.

Blood tests — FBC and liver function tests (LFTs) — are taken as a baseline before starting oral antifungal tablets; rare drug-related liver effects are worth having a baseline for.

First-line treatment

The core principle (eTG, BAD guidelines 2014, Australasian College of Dermatologists): oral antifungal is mandatory. The choice depends on the suspected or confirmed species:

Situation	Drug of choice	Duration
Microsporum species (cat/dog contact, Wood’s lamp positive)	Griseofulvin 10–20 mg/kg/day with fatty food	6–8 weeks (up to 12 wk)
Trichophyton species (urban, sport contact, Wood’s lamp negative)	Terbinafine (weight-banded: <20 kg = 62.5 mg/day; 20–40 kg = 125 mg/day; >40 kg = 250 mg/day)	4 weeks
Species uncertain	Griseofulvin (broader spectrum) or terbinafine if T. tonsurans epidemiologically most likely	Revise once culture returns

Both griseofulvin and terbinafine are on the PBS General Schedule. Griseofulvin must be given with a fat-containing meal — it is poorly absorbed without fat. Practical options include full-fat milk, peanut butter on toast, or avocado. Absorption failure is a common reason treatment doesn’t work.

Adjunct topical shampoo — ketoconazole 2% or selenium sulfide 2.5% shampoo, two to three times per week throughout the treatment course. This does not cure the infection but reduces the number of viable fungal spores being shed from the scalp, which helps protect household contacts and classmates during the weeks of treatment.

B. Evidence appraisal — griseofulvin vs terbinafine, and the kerion debate

Which antifungal?

A 2011 meta-analysis by Tey and colleagues (JAAD) comparing griseofulvin and terbinafine found that terbinafine was significantly more effective for Trichophyton infections and had the advantage of a shorter treatment course (four weeks rather than six to eight). For Microsporum infections, griseofulvin was more effective. The clinical implication is straightforward: match the drug to the likely species based on local epidemiology and the source of exposure, then confirm on culture and adjust if needed.

In Australian metropolitan centres, T. tonsurans has become the dominant isolate, particularly in schools serving diverse urban communities, and in wrestling, judo, and BJJ clubs. In suburban and rural areas, M. canis from cats and dogs remains common. In communities with large recent migrations from Sub-Saharan Africa or South Asia, T. violaceum is seen — this species also responds better to terbinafine.

Kerion: oral antifungal, no surgery

The kerion is frequently misdiagnosed as a bacterial abscess and surgically drained, with permanently disfiguring results. The kerion is caused by a type IV (delayed-type) hypersensitivity immune response to dermatophyte antigens in the hair shaft — it is the host immune system reacting vigorously, not pus from bacterial superinfection.

Per eTG and the BAD guidelines: continue the standard oral antifungal course; apply gentle saline soaks to loosen crusting; avoid cutting, draining, or shaving. Oral corticosteroids (prednisolone) have been trialled as adjuncts to reduce inflammation, but a randomised controlled trial by Hussain and colleagues (1999) found no significant benefit in scarring outcomes or speed of resolution. A short corticosteroid course can be considered for a very severe kerion causing significant pain or lymph-node enlargement affecting function, but this is not routine practice.

Secondary bacterial superinfection (most commonly Staphylococcus aureus) can complicate a kerion and may warrant a bacterial swab and targeted antibiotics if the clinical picture suggests it — but the primary treatment is always oral antifungal.

C. Contact management and school exclusion

Household contacts

Siblings and other household members should be examined for scaly patches, hair loss, or itching. Asymptomatic carriage (scalp colonisation without visible disease) is common, particularly with T. tonsurans, and maintains the reservoir for reinfection. In confirmed T. tonsurans outbreaks, screening cultures for asymptomatic contacts and antifungal shampoo prophylaxis are reasonable steps.

All household members should use antifungal shampoo (ketoconazole 2% or selenium sulfide 2.5%) two to three times per week during the treatment period, hot-wash all shared bedding, pillowcases, towels, and hats, and discard old combs, brushes, and hair accessories.

Pets

If the causative species is Microsporum canis — or even if suspected based on cat or dog exposure — a veterinary assessment of any household cats and dogs is important. Animals with patchy fur, skin scaling, or hair loss should be tested and treated. Without treating the source animal, the child will typically be reinfected once tablets are stopped. This is one of the most commonly missed reasons why a treatment course appears to “fail.”

School exclusion rules

Per the Communicable Diseases Network Australia (CDNA), children with tinea capitis do not need to be excluded from school or childcare once treatment has commenced. They can return from the day the first tablet is given. Individual states may have slightly different policies; checking local state health department guidance is worthwhile, but the national standard is that treatment started equals school cleared.

For wrestling, BJJ, judo, and other close-contact sport: a two-week suspension from skin-to-skin competition after treatment commences is the standard recommendation, consistent with guidelines on tinea gladiatorum, before return with clinical clearance.

D. Australian operations

Tinea capitis is assessed and managed in general practice. Initial consultations involve examination, Wood’s lamp, hair plucking and culture sampling, baseline blood tests, and a prescription for oral antifungal.

MBS items: standard consult items (23, 36, 44) apply. Fungal microscopy and culture is covered by pathology MBS item 69333. Baseline FBC (65070) and LFTs (66512) are bulk-billable.

PBS: griseofulvin tablets and terbinafine tablets are on the PBS General Schedule. Griseofulvin paediatric suspension availability in Australian pharmacies has been variable over recent years due to supply constraints; confirming availability with the dispensing pharmacy before prescribing saves a wasted trip. Itraconazole and fluconazole are also on the General Schedule and are alternatives for refractory or intolerant cases. Ketoconazole 2% and selenium sulfide 2.5% shampoos are available over the counter.

Follow-up: review at two weeks (tolerability, adherence, contact management, school/sport plan) and four weeks (clinical response, LFTs if symptomatic). A repeat fungal culture before stopping treatment is reasonable when Microsporum is the species, as clinical clearance does not always correlate with mycological cure.

E. Special populations

ATSI remote communities. Aboriginal and Torres Strait Islander children in remote communities carry a higher burden of dermatophyte infections alongside scabies and impetigo — all three conditions often coexist. Integrated Healthy Skin program approaches (screening, community treatment, household management) achieve better outcomes than treating one child at a time in isolation. GPs serving these communities should integrate tinea capitis into the broader healthy skin framework.

Adolescents on combined oral contraceptive pill. Griseofulvin is a CYP enzyme inducer and reduces the efficacy of the combined oral contraceptive pill. Adolescents on the OCP who need griseofulvin should be counselled to use additional contraception during treatment and for one month after stopping. An alternative is to use terbinafine if the species is Trichophyton.

Immunocompromised children. Tinea capitis in an immunocompromised child (HIV, transplant recipient, on biologics, or receiving oncology treatment) can be atypical, extensive, or refractory. Longer treatment courses, specialist dermatology input, and closer monitoring for drug toxicity are required.

Adult tinea capitis. Tinea capitis is rare in adults because the increased sebum production after puberty is naturally fungistatic. When it occurs in an adult, an underlying cause such as HIV, immunosuppressive therapy, or (in women) postmenopausal hormonal changes should be explored.

When to escalate

Refer to dermatology or paediatric dermatology when:

• Treatment failure after two full courses of appropriate antifungal at correct weight-banded dosing
• Kerion with severe inflammation, significant cervical lymphadenopathy, or pain affecting function
• Adult-onset tinea capitis — needs immunocompromise workup
• Suspected resistant species — terbinafine-resistant T. indotineae is an emerging concern globally; suspect if treatment failure despite correct species-directed therapy
• Atypical or scarring presentations — biopsy may be needed
• Outbreak in a school, childcare centre, residential facility, or sport club — contact the state public health unit

What this article is and is not

This article is general health information based on current Australian clinical guidelines — Therapeutic Guidelines (eTG), AMH, RCH Melbourne CPG, and Australasian College of Dermatologists guidance — and peer-reviewed evidence. It is not personal medical advice and does not create a doctor–patient relationship. Diagnosis, species identification, and antifungal prescribing require assessment by a GP or specialist.

For consumer resources: HealthDirect — Ringworm of the scalp, RCH Kids Health Info, Better Health Channel — Tinea.

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Sources cited

1. Therapeutic Guidelines (eTG) — Dermatology: Tinea capitis
2. Australasian College of Dermatologists — Tinea capitis
3. Royal Children’s Hospital Melbourne CPG — Tinea
4. Australian Medicines Handbook
5. CDNA — School exclusion guidance
6. Fuller LC et al. — BAD guidelines for tinea capitis (Br J Dermatol 2014)
7. Tey HL et al. — Griseofulvin vs terbinafine meta-analysis (JAAD 2011)
8. HealthDirect — Ringworm of the scalp
9. RCH Kids Health Info — Tinea
10. Better Health Channel — Tinea