Epidemiology^[1][2]

• The pattern of infection varies around the world. Microsporum canis is the most common agent in Europe, particularly the countries bordering the Mediterranean. Trichophyton tonsurans, an anthropophilic dermatophyte is mainly seen in the UK (more than 90% of cases). This is possibly linked to an influx of African children. Trichophyton soudanense[/i] and Microsporum audouinii are becoming increasingly common in France.
• The current measures for control have not been effective with spread of T. tonsurans in the USA, possibly because of difficulty distinguishing between carriers and children with minimal infections.^[3]
• T. tonsurans is not a new infection in the UK. There were outbreaks of infections in schools in the 1970s. However, control was achieved by rigorous surveillance. Although there are some differences in the new pattern of infection, improving early detection rates is likely to provide some of the answers.
• M. canis accounts for fewer than 10% of cases in the UK and is mainly seen in non-urban communities. It is principally acquired from puppies and kittens.
• Other animal hosts are occasionally identified - eg Trichophyton verrucosum in cattle.
• Trichophyton schoenleinii in contrast is becoming less common. This is because of its striking clinical appearances and the tendency to scar. It causes a characteristic scalp infection - favus. It is recognised even in remote communities and patients with favus, or their parents, are more likely to present for treatment.
• Ideally, the annual diagnostic figures for tinea capitis should be collected from a number of sentinel diagnostic laboratories in order to monitor the progress of this epidemic and the effect of control measures.^[3]

Risk factors^[3]

Little is known about the risk factors for anthropophilic infection. Those cited include:

• Overcrowding (households or schools).
• Hairdressing salons.
• Use of shared combs.
• Ethnicity.

The current spread of T. tonsurans in the USA, Europe and South America is most often seen in black communities but this species has been found in West and East Africa as well. Although prevalent in black communities, infection occurs in children from other ethnic backgrounds. Ethnicity, social and cultural factors and hair styling all seem to play in the spread of infection; however, definitive proof is lacking.

Presentation^[1]

• Clinical diagnosis alone is unreliable. There is a wide range of clinical presentations and it can, particularly in mild cases, be very difficult to detect. Infection in the hair and scalp skin is associated with symptoms and signs of inflammation and hair loss (mainly in prepubertal children). The main signs are scaling and hair loss but acute inflammation with erythema and pustule formation can occur.
  
  
  
  
  
  
• Laboratory methods should be used wherever possible to confirm the diagnosis.
• The dermatophytes that cause tinea capitis can affect nails and skin in other parts of the body (only very rarely the feet or groins).
• Children or adults who have neither signs nor symptoms of infection but from whose scalps causative fungi can be grown, are described as 'carriers'.
  The carrier state:^[3] Carriage of fungi, defined as positive cultures taken by brush sampling but absence of clinical signs of infection or positive direct microscopy of hair, can occur. However, in the case of T. tonsurans infection in some individuals, it is possible to overlook limited and symptom-free infections accompanied by hair shaft invasion without highly detailed examination of the scalp.

Differential diagnosis^[1]

• Alopecia areata.
• Atopic dermatitis.
• Bacterial folliculitis.
• Drug-related rashes.
• Id reaction (autoeczematisation).
• Impetigo.
• Subacute cutaneous lupus erythematosus.
• Psoriasis (including plaque and pustular varieties).
• Seborrhoeic dermatitis.
• Syphilis (including secondary syphilis).
• Trichotillomania.

Investigations^[4]

• Definitive diagnosis depends on an adequate amount of clinical material submitted for examination by direct microscopy and culture:
  • Scalp scrapings - including hairs and hair fragments - should, wherever possible, be used as the primary method of detection. At least 5 mm² of skin flakes and hair should be obtained wherever possible.
  • This may be difficult (some children may not tolerate the plucking) and the second-line approach is to use sterile brushes (such as disposable toothbrushes).
  • Any treatment cream should be wiped off before sampling.
  • Do not refrigerate samples: keep at room temperature.
  • Cultures should be repeated after therapy.
• Microscopy and culture:
  • Routine direct microscopy takes 24 hours (depending on the laboratory). Microscopic examination of the infected hairs may provide immediate confirmation of the diagnosis of ringworm and establishes whether the fungus is small-spore or large-spore, etc.
  • Culture may take several weeks. Culture provides precise identification of the species (for epidemiologic purposes).
• Conventional sampling of a kerion (pus-filled boggy mass which looks like a bacterial abscess) can be difficult. Negative results are not uncommon in these cases.
• Include any treatment, animal contact and overseas travel in the details on the request form.
• Scrape material directly on to special black cards provided by the laboratory.
• Send samples for microscopy (results available within 24 hours) and culture (takes 2-3 weeks).

Management^[1][3][4]

• Treatment of scalp ringworm can be carried out in primary care and, for most cases, it is not necessary to refer children to a dermatologist. However, the importance of confirming the diagnosis by laboratory procedures, including culture, before starting treatment should again be emphasised.
• There is no currently approved treatment for tinea capitis in childhood in the UK apart from griseofulvin (tablet formulation). However, there are a number of options.

The options for treatment in the following clinical scenarios are:

• Confirmed infection:
  • Children - griseofulvin (1 month-12 years 15-20 mg/kg, maximum 1 g) once daily or in divided doses in patients with T. tonsurans infection.There is no UK approved liquid paediatric formulation of griseofulvin but, in younger children, crushed tablets or suspensions of crushed tablets can be used. It provides broad cover for all the different organisms that cause tinea capitis^[5].
  • Terbinafine is now well documented as a treatment for trichophyton infections, particularly those caused by T. tonsurans; the duration of treatment is four weeks. It is equivalent to griseofulvin given for eight weeks and it is increasingly recommended as the first treatment for T.tonsurans infections. Its dose is doubled in Microsporum spp. infections.
  • Itraconazole and fluconazole are alternatives, particularly with Microsporum spp. infections.
  • Topical treatment (usually selenium sulphide or ketoconazole shampoo but, occasionally, also topical antifungals like terbinafine cream) is recommended at least twice-weekly during the first two weeks of therapy, to minimise transmission to others.
  • Children on treatment should NOT be kept off school unless their clinical condition warrants it (for example, a severe kerion).

  Antifungals for tinea capitis[3]
  Antifungal agent	Daily dosage (weekly or intermittent dosage)
  Griseofulvin	10 mg/kg/day (some physicians use 20 mg/kg/day for T. tonsurans).
  Terbinafine	<10 kg 62.5 mg, 10-20 kg 125 mg, >20 kg 250 mg - all daily.
  Itraconazole	2-4 mg/kg/day. Some data suggest that 5 mg/kg in weekly pulses each month is effective - 2-3 pulses.
  Fluconazole	2-5 mg/kg/day. Weekly treatment with 8 mg/kg may be as effective.
  Note: there is no paediatric licence for this indication at present for any of the agents except griseofulvin. The doses recommended are based on non-comparative trial data.

• Carriers:
  • Do not generally need oral antifungals.
  • They are given a topical preparation such as selenium sulphide shampoo at least twice-weekly.
  • However, if there is heavy growth of dermatophytes from scalp brushes taken from children with clinically normal scalps, they should be treated with oral therapy as for infected cases.
• Children in contact with tinea capitis:
  • Should be examined very carefully for signs of infection (may be just a few visible broken hairs).
  • If infected hairs are seen and confirmed by mycological examination, the children should receive oral therapy.
• Treatment of kerions:
  • The same treatment strategy for normal infections is used.
  • However, it is more difficult to clear with 6-8 weeks of treatment. It is therefore recommended to continue therapy for 12-16 weeks.
  • There is uncertainty over the need for anti-inflammatory treatments. There have been few clinical trials on the use of systemic corticosteroids in kerions.^[3] The use of systemic corticosteroids for routine treatment of kerions is not recommended but they may be used with antifungal therapy if there is a severe allergic response (dermatophyte id reaction).
  • Removal of surface crusts is often helpful (relieves itching and secondary infection). It can be painful and should be carried out after soaking with lukewarm water or saline with moistened dressings and then teasing off the crusts.
  • Sometimes secondary bacterial infection (typically Staphylococcus aureus) requires antibiotics (for example, flucloxacillin) and an antifungal cream which also has anti-Gram-positive activity (miconazole, clotrimazole, econazole). This allows the scalp to heal and avoids the formation of new crusts.

Complications^[1][3]

• Severe hair loss.
• Scarring alopecia.
• Psychological impact (ridicule, bullying, isolation, emotional disturbance, family disruption).

Prognosis^[1][3]

Continuous shedding of fungal spores may last several months even with active treatment. Keeping patients with tinea capitis out of school is impractical.
The treatments are very effective. Treatment failure can occur because of:

• Re-infection.
• Relative insensitivity of the organism.
• Poor absorption of the medication.
• Poor compliance (the long courses of treatment).

In persistent positive cases (often T. tonsurans and Microsporum spp.) - that is, when fungi can still be isolated at the completion of treatment but clinical signs have improved - the recommendation is to continue the treatment for another month.

Prevention

Asymptomatic carriers should be detected and treated. Increased surveillance in schools would be helpful.^[2] Spread should be prevented (avoid sharing of toys or other personal objects, such as combs and hairbrushes, with siblings and playmates of patients).^[3]