Tinea Capitis

See separate related article on Dermatophytosis (Tinea Infections).

Tinea capitis, or scalp ringworm, is an exogenous infection caused by the dermatophytes Microsporum spp. and Trichophyton spp. These originate from a number of possible sources including other children or adults (anthropophilic), animals (zoophilic) or soil (geophilic).

• The pattern of infection varies around the world.

  Tinea capitis - range of infection around the world
  Area	Dermatophyte
  Europe	M. canis, (T. verrucosum – less common) T. tonsurans, T. soudanense, M. audouinii – including M. langeroni
  USA, Canada	T. tonsurans, M. canis
  Mexico, Central America	T. tonsurans, (M. canis)
  South America	M. canis
  West Africa	M. audouinii, M. langeroni, M. rivalieri T. soudanense, T. yaoundei, T. gourvilii
  East Africa	T. violaceum (north), T. schoenleinii M. canis, M. audouinii
  Middle East	M. canis, T. violaceum
  Indian subcontinent	T. violaceum, T. tonsurans
  SE Asia	M. canis, M. ferrugineum, T. tonsurans,
  Russia and Central Asia	M. canis, T. violaceum, M. ferrugineum
  China, Japan, East Asia	M. canis, T. tonsurans
  Australasia	M. canis
  T. schoenleinii causes favus, which is a clinically distinct form of tinea capitis.

• The pattern of tinea capitis in the UK has changed in the past ten years. In particular there has been a dramatic rise in the incidence and prevalence of of infection due to anthropophilic dermatophytes such as T. tonsurans.
• This epidemic has been mainly in cities within black communities. However it is clear that infection can occur in any child irrespective of their ethnic origin.
• It occurs mainly in prepubertal children.
• 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.¹
• 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.
• T. 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.¹

Risk factors

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.

• 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. affect nails and skin in other parts of the body
• 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:1carriage 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.

• 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

• 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.
  • This may be difficult and, therefore the second-line approach is to use sterile brushes (such as disposable toothbrushes).
  • 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 can be difficult. Negative results are not uncommon in these cases.
• Skin and nail specimens may be scraped directly on to special black cards (easier to see how much material has been collected and provide ideal conditions for transportation to the laboratory).

• 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 (dose of at least 10 mg/kg and up to 20 mg/kg in patients with T. tonsurans infection or where there is failure to respond after six weeks of treatment). 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.
  • 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.
  • Children on treatment should NOT be kept off school unless their clinical condition warrants it (for example a severe kerion).

  Antifungals for tinea capitis1
  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 (pus filled inflammatory swellings which may look like bacterial abscesses):
  • 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.¹ 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.

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

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.

Asymptomatic carriers should be detected and treated.
Spread should be prevented (avoid sharing of toys or other personal objects, such as combs and hairbrushes, with siblings and playmates of patients).¹