Tinea capitis: etiology, clinical manifestation, diagnosis and treatment




Tinea capitis: etiology, clinical manifestation, diagnosis and treatment
Tinea capitis: etiology, clinical manifestation, diagnosis and treatment

What is Tinea capitis?

  • The term tinea capitis is used to refer the infections caused by the dermatophytes on the hair scalp and hair skin.
  • The major clinical signs are hair loss and scaling along with the possibilities of inflammation.
  • Certain individuals are termed as carriers, as dermatophytes can be isolated from their scalp but they lack any signs and symptoms.
  • Geographical distribution of Tinea capitis:
    • Tenia capitis has been distributed world-wide, but is more common in Africa, Asia and southern and eastern Europe.
    • It occurs mainly in prepubescent children.
    • It is seen as increasing incidence.

Epidemiology:

  • Etiological agents:
    • Tinea capitis caused by anthropophilic Microsporum and Trichophyton species is a contagious disease endemic in many countries.
  • It is primarily a disease of pre-pubertal children, being more common in males than females, and most prevalent between 6 and 10 years of age.
  • The disease seldom persists beyond the age of 16.
  • The predominant aetiological agents of anthropophilic tinea capitis differ from one region to another, and can change within a particular region over time.
  • At least two factors are thought to be responsible for this shift in species distribution.
  • The first is the wide- spread use of griseofulvin to treat scalp infections. Because M. audouinii is susceptible to this antifungal agent, this species may have been eradicated, allowing T. tonsurans, which is less susceptible to griseofulvin, to become predominant.
  • The second factor is changes in immigration patterns and the increase in international travel which might have facilitated the spread of T. tonsurans to new regions.
  • In addition to T. tonsurans, other anthropophilic species, such as T violaceum, have appeared and in- creased in prevalence in urban populations in the UK and Europe.
  • Children from all ethnic back- grounds are susceptible.
  • In the USA, T. tonsurans is also more common in urban populations, particularly among African American children.  
  • The distribution of zoophilic infections in humans mirrors the geographic range of the animal host.
  • The most common zoophilic cause of tinea capitis is M. canis which is spread from cats and dogs.
  • Household pets are a common source of infection, but feral cats are another prolific source of M. canis.
  • Sporadic cases of M. canis infection occur worldwide.
  • T. verrucosum, which is acquired from cattle, is the second most frequent cause of zoophilic tinea capitis in the UK.

Clinical manifestations of Tinea capitis:

  • The clinical manifestations of tinea capitis are varied and can range from mild scaling  and hair loss to widespread alopecia, or less commonly to a highly inflammatory suppurating lesion termed a kerion.
  • The suppurating lesion (Kerion) is usually caused by infection with a zoophilic dermatophyte. Different dermatophytes give different characteristic lesion.
  • i) lesion:
  • a) In Microsporum audouinii infection the lesions consist of one or more discrete, round or oval, erythematous patches of scaling and hair loss (2-6 cm in diameter).
    • These may extend with time to involve the entire scalp. Fine scaling being the characteristic, inflammation is minimal.
    • The hairs in these lesions are all parasitized and most of them are broken about 2-3 mm above the surface of the scalp.
    • In Microsporum canis infection the scene is similar, but there is usually more inflammation.
    • In both these infections the hair surface is covered with a dense mass of small (2-3 pm in diameter) arthrospores (ectothrix infection).
    • The infected hairs show green fluorescence under Wood’s light.
  • b) In Tricophyton tonsurans, T. violaceum and T. soudanense infections, the lesions are often inconspicuous and inflammation may be minimal.
    • The typical lesions are irregular patches of scaling (0.5-1.0 cm in diameter).
    • The affected hairs often break off at the scalp surface, leading to alopecia and giving a black-dot appearance in dark- haired patients.
    • Other hairs are broken off 1-2 mm from the scalp surface and are often obscured under a layer of scales.
    • The infected hairs are filled with arthrospores (endothrix infection) and do not fluoresce under Wood’s light.
  • ii) Kerion:
    • The most florid form of tinea capitis is a kerion and is a painful inflammatory mass in which the hairs that remain are loose.
    • Thick crusting with matting of adjacent hairs is common.
    • Pus may be discharged from one or more points.
    • A kerion may be limited in extent, but a large confluent lesion can develop that involves most of the scalp.
    • In most cases, infection with a zoophilic dermatophyte such as Trichophyton verrucosum or T. mentagrophytes results in the kerion formation.
    • In T. verrucosum infections, the hairs are coated with chains of large arthrospores however they do not fluoresce under Wood’s light.
  • iii) Favus:
    • The main clinical manifestations of favus are the formation of crusted, inflamed patches on the scalp, with permanent hair loss due to follicular scarring.
    • The scalp itches and gives off a foetid odour.
    • The crusts (scutula) develop around the follicular openings and can fuse to cover large areas of the scalp.
    • Long-standing favus can lead to permanent diffuse patches of alopecia.
    • Although infected, the hairs tend not to break off and can grow to normal length.
    • Infected hairs give off a dull green fluorescence under Wood’s light.

Differential diagnosis of Tinea capitis:

  • Tinea capitis is often difficult to differentiate from other causes of scaling (such as psoriasis and seborrhoeic dermatitis) or hair loss (such as alopecia areata and discoid lupus erythematosus).
  • Thus, Wood’s light examination and laboratory tests should be performed in any patient with scaling scalp lesions or hair loss of undetermined origin.
  • A kerion can be misdiagnosed as a bacterial abscess, and then incised, drained and treated with antibiotics.
  • Antibiotics treatment has no effect on the fungus.
  • The longer the infection remains undiagnosed, the greater the risk of scarring alopecia.
  • It is essential that any pustular eruption, particularly of the scalp, is identified as a possible fungal infection and examined accordingly.

lab diagnosis of tinea capitis

  • Specimens:
    • Specimens from the scalp should consist hair roots, the contents of plugged follicles and skin scales.
    • Excluding favus, the distal portion of infected hair rarely carry any fungus.
    • Thus, cut hairs without roots are unsuitable for mycological investigation.
    • One method which is useful for collecting material from the scalp is hair brush sampling.
  • Microscopy:
    • Hairs infected with Trichophyton tonsurans do not fluoresce under Wood’s light whereas those infected with Microsporum audouinii or M. canis produce a brilliant green fluorescence under Wood’s light in a darkened room.
    • However, in recent infections, or at the spreading margin of lesions, the fluorescent part of the hair may not yet have emerged from the follicle and fluorescence can only be detected after the hair is plucked.
    •  T. schoenleinii causes a pale dull green fluorescence of infected hair.
    • The fluorescent hairs tend to be long, in contrast to the short hair stumps characteristic of Microsporum infection.
    • The creams and ointments applied to scalp lesions, as well as host tissue and exudates, can produce a pale bluish or purplish fluorescence under Wood’s light.
    • Direct microscopic examination of infected material should expose arthrospores of the fungus located outside (ectothrix) or inside (endothrix) the affected hair.
    • The arthrospores can be either small ( 2-4 m in diameter) or large (up to 10m in diameter) in size.
    • Skin scales will contain hyphae and arthrospores.
    •  In T. schoenleinii infection (favus), loose chains of arthrospores and air spaces are seen within the affected hairs.
    • The crust as termed as scutulum comprises of neutrophils, mycelium and epidermal cells.
  • Culture:
    • Isolation of the aetiological agent in culture will allow the species of fungus involved to be determined.
    • This will grant information as to the source of the infection and help in the selection of appropriate treatment.

Treatment of Tinea capitis

  • It is essential to have mycological confirmation before the initiation of the oral treatment.
  • Treatment can be done with these alternatives:
  • Griseofulvin:
    • 10 mg/kg for up to 3 months
    • absorption and bioavailability vary with dietary fat intake
    • rapidly eliminated from body when discontinued; some side effects
  • Itraconazole:
    • 100 mg/day for 4–6 weeks in adults
    • depending on causative species
    • note potential drug interactions
  • Itraconazole pulse therapy:
    • for children
    • oral solution, 5 mg/kg/day for 1 week per month for 3–4 months
  • Terbinafine:
    • 250 mg/day for 4 – 6 weeks
    • higher dose and longer duration if Microsporum canis is present; only mild and transient side effects
  • Fluconazole:
    • oral suspension, daily or weekly regimens
    • good absorption
    • optimum dose to be determined
    • Fluconazole is licensed for use in children (although not for dermatophytosis)
    • It is a useful alternative treatment for patients with Microsporum infections that fail to respond to griseofulvin
  • 2% ketoconazole shampoo, or 1% selenium sulphide shampoo regarded as topical treatment of lesions with an azole, may decrease spread.
  • One of the essential component in management of tinea capitis is the regular epidemiological observation of causative fungal organisms in the community and their antifungal sensitivity.

Tinea capitis: distribution, etiology, clinical manifestation, diagnosis and treatment