Tinea capitis Scalp ringworm or tinea capitis has become an increasingly important public health problem in the past

decade.97,98 It was once almost exclusively an infection of children, and associated with either M. canis or M. audouinii.99101 M. canis is the causative organism in only 10% of all tinea capitis infections in the UK.102 This organism is still common in some countries.103 Now, T. tonsurans and T. violaceum are the most common isolates in some geographical areas,104122 causing an endothrix type of hair invasion with the fungus entering the cortex just above the hair bulb and encircling the shaft beneath an intact cuticle.123 Endothrix infections do not produce fluorescence with Woods light, as opposed to ectothrix infections (M. canis and M. audouinii), which give a typical green fluorescence. T. rubrum, the commonest cause of tinea corporis, is not usually regarded as a scalp pathogen, although very occasional cases occur.124126 T. soudanese is a common cause of tinea capitis in Africa; it is rare elsewhere except in immigrants from Africa.127129 The effects vary from mild erythema with persistent scaliness and minimal hair loss through to inflammatory lesions with pustules and folliculitis and kerion formation.130,131 Adults generally present with alopecia and scale,132 but it may also masquerade as a bacterial pyoderma.133,134 Tinea capitis may also mimic dissecting cellulitis.135 Tinea capitis seems to be surprisingly rare in patients with HIV infection. 136,137 It is also uncommon in the first year of life.138140 Transmission at the hairdresser has been recorded in two elderly women.141 Household contacts are a potential reservoir of infection.142 The production of extracellular proteases by the fungi facilitates their dissemination through the stratum corneum of the scalp.143

Tinea of the scalp (tinea capitis; see also p. 210, Fig. 14.8) This is usually a disease of children. The causative organism varies from country to country. Fungi coming from human sources (anthropophilic organisms) cause bald and scaly areas, with minimal inflammation and hairs broken off 34 mm from the scalp. Fungi coming from animal sources (zoophilic fungi) induce a more intense inflammation than those spread from person to person. In ringworm acquired from cattle, for example, the boggy swelling, with inflammation, pustulation and lymphadenopathy, is often so fierce that a bacterial infection is suspected; such a lesion is called a kerion and the hair loss associated with it may be permanent. Tinea of the beard area is usually caused by zoophilic species and shows the same features (Fig. 16.42). In favus, caused by Trichophyton schoenleini, the picture is dominated by foul-smelling yellowish crusts surrounding many scalp hairs, and sometimes leading to scarring alopecia. The scalp and hair of black children are especially prone to infection with Trichophyton tonsurans (p. 210). ABC OF DERMATOLOGY FOURTH EDITION Paul K Buxton BMJ Scalp and face Scalp ringworm in children may be caused by anthropophilic fungi such as Trichophyton tonsurans, which is spreading in cities in the United Kingdom, or Microsporum audouinii. Sporadic cases are caused by M.canis which is acquired from cats or dogs. In all cases there is itching, hair loss, and some degree of inflammation which is worse with M. canis infections. Kerion, an inflamed, boggy, pustular lesion, is often due to cattle ringworm and is fairly common in rural areas. It is often seen in children in the autumn when the cows are brought inside for the winter. THE SUPERFICIAL MYCOSES Tinea capitis Tinea capitis, also known as scalp ringworm, can be caused by all the pathogenic dermatophytes except for Epidermophyton floccosum and Trichophyton concentricum. In the US, most cases are caused by Trichophyton tonsurans (which has replaced Microsporum audouinii as the most common pathogen). Pet exposure is associated with tinea capitis caused by M. canis. Immigrant populations have a high incidence of tinea capitis with organisms common in their regions of origin. Among African and Arab immigrants, Trichophyton soudanense, Trichophyton violaceum and M. audouinii are particularly common. Tinea capitis occurs mainly in children, although it may be seen at all ages. Boys have tinea capitis more frequently than girls; however, in epidemics caused by T. tonsurans there is often equal frequency in the sexes. African American children have a higher incidence of T. tonsurans infections than Anglo Americans. The infection is also common among Latin American children. T. tonsurans produces black dot ringworm, as well as subtle

seborrheic-like scaling and inflammatory kerion. Black dot tinea may also be caused by T. violaceum, an organism rarely seen in the US. Both of these organisms produce chains of large spores within the hair shaft (large spore endothrix) (Fig. 15-1). They do not produce fluorescence with a Woods light. The M. canis complex includes a group of organisms that produce small spores visible on the outside of the hair shaft (small spore ectothrix). These fungi fluoresce under Woods light examination. The M. canis complex includes M. canis, M. canis distortum, Microsporum ferrugineum, and M. audouinii. M. canis infections begin as scaly, erythematous, papular eruptions with loose and broken-off hairs. The lesions commonly become highly inflammatory, although M. audouinii has less of a tendency to produce inflammatory lesions. Deep, tender, boggy plaques exuding pus are known as kerion celsii (Fig. 15-2). Kerion may be followed by scarring and permanent alopecia in the areas of inflammation and suppuration. Systemic steroids for a short period along with appropriate antifungal therapy will greatly diminish the inflammatory response and reduce the risk of scarring, and should be considered in the setting of highly inflammatory lesions. Asymptomatic carriers of T. tonsurans are common, and represent a source of infection for classmates and siblings. Numerous studies have shown that 515% of urban children in western countries have positive scalp dermatophyte Fig. 15-1 Endothrix hair mount, note spores within the hair shaft.

Fig. 15-2 Kerion. cultures. In one study, 60% of children with a positive scalp culture were asymptomatic. All of these children were African

American. The presence of scalp scaling and the use of a dandruff shampoo were associated with an increased likelihood of carrying a fungal organism. It is unlikely that dandruff shampoos predispose to tinea. More likely, they provide incomplete treatment of minimally symptomatic tinea that produces a subtle seborrheic scale. The prevalence of various dermatophytes varies throughout the world. Where animal herding is an important part of the economy, zoonotic fungi account for a significant proportion of cases of tinea. In Asia, organisms vary significantly by region. In a study of 204 Iraqi schoolchildren with tinea capitis, Trichophyton verrucosum was the most common organism. Both T. rubrum and T. mentagrophytes var. mentagrophytes were more common than T. tonsurans. In south central Asia, T. violaceum is the most common dermatophytic species isolated, with M. audouinii a close second. Other common organisms include Trichophyton schoenleinii, T. tonsurans, Microsporum gypseum, T. verrucosum, and T. mentagrophytes. In east Asia, T. violaceum and M. ferrugineum are important pathogens. In Europe, African/Caribbean immigrants account for a large proportion of new patients with tinea capitis. Important pathogens include T. tonsurans, M. audouinii var. langeronii, Trichophyton soudanense, and T. violaceum. Trichophyton megninii is a rare cause of tinea capitis largely restricted to southwest Europe. In Africa, large-scale epidemics are associated with T. soudanense, T. violaceum, T. schoenleinii and Microsporum spp. In Australia, the predominantly white population experiences infections, mostly with M. canis, but T. tonsurans is now equal in prevalence in some areas of the continent. Favus Favus, which is very rare in the US, appears chiefly on the scalp but may affect the glabrous skin and nails. On the scalp, concave sulfur-yellow crusts form around loose, wiry hairs. Atrophic scarring ensues, leaving a smooth, glossy, thin, paper-white patch. On the glabrous skin the lesions are pinhead to 2 cm in diameter with cup-shaped crusts called scutulae, usually pierced by a hair as on the scalp. The scutulae have a distinctive mousy odor. When the nails are affected they become brittle, irregularly thickened, and crusted under the free margins. Favus among the Bantus in South Africa is called, in Afrikaans, witkop (whitehead). It is also prevalent in the Middle East, southeastern Europe, and the countries bordering the Mediterranean Sea. Pathogenesis and natural history The incubation period of anthropophilic tinea capitis lasts 24 days, although the period is highly variable and asymptomatic carriers are common. The hyphae grow downward into the follicle, on the hairs surface, and the intrafollicular hyphae break up into chains of spores. There is a period of spread

(4 days to 4 months) during which the lesions enlarge and new lesions appear. At about 3 weeks hairs break off a few millimeters above the skin surface. Within the hair, hyphae descend to the upper limit of the keratogenous zone and here form Adamson fringe on about the 12th day. No new lesions develop during the refractory period (4 months to several years). The clinical appearance is constant, with the host and parasite at equilibrium. This is followed by a period of involution in which the formation of spores gradually diminishes. Zoonotic fungal infections are commonly more highly inflammatory, but undergo similar phases of evolution. Diagnosis Woods light Ultraviolet (UV) light of 365 nm wavelength is obtained by passing the beam through a Woods filter composed of nickel oxide-containing glass. This apparatus, commonly known as the Woods light, is commonly used to demonstrate fungal fluorescence. Fluorescent-positive infections are caused by M. audouinii, M. canis, M. ferrugineum, M. distortum, and T. schoenleinii. In a dark room the skin under this light fluoresces faintly blue, and dandruff commonly is bright blue white. Infected hair fluoresces bright green or yellowgreen. The fluorescent substance is a pteridine. Large spore endothrix organisms (such as T. tonsurans and T. violaceum) and T. verrucosum (a cause of large spore ectothrix) do not fluoresce. Laboratory examination For demonstration of the fungus in a highly inflammatory plaque, two or three loose hairs are carefully removed with epilating forceps from the suspected areas. If fluorescence occurs, it is important to choose these hairs. Bear in mind that hairs infected with T. tonsurans do not fluoresce. In black dot ringworm or in patients with seborrheic scale, small broken fragments of infected hair will adhere to a moist gauze pad rubbed across the scalp. The hairs are placed on a slide and covered with a drop of a 1020% KOH solution. Then a coverslip is applied, and the specimen is warmed until the hairs are macerated. Dimethyl sulfoxide (DMSO) can be added to the KOH solution in concentrations of up to 40%. This additive allows for rapid clearing of keratin without heating. Once the hairs have softened, they are compressed through the coverslip and examined first with a low-power objective and then with a high-power objective for detail. The patterns of endothrix and ectothrix involvement described above, together with local prevalence data, allow for identification of the organism. Exact identification of the causative fungus is generally determined by culture, although molecular sequencing offers a more rapid alternative. For culture, several infected hairs are planted on Sabouraud dextrose agar, Sabouraud agar with chloramphenicol, Mycosel agar, or dermatophyte test medium

(DTM). Cultures are best collected by rubbing the lesion vigorously with a moistened cotton swab or gauze pad, then streaking the cotton over the agar surface. On the first three media, a distinctive growth appears within 12 weeks. Most frequently, the diagnosis is made by the gross appearance of the culture growth, together with the microscopic appearance. In the case of Trichophyton spp, growth on different nutrient agars is often required to identify the organisms beyond genus. DTM not only contains antibiotics to reduce growth of contaminants but also contains a colored pH indicator to denote the alkali-producing dermatophytes. A few nonpathogenic saprophytes will also produce alkalinization and in the occasional case of onychomycosis of toenails caused by airborne molds, a culture medium containing an antibiotic may inhibit growth of the true pathogen. T. tonsurans This microorganism grows slowly in culture to produce a granular or powdery yellow to red, brown, or buff colony. Crater formation with radial grooves may be produced. Swollen microconidia may be seen regularly. Diagnosis is confirmed by the fact that cultures grow poorly or not at all without thiamine. T. mentagrophytes The colony is velvety, granular, or fluffy. It may be flat or furrowed, light buff, white, or sometimes pink. The back of the culture can vary from buff to dark red. Round microconidia borne laterally and in clusters confirm the diagnosis within 2 weeks. Spiral hyphae are sometimes prominent. T. verrucosum Growth is slow and cannot be observed well for at least 3 weeks. The colony is compact, glassy, velvety, heaped or furrowed, and usually white, but may be yellow or gray. The colony may crack the agar. Chlamydospores (round swellings along the hyphal structure) are present in early cultures, and microconidia may be seen. M. audouinii Culture typically shows a slowly growing, matted, velvety, light brown colony, the back of which is reddish brown to orange. The colony edge is generally striate, rather than smooth. Under the microscope a few large multiseptate macroconidia may be seen. Microconidia in a lateral position on the hyphae are clavate. Racquet mycelia, terminal chlamydospores, and pectinate hyphae are sometimes seen. M. canis The culture grossly shows profuse, cottony, aerial mycelia that are distinctly striate at the periphery, while sometimes tending to become powdery in the center. The color is buff to light brown. The back of the colony is lemon to orangeyellow. There are numerous spindle-shaped, thick-walled echinulate macroconidia. Clavate microconidia may be found, along with

chlamydospores and pectinate bodies. Differential diagnosis Tinea capitis must be differentiated clinically from chronic staphylococcal folliculitis, pediculosis capitis, psoriasis, seborrheic dermatitis, secondary syphilis, trichotillomania, alopecia areata, lupus erythematosus, lichen planus, lichen simplex chronicus, and various inflammatory follicular conditions. The distinctive clinical features of tinea capitis are broken-off stumps of hairs, often in rounded patches in which there are crusts or pustules and few hairs. The broken-off hairs are loose and when examined are found to be surrounded by, or to contain, the fungus. Diffuse seborrheic scaling with hair loss is a common presentation of T. tonsurans infections. In alopecia areata the affected patches are bald, and the skin is smooth and shiny without any signs of inflammation or scaling. Stumps of broken-off hairs are infrequently found, and no fungi are demonstrable. In seborrheic dermatitis the involved areas are covered by fine, dry, or greasy scales. Hair may be lost, but the hairs are not broken. Atopic dermatitis is rarely associated with localized scalp involvement, and clinical examination frequently reveals more typical generalized findings. In psoriasis, well-demarcated, sometimes diffuse, areas of erythema and white or silver scaling are noted. Lichen simplex chronicus is frequently localized to the inferior margin of the occipital scalp. In trichotillomania, as in alopecia areata, inflammation and scaling are absent. Circumscribed lesions are very rare. Serologic testing, scalp biopsies, and immunofluorescent studies may be indicated if the alopecia of secondary syphilis or lupus erythematosus is a serious consideration. It should be noted that adult patients with lupus erythematosus are susceptible to tinea capitis, which may be photosensitive and difficult to distinguish from plaques of lupus without biopsy and KOH examinations. Treatment Numerous clinical trials exist that demonstrate the effectiveness of itraconazole, terbinafine, and fluconazole. Despite these studies, griseofulvin remains the most commonly used antifungal agent in children. It has a long safety record, and pediatricians and family practitioners are generally comfortable with the drug. A meta-analysis of published studies shows mean efficacy for griseofulvin treatment of about 68% for Trichophyton spp and 88% for Microsporum. For the ultramicronized form, doses start at 10 mg/kg/day. The tablets can be crushed and given with ice cream. Grifulvin V oral suspension is less readily absorbed. The dose is 20 mg/kg/day. Treatment should continue for 24 months, or for at least 2 weeks after negative laboratory examinations are obtained. Doses much higher than those reflected in drug labeling are commonly needed. For Trichophyton infections, terbinafine is commonly effective in doses of 36 mg/kg/day for 14 weeks.

Alternate dosing schedules for terbinafine include one 250 mg tablet for patients over 40 kg, 125 mg (half of a 250 mg tablet) for those 2040 kg, and 62.5 mg (one-quarter of a 250 mg tablet) for those under 20 kg. Microsporum infections require higher doses and longer courses of therapy with terbinafine. Itraconazole has been shown to be effective in doses of 5 mg/ kg/day for 23 weeks, and fluconazole at doses of 6 mg/kg/ day for 23 weeks. Reports of heart failure with itraconazole have limited its use. Selenium sulfide shampoo or ketoconazole shampoo left on the scalp for 5 min three times a week can be used as adjunctive therapy to oral antifungal agents to reduce the shedding of fungal spores. Combs, brushes, and hats should be cleaned carefully and natural bristle brushes must be discarded. Prognosis Recurrence usually does not occur when adequate amounts of griseofulvin, fluconazole, or terbinafine have been taken, although exposure to infected persons, asymptomatic carriers, or contaminated fomites will increase the relapse rate. Without medication there is spontaneous clearing at about the age of 15, except with T. tonsurans, which often persists into adult life.