**3. Fungal infections of scalp**

#### **3.1. Tinea capitis**

Tinea capitis (TC) is a disease caused by dermatophytes of the skin of the scalp with a propensity for attacking hair shafts and follicles. It occurs predominantly in pre-pubertal children aged between 3 and 7 years. It is reported more in boys than in girls within pre-pubertal age. Tinea capitis is the most seen pediatric dermatophyte infection worldwide [35]. All species of *Trichophyton* and *Microsporum* can cause TC. *Microsporum canis* is the cause of the most seen dermatophyte worldwide, whereas in the United States *Tricophyton tonsurans* is the most common organism. Transmission occurs by direct head-to-head contact through fomites, from animals to humans, and, least commonly, acquired from soil. Asymptomatic carriers of *Tricophyton tonsurans* are common, making it difficult to treat [36].

From the site of inoculation, the fungal hyphae grow centrifugally in the stratum corneum. According to the patterns of contamination, tinea of the scalp is classified into two types: ectothrix and endothrix. In an ectothrix infection, the fungi continue downward growth into the follicle and they invade the keratin part of the hairs. Ectothrix invasion is usually associated with *Trichophyton verrucosum, Trichophyton mentagrophytes* and all *Microsporum* species. The endothrix hair invasion caused by *Trichophyton tonsurans* and *Trichophyton violaceum* is characterised by the development of the fungi within the hair shaft only. While the ectothrix-infected hairs can be of fluoresce bright green or yellow green caused by the destruction of the cuticle of the hair, the endothrix infection do not fluoresce, because the cuticle of the hair remains intact in endothrix infection. The hair is very fragile and breaks the surface of the scalp. Therefore, leaves the infected dark stubs visible in the follicular orifices. Thus, endothrix infection is often described as a 'black dot' appearance [37].

the area by clothing stimulating an inflammatory reaction, secondary bacterial infection, mast cell density and medications such as antiepileptic drugs or cyclosporine [24, 26–28]. Histological studies show evidence of follicular and perifollicular infiltrate at the upper onethird of the hair follicle in early lesions, whereas more advanced lesions reveal disrupted hair follicles, a foreign-body reaction with granulomatous inflammation and fibrotic dermis [25, 29]. Differential diagnosis of AKN consists of the other chronic scarring folliculocentric

First step in treatment is patient education. It should be advised that the patient should avoid from mechanical irritation from clothing for prevention. Prognosis becomes good if the treatment begins at early stage. However, once major scarring develops, therapy is more difficult and morbidity is increased. If pathogenic microorganism with culture are identified, appropriate antibiotics should be prescribed. Conventional treatment modalities usually involve use of topical, intralesional or systemic steroids in combination with retinoids and/or oral antibiotics such as doxycycline or minocycline to decrease inflammation. Oral isotretinoin of 20 mg daily may be used alone or in combination with topical fusidic acid and oral cefadroxil [500 mg twice daily for 2 weeks] to treat the patient [30]. Other treatment options are cryotherapy and targeted ultraviolet B [290–320 nm] phototherapy. Combination of cryotherapy and intralesional steroid may help to reduce the size and firmness of papules and nodules [31]. Radiation therapy and intralesional 5-fluorouracil are alternative treatment strategies

59-nm pulse dye laser [PDL] and 810-nm diode laser have been used which allow for 82–95% improvement in one to five sessions [33]. Patients who present with big fibrotic nodules would benefit most from surgical excision. Excision with primary closure may be used for excellent

Tinea capitis (TC) is a disease caused by dermatophytes of the skin of the scalp with a propensity for attacking hair shafts and follicles. It occurs predominantly in pre-pubertal children aged between 3 and 7 years. It is reported more in boys than in girls within pre-pubertal age. Tinea capitis is the most seen pediatric dermatophyte infection worldwide [35]. All species of *Trichophyton* and *Microsporum* can cause TC. *Microsporum canis* is the cause of the most seen dermatophyte worldwide, whereas in the United States *Tricophyton tonsurans* is the most common organism. Transmission occurs by direct head-to-head contact through fomites, from animals to humans, and, least commonly, acquired from soil. Asymptomatic carriers of

From the site of inoculation, the fungal hyphae grow centrifugally in the stratum corneum. According to the patterns of contamination, tinea of the scalp is classified into two types: ectothrix and endothrix. In an ectothrix infection, the fungi continue downward

laser, 1064-nm Nd:YAG laser,

for refractory cases [32]. Recently, laser treatment such as CO2

*Tricophyton tonsurans* are common, making it difficult to treat [36].

cosmetic results for the management of extensive cases of AKN [23, 28, 34].

pustules localised to the scalp.

204 Hair and Scalp Disorders

**3. Fungal infections of scalp**

**3.1. Tinea capitis**

Among predisposing factors for dermatophyte infections are humid environment, atopic diathesis, such as cell-mediated immune deficiency, systemic immunocompromised states, prolonged immunosuppression with the use of topical glucocorticoids and broad-spectrum antibiotic use [38].

Typical clinical features are small areas of fine scale with minimal hair loss. 'Moth-eaten' alopecia is seen. When *Tricophyton tonsurans* is responsible, black dots are seen. Erythema is also a clue for *Microsporum canis*. Shedding of fungal spores may continue several months despite active treatment; therefore, children with tinea capitis may attend school. Also, short haircuts and wearing a cap during treatment are not necessary. Clinical manifestations of TC may resemble pityriasis amiantacea, seborrheic dermatitis, bacterial folliculitis, pediculosis capitis, trichotillomania, alopecia areata or pustular psoriasis, which are often treated incorrectly [39].

Definitive diagnosis of TC is made through 10–20% potassium hydroxide [KOH] examination and culture from lesions. The turn-around time for culture may take several weeks. Wood light examination is also helpful to demonstrate fungal fluoresce. Infected hair produces bright green or yellow green fluorescence. It should be kept in mind that endothrix organisms do not fluoresce. Trichoscopy is an additional tool for the diagnosis of tinea capitis. Comma shaped hairs, corkscrew hairs and zigzag shaped hairs are the diagnostic trichoscopic features of tinea capitis [40, 41]. Skin biopsy can be done for differential diagnosis. Fungal hyphae in the stratum corneum can be demonstrated histopathologically.

As the dermatophyte penetrate the hair follicle, oral antifungals is required for the treatment of TC. Basically, three different groups of systemic antifungals are used to eliminate TC: Griseofulvin, azoles [itraconazole, fluconazole, ketoconazole] and allylamines [terbinafine]. Of these agents, itraconazole and terbinafine are most commonly used. Griseofulvin [10–25 mg/kg/day for 6–8 weeks] is the most frequently used antifungal agent, but recently it has also been reported that newer agents such as terbinafine [10–20 kg: 62.5 mg/day; 20–40 kg: 125 mg/ day; >40 kg: 250 mg/day for 2–4 weeks], itraconazole [5 mg/kg/day for 2–6 weeks] and fluconazole [first dose 6–12 mg/kg, then 3–6 mg/kg/day for 2–4 weeks] to be effective. Selenium sulphide, zinc pyrithione, povidone iodine or ketoconazole shampoos have been shown to help to decrease the shedding of fungal spores. Common recommendations are to use these shampoos two to four times weekly for 2–4 weeks [42, 43].

#### **3.2. Favus**

Favus or tinea favosa is the most severe form of tinea capitis. It is caused by *Tricophyton schoenleinii*. The disease frequently occurs in children and is seen rarely in adults. If untreated, the disease persists forever. Favus is seen almost exclusively in Africa, the Mediterranean and the Middle East and, rarely, in North America and South America [44].

The most common clinical manifestations on the scalp are yellowish cup-shaped crusts termed scutula, which surround the infected hair follicles. The scutula have an unpleasant mousy odour. Besides the scalp, it may involve glabrous skin, hairy regions and nails. If not treated properly, the lesion advances peripherally and it can leave scarring alopecia [45, 46].

The diagnosis is confirmed by direct mycological examination and culture. A greyish-green fluorescence may be observed with Wood's lamp examination. Optical microscopy with KOH preparation shows invasion by the fungus, hyphae parallely arranged to the axis, air spaces and a few spores.

In presence of scaly patches without alopecia, favus is misdiagnosed as seborrheic dermatitis, psoriasis, tinea amiantacea or lichen planus [47, 48].

The treatment of tinea favosa lies on the combination of an oral and topical antifungal agents. The local treatment consists in cutting of hair around the alopecia patches and applying once or twice a day of antifungal imidazol [shampoo, foam gel, lotion and spray]. Griseofulvin terbinafine and itraconazole could be used in systemic therapy [44, 45].

#### **3.3. Kerion**

Kerion celsi [KC] [so-called deep tinea capitis] is an uncommon inflammatory presentation of tinea capitis [TC], which appears as a boggy, large inflammatory painful mass studded with broken hairs, pustules and, often, purulent drainage from its surface (**Figure 5**). Hair loss is frequently seen in KC. It is usually solitary but multiple lesions may be found. Reactive lymphadenopathy, especially cervical or suboccipital, is a very common associated feature. KC often occurs in children but it has been described in elderly patients [49–51]. The higher

**Figure 5.** Boggy, large inflammatory painful plaque lesion is seen.

prevalence in females may be related to fact that they generally have longer hair [52]. KC is a markedly inflammatory type of TC secondary to a vigorous host immune response. It is generally caused by zoophilic dermatophytes [*Microsporum canis and Trichophyton mentagrophytes*], but also by anthropophilic [*Trichophyton rubrum*] and rarely by geophilic [*Microsporum gypseum*] species. KC is thought to be the result of a hypersensitivity reaction to dermatophytes [49].

The main source of the fungi responsible for KC is from humans or animals, though dermatophytes may spread via fomites [combs, hairbrushes, hats and contaminated wearing materials]. Although the gold standard diagnostic method is fungal culture, conventional sampling of a kerion can be difficult. Negative results are not uncommon in these cases. The diagnosis of kerion is usually made clinically. A moistened standard bacteriological swab taken from the pustular areas and inoculated onto the culture plate may yield a positive result [53].

Id reactions [so-called dermatophytid] are noted in patients with KC. This is an often pruritic dermatitis based on sensitisation to fungal antigens, reported in 4–5% of fungal infection. Although it may mimic an allergic reaction, it should not lead to discontinuation of antifungal treatment [54]. Acute vesicular dermatitis of the hands and feet is the most common type of id reaction. Other less common types of id reactions include annular erythema and erythema nodosum. These patients have a strong delayed-type hypersensitivity [DTH] reaction to intradermal trichophytin. EN is thought to be due either the deposition of immune complexes in capillaries and venules of the dermal and adipose plexus, or to a DTH reaction to an antigen [55, 56].

The principal differential diagnoses consist of impetigo and bacterial or sterile folliculitis or abscesses. KC is usually misdiagnosed as bacterial abscesses. However, bacterial infections do not cause alopecia, and hairs plucked from a kerion are painless. Diagnostic errors causes patients to undergo unnecessary surgery or antibiotic treatment. However, there is little evidence to support the use of antibiotics for severe KC [49]. Kerion celsi requires treatment with systemic antifungals to penetrate the affected hair shafts. Early short course of glucocorticosteroids with a dose of 1 mg/kg/day were often used in severe KC to reduce inflammation. Oral steroid is tapered to withdraw in 10 days. Manual pressure to remove pus from sinuses was an adjuvant therapy to systemic oral antifungal agents for severe KC.
