Superficial Fungal Infections

Epidemiology and Microbiology

Tinea capitis largely affects children, with the peak incidence between 4 and 7 years of age. ^, Age prevalence probably is due to the antifungal effect of sebum, which becomes abundant around puberty and inhibits the growth of dermatophytes consequent to the presence of saturated fatty acids with chain lengths of 7, 9, 11, and 13 carbon residues in sebum.

The epidemiologic relevance of tinea capitis is its propensity for rapid spread within schools and childcare facilities. Early recognition and treatment of cases and identification of infection in contacts are essential. There is no clear-cut sexual predilection for the infection, with speculation of higher incidence in boys due to easy implantation of spores in shorter hair, and a higher incidence in girls due to tight braiding.

Tinea capitis is caused by dermatophytes with the ability to invade hair shafts. Based on the location of formation of spores (arthroconidia) from hyphae, the pattern of invasion is termed ectothrix (sporulation occurring over the surface of shaft) or endothrix (sporulation occurring within hair shafts). The two patterns of invasion may lead to distinct clinical presentations, although significant overlap exists.

Dermatophyte strains causing tinea capitis vary in different geographical locations. While Trichophyton tonsurans has emerged as the predominant cause in the US, Western Europe, South America, and West Africa, Microsporum canis predominates in other parts of Europe. Trichophyton soudanense and Trichophyton violaceum predominate in niche areas of Africa and India, with occasional reports from the US. T. tonsurans , T. soudanense, and T. violaceum are anthropophilic, while M. canis is zoophilic with cats and dogs as the major vectors. The inflammatory kerion is predominantly caused by zoophilic strains Trichophyton verrucosum and Trichophyton mentagrophytes, although rarely anthropophilic infections can suddenly become inflammatory. ^{, ,} The rare variant favus is caused by the anthropophilic dermatophyte Trichophyton schoenleinii .

Clinical Manifestations and Differential Diagnosis

The characteristic presentation of tinea capitis is a patch of partial (never total) hair loss, along with varying degrees of inflammation (scaling/erythema/pustulation). Hairs within the patch are easily pluckable because of damage by the fungus. Lymphadenopathy often is present in the posterior auricular, occipital, and submandibular groups, especially with the inflammatory types, and helps to differentiate tinea capitis from clinical mimickers. Tinea capitis is variably pruritic and can take one of the following clinical forms.

• 1.

  Grey patch tinea capitis —patches of partial alopecia with broken off dull grey hair (representing spores on the surface of hair shafts in an “ectothrix” type invasion) within the patch, and fine scaling all throughout the lesion ( Fig. 254.1 )

  

• 2.

  Black dot tinea capitis —patches (single/multiple) of partial hair loss with black dots representing hair broken off at the scalp surface in an “endothrix” type invasion

• 3.

  Kerion ( kerion celsi )—boggy fluctuant mass with loss of hair and pustulation on the surface. Secondary bacterial infection can occur, although follicular pustules primarily represent an inflammatory response to the fungus itself ( Fig. 254.2 ). Another inflammatory variant is the diffuse pustular form in which patchy alopecia occurs with extensively scattered pustules.

  

• 4.

  Favus —a distinct pattern, endemic in certain regions of Africa, characterized by the presence of cup-shaped crusts (scutula) around hair follicles. The affected hair appears less damaged initially and may grow long, but the infection is persistent and leads to scarring and permanent hair loss over time. ^,

• 5.

  Other manifestations —diffuse erythema and scaling with mild hair loss and less discernible alopecic patches (seborrheic dermatitis-like tinea capitis) or visibly bland patches with no inflammation (alopecia areata-like tinea capitis ). ^, Inflammatory variants can be associated with an id eruption, with tiny papulovesicles over helices of ear, face, neck, or more extensively distributed eczematous lesions over the trunk and extremities. Typically, these lesions are pruritic, appear either before or after initiation of antifungal treatment, do not contain fungal elements on smear examination, and require topical or systemic corticosteroid therapy (depending on the extent) for resolution in addition to a continuation of antifungal treatment.

Tinea capitis must be differentiated from other causes of patchy hair loss in children, the most important of which is alopecia areata . Alopecia areata manifests as smooth bald patches with no hair or only a few non-pigmented hairs within the patch. There is no scaling or signs of inflammation or lymphadenopathy ( Fig. 254.3A ). The patient may have a history of similar lesions, having developed previously with self-resolution or resolution with treatment over a few months. There may be simultaneous involvement of eyebrows or eyelashes. Trichotillomania is a disorder in which the patient pulls out hair from accessible regions of the scalp/eyebrows/eyelashes, leaving areas of partial hair loss with hair of unequal lengths ( Fig. 254.3B ). Both alopecia areata and trichotillomania are distinguishable from tinea capitis on trichoscopy (see below). Kerion is often confused with bacterial scalp infections such as a furuncle, but the presence of loose hair, other patches of noninflammatory tinea capitis, and demonstration of fungal hyphae on KOH smear differentiates tinea capitis. Seborrheic capitis and psoriasis manifest variable amounts of scaling and erythema, but generally, there is no hair loss.

Diagnosis

Apart from the clinical appearance of lesions and the presence of lymphadenopathy, in-clinic procedures—trichoscopy and potassium hydroxide (KOH) smear are extremely useful. Trichoscopy usually is diagnostic and shows the presence of abnormally shaped short hair shafts with a comma, corkscrew, or zig-zag appearance ( Fig. 254.4 ). To prepare a KOH smear, damaged hairs (appearing dull grey) are plucked from within the lesion, taking care to pluck with roots intact. A 10% KOH concentration is applied, and the smear must be examined immediately after mounting in order to visualize fungal spores and hyphae and to determine the location of spores within (endothrix) or outside (ectothrix) the hair shaft. Cultures can be performed using brush samples when this capability is available, although culture does not have a primary diagnostic role in routine patient management.

Treatment

Treatment of tinea capitis largely consists of the administration of an oral antifungal agent because topically applied agents cannot penetrate the infected hair shaft. Topical antifungal therapy, such as with ketoconazole, ciclopirox, and selenium sulfide shampoos, is prescribed to lower the spore count, thus preventing spread. Ideally, KOH testing is repeated at the end of therapy to confirm the cure. The child’s hair gear, towels, pillows, and combs should be separate from others’ during treatment to mitigate contagiousness. Some experts advise screening of all family members, especially when tinea capitis is associated with highly infectious anthropophilic strains. Restriction from school is not necessary once treatment is started.

The two most widely used oral drugs for tinea capitis are griseofulvin and terbinafine ( Table 254.1 ). Both are FDA-approved for this indication. Griseofulvin should be taken with a fatty meal to enhance absorption. Concerns with its use are the long duration of treatment (e.g., ≥6–8 weeks) and intolerance by some patients. Headache and gastrointestinal effects such as nausea and diarrhea are the commonest reported adverse effects. Terbinafine has an advantage over griseofulvin in terms of shorter courses of treatment (4–6 weeks) likely due to the long persistence of the drug in hair shafts where detectable levels are measurable 50 days after a course of 14 days). A granule formulation containing 125 mg or 187.5 mg is available in packets to be sprinkled on food and is licensed for use in children >4 years of age in the US. Terbinafine is well tolerated in children.

Terbinafine has shown higher efficacy against tinea capitis caused by endothrix organisms (e.g., T. tonsurans ), while griseofulvin has higher efficacy for ectothrix infections (e.g., M. canis ). The higher efficacy of terbinafine against endothrix organisms likely is because the drug accumulates preferentially in the hair shaft where the bulk of infection lies. In case of ectothrix infection, however, arthroconidia lie on the scalp surface, and in prepubertal children with low sebum concentrations (sebum being the mode of secretion of terbinafine onto the skin), terbinafine may not achieve sufficient levels at the site of infection. Recent evidence suggests the requirement of higher doses of griseofulvin (25 mg/kg/day) for longer periods (12–18 weeks) in the case of Trichophyton infections. Thus for geographical locations such as in the US, where T. tonsurans is the predominant causative organism, terbinafine would be the preferred drug and is effective in the majority of patients.

Itraconazole administered for 4–6 weeks ( Table 254.1 ) has comparable efficacy with griseofulvin and terbinafine and has activity against both Microsporum and Trichophyton species. Itraconazole has a good safety profile in children and also is available as an oral solution that has higher bioavailability than capsules and is convenient for use in children. Itraconazole also has been used as consecutive pulse therapy (5 mg/kg once daily for 1 week followed by 2 weeks without therapy). One, two, and three pulses produced complete clinical and mycological cure in 1, 6, and 3 of 10 patients, respectively, in one study.

Fluconazole (6 mg/kg once daily or 8 mg/kg once weekly) has been used less frequently as it offers no advantage in terms of efficacy, availability, or cost over other existing treatment options. ^,

An antibiotic usually is not given even for inflammatory lesions as a secondary bacterial infection is uncommon. It is good practice to obtain a swab to confirm secondary bacterial infection and prescribe an antibiotic only when the culture is positive for an expected pathogen. A short course on an oral corticosteroid (e.g., prednisolone 1–2 mg/kg/day for 1–2 weeks) occasionally is in severe inflammatory forms to reduce the chance of sequela of permanent scarring, or occasionally for severe id reactions.

Treatment usually is curative. In case of failure to resolve, the following should be considered consecutively: prolongation of therapy when there has been a lack of adherence, increasing the dose if griseofulvin was used, or changing to an alternative drug. The possibility of re-infection with the same or a different species also is considered, and if feasible, a culture is performed.

A simple bleach solution may be used to disinfect the child’s headgear, combs, and other fomites throughout and at the end of treatment. Parents and patients should be reassured that normal hair growth usually ensues following successful treatment, although it may take time for a full recovery.

Clinical Manifestations and Differential Diagnosis

Clinical features of onychomycosis primarily are a combination of subungual debris and nail plate changes ( Fig. 254.5 ). Similar to adults, toenails are affected more commonly than fingernails. The most common clinical type is distal and lateral subungual onychomycosis, in which the nail plate is lifted distally along one of the lateral nail folds. This gives the involved area of the nail plate a yellowish appearance, with nail bed hyperkeratosis (debris) visible beneath. Other clinical forms of onychomycosis include a proximal subungual form (changes similar to the distal/lateral form except in the proximal nail unit) , superficial white form (classical superficial white patches without subungual debris or lifting of the nail plate), total dystrophic form (complete destruction of the entire nail apparatus with resulting nail thickening, dystrophy and crumbling) and endonyx (lamellar splits and pits within the nail plate without lifting). Candidal onychomycosis often is associated with paronychia ( Fig. 254.6 ).

It is important to examine the patient for tinea pedis and for tinea infections elsewhere on the skin and also to examine or query about similar conditions in parents and siblings. In one series, 47% of children with onychomycosis had concurrent tinea pedis, and 65% had a sibling, parent, or grandparent with onychomycosis or tinea pedis.

Onychomycosis must be distinguished from noninfectious cutaneous disorders affecting the nail such as psoriasis, lichen planus, eczematous dermatoses, and alopecia areata, all of which have simultaneous skin or hair abnormalities, and post-traumatic nail dystrophy, which can mimic onychomycosis and frequently leads to secondary fungal infection. Laboratory testing confirms the diagnosis of onychomycosis.

Diagnosis

It is ideal to confirm the diagnosis and etiology of onychomycosis in children as treatment is prolonged, and failures can occur. Obtaining a specimen may cause discomfort. The child and parent need to be informed and counseled regarding this. Additionally, isolation of the fungus from nails is more difficult than from skin. For KOH smear examination, subungual debris and small nail clippings are ideal specimens. A 10%–30% KOH is applied to digest keratin. Clearing takes longer than skin samples, and the sample may need to be kept overnight or incubated at 37°C for one hour. Dermatophytic hyphae are uniformly broad with visible regular septations and branching ( Fig. 254.7 ). The sensitivity of KOH examination varies from 53% to almost 80%, depending on the specimen and the observer’s expertise. ^, For culture, more proximal samples are needed as the fungus is more likely to be viable proximally, and the sensitivity of diagnosis is low (33%–53%) ( Fig. 254.8 ). Histologic examination of large nail plate clippings using periodic acid Schiff (PAS) stain is the current gold standard for diagnosis of onychomycosis with a reported sensitivity approaching 90% ( Fig. 254.9 ).

Treatment

While adults usually are treated with systemic antifungal agents, children are more likely to respond to topical therapy as their nails are thin and faster growing. Treatment with a systemic antifungal agent alone in children results in the cure rate of 71%, which increases to 80% with the use of combined systemic and topical therapy. Although no systemic antifungal agent is currently US FDA approved for onychomycosis in the pediatric age group; many studies report their use in children with onychomycosis ( Table 254.1 ).