White : Diseases of the Skin - Fungal Infections

Table of Contents
This Chapter	All Chapters

Gary M. White & Neil H. Cox

Diseases of the Skin

26	Fungal Infections

DERMATOPHYTE (RINGWORM) INFECTIONS

Tinea pedis

Etiology and pathogenesis

Tinea pedis is usually due to one of three organisms: Trichophyton rubrum, T. mentagrophytes var. interdigitale, or Epidermophyton floccosum. These organisms are commonly found at swimming pools or public showering facilities. Shoe-wearing is key, and in fact there is a maxim that ‘tinea pedis follows in the footsteps of shoe-wearing nations’. Evidence suggests that many people with chronic tinea pedis do not mount an adequate cell-mediated immune response.
The three main patterns of tinea pedis are discussed separately, as they have different clinical features, differential diagnoses, and therapeutic implications; they comprise:

•	interdigital tinea infection,
•	moccasin pattern tinea pedis, and
•	bullous tinea pedis

Interdigital tinea infection (athlete’s foot)

Etiology and pathogenesis

The term dermatophytosis simplex has been used to describe this common, relatively asymptomatic, uncomplicated, scaling fungal infection between the toes (the term athlete’s foot is commonly used but may be loosely used for any toe web maceration).
This may progress to dermatophytosis complex by prolonged occlusion. This condition represents a mixed infection of both dermatophytes and bacteria (e.g. Staphylococcus aureus, Micrococcus sedentarius, S. epidermidis, Corynebacterium minutissimum, Pseudomonas, and Proteus) in the moist, occluded environment of the toe web. These specific bacteria are thought to proliferate because the dermatophytes produce penicillin- and streptomycin-like substances that inhibit other organisms. M. sedentarius and S. epidermidis also produce a variety of thioesters, which can cause malodor. The toe web is scaly, macerated, and inflamed.
Dermatophytosis complex may progress to a gram-negative toe-web infection, in which there is severe inflammation with erosions, weeping, and vesiculation extending on to the foot. A green color is common and indicates the presence of Pseudomonas organisms.

Fig. 26.9 Dermatophytosis simplex of multiple web spaces. The skin is dry and scaly.

Clinical

In dermatophytosis simplex, the web spaces are dry and scaly (Fig.26.9). Usually the fourth web space between the fourth and fifth toes is affected. As the area progresses to dermatophytosis complex, the skin of the web space becomes white, macerated, and malodorous (Fig. 26.10).

Differential diagnosis

Other causes of toe web maceration include the following.

•	Simple intertrigo.
•	Other infections-erythrasma, candidiasis, staphylococcal, streptococcal, and gram-negative (including Acinetobacter spp. and Pseudomonas spp.).
•	Soft corn.

Fig. 26.10 Dermatophytosis complex: white, macerated, malodorous fourth toe interspace.

Fig. 26.11 Tinea pedis. Redness and scaling of the web spaces initially but later over some or all of the sole (moccasin distribution) is characteristic. KOH examination or culture is confirmatory.

Fig. 26.12 Tinea pedis. The fungal infection has spread from the web spaces to cover the distal half of the sole.

Fig. 26.13 KOH examination. Virtually any relatively flat, scaly lesion should raise the suspicion of fungal infection. The KOH examination is invaluable due to its ease, simplicity, and quick results. Abundant scale is scraped on to a microscope slide with a blade and covered with a coverslip. (Courtesy of Terence C. O’Grady, M.D.)

Treatment

A topical antifungal solution or cream twice daily is usually sufficient. The area may be kept dry by avoiding occlusive footwear, using cotton socks, and applying a superabsorbent powder. Broad-spectrum antibacterial and astringent agents (e.g. aluminum chloride, Castellani’s paint, and 2% aqueous eosin) may also be helpful.

Moccasin pattern

Etiology and pathogenesis

This is due to chronic T. rubrum infection.

Clinical

In this pattern of tinea pedis, redness and scaling of the web spaces occurs initially, but later spreads over some or all of the sole (moccasin distribution, Figs 26.11 and 26.12). Often, onychomycosis is present and can serve as a source for reinfection. KOH examination or culture is confirmatory (Fig. 26.13).

Differential diagnosis

The main differential is ‘eczema’ of some sort. Indeed, a dry, scaly, minimally inflammatory eczema can be difficult to distinguish from tinea pedis of this type, and a shoe dermatitis due to contact allergy should always be considered, especially if any eczematous component extends on to the dorsal foot. However, the chronicity, degree of scaling, relative lack of symptoms, and frequently associated onychomycosis should suggest the diagnosis.
Psoriasis, keratodermas, and juvenile plantar dermatosis may be considered.

Fig. 26.14 Bullous tinea. The immune response can occasionally be so strong as to cause bullae.

Treatment

A topical antifungal cream or solution twice daily is often appropriate, although those with thick plantar skin may not achieve clearance. Any of the many topical antifungal medications are appropriate; the new allylamines are fungicidal and are more effective than the fungistatic imidazoles. Adequate control without cure is all that may be achieved in some patients who do not mount a sufficient immune response to aid in clearing the fungus, which allows quick recurrence. An oral antifungal medication is justified if there is failure or if there is onychomycosis.
Since recurrences are common after any method of clearing, prophylactic application of a topical antifungal for years is appropriate.

Bullous tinea pedis

Etiology and pathogenesis

The immune system may react against a fungal infection to such a level that bullae form. Often T. mentagrophytes var. interdigitale is the causative fungus. The method of bulla formation appears to be the same as that for allergic contact dermatitis.

Clinical

An acute eruption of vesicles or bullae on the arch or sides of the foot is characteristic (Fig.26.14). The lesions are usually pruritic and rarely painful.

Differential diagnosis

This includes the following.

•	Allergic contact dermatitis.
•	Pompholyx-the blisters are smaller vesicles.
•	Other forms of dermatitis, exanthems, drug eruptions, or scabies-very acute tinea of this type may provoke an ‘id’ hypersensitivity rash, greatly widening the differential if it is not appreciated that the feet are the primary cause.
•	Epidermolysis bullosa, Weber-Cockayne type-usually patients are aware of this inherited condition, which may also affect the hands.
•	Friction blister-occurs after the wearing of new shoes or prolonged, unusual physical activity.

Fig. 26.15 Candidal infection of the nail. Candida tropicalis and C. albicans were cultured.

Fig. 26.16 Candidal infection of the nail.

Treatment

A topical antifungal solution or cream twice a day is appropriate. An oral antifungal medication may be needed. Tense vesicobullae may be punctured sterilely, but the roof should be left on for protection. Warm water, saline, or astringent soaks to the feet twice daily are recommended for any crusting or maceration. A potent topical or even a systemic steroid may be needed acutely.

Onychomycosis

Etiology and pathogenesis

Dystrophy of the nails is very common, especially in the elderly. It is important to remember, however, that not all dystrophy is caused by a fungus. In fact, in a recent study of patients aged 61 years and older, 66% had dystrophic nails suspicious for onychomycosis, but only two-thirds of those actually proved to have a fungal infection. Still, the most common disease of the nails is infection by a fungus (Figs 26.15 and 26.16).
The most common pattern of infection is termed distal and lateral subungual onychomycosis (DLSO). In this variant, the fungus takes hold in the skin, usually the web, and advances distally to the digital tip and then to the skin just below the distal nail, the hyponychium. From there, the fungus invades the undersurface of the nail. Dermatophytes are much the commonest cause of onychomycosis, accounting for most toenail infections. Fingernails are less frequently affected than toenails, but at this site Candida spp. may account for up to 70% of infections.
Other patterns of onychomycosis include the following.

•	Superficial white onychomycosis (SWO)-the dermatophyte invades the upper surface of the nail plate; usually due to T. mentagrophytes var. interdigitale.
•	Proximal subungual onychomycosis (PSO)-the dermatophyte invades the nail apparatus via the proximal nail fold and then spreads in a distal direction underneath the nail plate (Fig.26.17). T. rubrum is the usual cause (Fig.26.18), although yeast (e.g. Candida) or a mold (e.g. Aspergillus) may be found. This disease has been seen more frequently in patients with AIDS.
•	Endonyx onychomycosis-a rare superficial infection.
•	Total dystrophic onychomycosis-the end stage of DLSO.

Fig. 26.17 Proximal subungual onychomycosis. No immunologic cause was found.

Fig. 26.18 Onycholysis of great toe, caused by a dermatophyte in a child.

Fig. 26.19 Pigmented nail caused by onychomycosis.

Fig. 26.20 Distal subungual onychomycosis. Fungal organisms enter at the distal edge of the nail bed. Subungual debris accumulates, lifting the nail and causing onycholysis. Invasion of the nail plate causes it to thicken and turn yellow, brown, or white. The causative agent is usually a dermatophyte, but one may also find a yeast (e.g. Candida) or a mold (e.g. Aspergillus).

Fig. 26.21 Superficial white onychomycosis. The surface of the nail is white and powdery.

Fig. 26.22 Collection of nail for culture. The subungual debris is the most valuable material for culture. After cutting back the nail, a curette may be used. Clippings of the nail may be added to the culture.

Clinical

The various clinical patterns of onychomycosis are found most commonly on the toenails along with tinea pedis. In fact, the patient may clear the fungal infection of the skin with topical therapy, only to suffer relapse as the fungus seeds the skin from the nail. In the early stages of DLSO, the nail plate separates from the nail bed and takes on a yellowish color. At times, the fungal infection may darken the nail (Fig.26.19). This separation advances proximally, and subungual debris accumulates (Fig. 26.20). Ultimately, the entire nail may be destroyed. In SWO, the surface of the nail is white and powdery (Fig.26.21). In PSO, a yellowish discoloration may be seen under the proximal nail, although the surface remains smooth.
Culture of the nail is appropriate in most situations, to document the infection and to determine the organism, which may influence therapy. For DLSO, the nail is cut back and the subungual debris is harvested with a curette (Fig.26.22) or a no. 15 blade. The best culture utilizes both nail clippings and some of this subungual debris. In SWO, the affected nail plate is scraped with a no. 15 blade. In PSO, the superficial part of the nail is removed with a blade and the deeper, involved nail removed with a curette.
In very suspicious but repeatedly culture-negative cases, sending nail for histologic examination may help, but it won’t identify the type of fungus.
Differential diagnosis
There are several important differentials (many are discussed in Ch.29, which deals with nail diseases).

•	Old age-in the older patient, the nail may be dystrophic for a variety of reasons, including poor circulation and old age itself. Often there is thickening and malformation, without the buildup of subungual debris.
•	Trauma.
•	Psoriasis-there should be evidence of psoriasis elsewhere, and there are usually changes affecting the surface of the nail plate.
•	Colonization in an area of onycholysis-in such cases, the organisms identified are often unusual as pathogens, for example Scopulariopsis brevicaulis. This is another situation where histologic examination may help by identifying whether there is actually nail plate invasion.
•	Other subungual infection-especially that due to Pseudomonas.
•	Skin disease-chronic inflammation of the proximal nail fold can induce dystrophy of the nail, for example in chronic paronychia and chronic eczema.
•	In children, consider congenital or hereditary abnormalities, for example pachyonychia congenita.

Treatment

As a general rule, topical agents are ineffective against onychomycosis. Oral agents are needed and have a cure rate of 70-80%. They are usually given over 2 months for fingernails and 3 months for toenails. After this treatment period, the patient must wait up to a year or longer for the new nail to grow out. Relapse is common. Because of all this, treatment may not be desired after patient education. Current evidence is that terbinafine (250mg/day for 6 weeks for fingernails and 12 weeks for toenails) is the most effective therapy for dermatophyte infections. Itraconazole (200mg twice a day for 1 week of each month) is also useful, with a recommended regimen of three cycles for toenails and two cycles for fingernails; it has the potential advantage of being effective for other molds as well as for dermatophytes (this is why awaiting a culture result is important). Similar pulsed therapy has been described with fluconazole.
Recurrence of onychomycosis may occur because the patient is predisposed to tinea pedis, which then invades the nail. Therefore it is very important to use a topical antifungal agent once or twice a week prophylactically. Persistent disease (i.e. the nail was never cleared) occurs about 20% of the time and seems more prevalent when there is involvement of the lateral nail. When persistent disease is a problem, another oral agent may be tried or the same agent given for a longer time. It remains to be seen if there are some patients who cannot be cleared of their disease.
A topical antifungal medication applied twice daily is usually curative for SWO unless there is deeper penetration of the nail, in which case an oral antifungal medication is needed. An oral antifungal medication is needed for PSO.

PRACTICE POINTS

•	Nobody can consistently diagnose fungal infection and the type of causative fungus by clinical inspection of the nail; as treatment is systemic, and the best choice may depend on the organism, always send samples for mycologic culture and wait for the proof.
•	Unusual organisms cultured from nail clippings may be commensals rather than actually invading the nail plate; this is a common reason for use of repeated but totally ineffective therapy. Seek more expert advice if in doubt.
•	Having psoriasis does not exclude the possibility of fungal nail infection; culture of nail clippings will resolve the query.
•	Clearing onychomycosis of the toenails can take a year or longer, as one needs to let the new normal nail grow out.
•	Changes in the surface of the nail plate (other than in SWO, which is uncommon) suggest that the diagnosis is not onychomycosis.
•	Compared with dermatophyte infection, chronic paronychia is a far commoner cause of fingernail dystrophy.
•	Once the nail is cleared, the patient should prevent tinea pedis to prevent recurrence.
•	There is an old dermatologic saying for nail dystrophy: ‘If it’s fungal we can fix it; if it’s not, we can’t’.

Fig. 26.23 Majocchi granuloma. (a) This fungal infection (usually by Trichophyton rubrum) occurs deep and therefore may resist topical antifungal therapy. Clinically, one sees a papulopustular perifollicular eruption, usually on one leg. It is often mistaken for a bacterial folliculitis. (b) Majocchi granuloma of the wrist. This infection often starts under a watch band and may be misdiagnosed as an allergic contact dermatitis.

Fig. 26.24 Tinea cruris in a male patient. Scaly plaques radiating out from the inguinal fold on to the inner thigh are characteristic of tinea cruris. The border is usually scaly, raised, and KOH-positive. Itching may vary from absent to severe.

Fig. 26.25 Tinea of the gluteal cleft. Note the annular shape and involvement of the nail.

Fig. 26.26 Tinea cruris in a female patient. Rarely, a woman may develop a dermatophyte infection of the groin.

Fig. 26.27 Tinea corporis (‘ringworm’). Red, scaly lesions on the body, often with an active border, are characteristic. Nummular eczema, in contrast, usually shows uniform inflammation, scale, or crust throughout (see Fig. 6.28).

Fig. 26.28 Tinea corporis. Concentric circles may occur, creating beautiful patterns.

Majocchi granuloma

Majocchi granuloma represents a fungal infection of the follicle. It most commonly occurs on the lower leg, the most common organism being T. rubrum. It usually occurs in normal hosts, but there are several reports of Majocchi granuloma occurring in various iatrogenic immune-suppressed states; it may also affect other sites, such as the beard area.
Perifollicular granulomatous papules aggregated together in an inflamed and slightly scaly patch are characteristic (Fig.26.23). KOH testing of the scale is usually positive, but sometimes a biopsy is needed to establish the diagnosis correctly. A topical antifungal medication may be tried, but often an oral antifungal agent is needed.

PRACTICE POINTS

•	Always examine the feet in patients with tinea cruris; tinea of the skin or nail will be present.
•	Always examine the feet in patients with unilateral hand scaling. You are likely to find that the patient has two foot, one hand disease and/or onychomycosis. Do not believe patients who declare their feet to be normal: moccasin tinea pedis may be so chronic that it is not felt to be a problem.
•	Always obtain mycology samples from a chronically scaly foot or feet.
•	Always consider fungal infection for any annular and scaling rash.
•	Always consider fungal infection for any asymmetric rash.

Fig. 26.29 Tinea corporis in a dark-skinned patient.

Fig. 26.30 Tinea corporis with pustules. A fungal infection may result in pustules. The clinician may misdiagnose this as a bacterial infection.

Fig. 26.31 Tinea corporis, inflammatory. The body’s level of immune response greatly influences the clinical appearance. Here, the inflammation is substantial.

Fig. 26.32 Tinea corporis, inflammatory. Tinea of the arm and trunk acquired from cattle. Cattle ringworm is typically inflammatory and often pustular. This pattern on the trunk occurs because the head of the cow is held between the arm and the flank for procedures such as dehorning.

Fig. 26.33 Tinea corporis affecting the entire back.

Fig. 26.34 Tinea of the arm. Note the active border.

Fig. 26.35 (a,b) Two foot, one hand disease. Scale without inflammation on just one hand is classic. Patients often deny any problem with the feet, but usually are found to have bilateral tinea pedis when they are persuaded to take off the shoes.

Fig. 26.36 Two foot, one hand disease. Unilateral onychomycosis develops in chronic cases and clinches the diagnosis.

Fig. 26.37 Tinea barbae. Fungal infection occasionally affects the beard area as aggregated follicular pustules. The condition is often misdiagnosed as a bacterial infection.

Fig 26.38 Tinea barbae, kerion. Cattle-acquired Trichophyton verrucosum in a farmworker who handled cattle. Significant scarring occurred in this case. Oral steroids may be given to prevent alopecia in patients with significant inflammation.

Fig. 26.39 Tinea barbae, kerion.

Fig. 26.40 Tinea faciei. The clinical clues to this being a fungal infection are the asymmetric nature and the raised, red, scaly border.

Fig. 26.41 Tinea faciei of the upper lip.

Tinea cruris

Etiology and pathogenesis

Tinea cruris refers to fungal infection of the groin. It occurs mainly in men as the scrotum and inner thigh press together, causing the perfect moist, occluded environment. It is almost invariably associated with tinea pedis or with onychomycosis.

Clinical
A red, scaly area with annular border emanates from the inguinal fold (Figs 26.24-26.26). Both sides are usually affected.

Differential diagnosis

The main differential diagnoses of groin rash are as follows.

•	Erythrasma-red-brown plaques, and there may be positive Wood’s light fluorescence.
•	Intertrigo-a hot, sweaty, itchy groin.
•	Psoriasis-flexural psoriasis, especially if it occurs without involvement of other sites, may cause diagnostic confusion (tip: check the nails and scalp if in doubt).
•	Hailey-Hailey disease-a rare inherited condition that patients would usually know about from previous episodes or from relatives.

Treatment

The most basic but valuable advice on treating a man with a groin rash is that if the KOH preparation and Wood’s light are negative, treat with a superabsorbent powder and a mild topical steroid. For those with positive mycology, a topical antifungal medication is usually adequate. The feet should be examined as well and any tinea pedis or onychomycosis treated, as this is usually the source of the infection.

Tinea corporis

Tinea corporis refers to ringworm of the body. The standard appearance is that of multiple, large, red, scaly lesions with raised, red, scaly borders (Figs 26.27-26.34). It may occur due to human ringworm species or those from animals. Often the infection is so extensive as to warrant oral antifungal agents.

Tinea manuum and two foot, one hand disease

The term tinea manuum refers to any dermatophyte infection of the hand. It is commonly unilateral and may present as red scaly areas, vesicular lesions, or hyperkeratosis.
The term two foot, one hand disease refers to a curious but common pattern of T. rubrum infection of either the dominant or non-dominant hand, associated with chronic (but often unrecognized) infection of both feet (Figs 26.35 and 26.36). Often the patient thinks the scaling is due only to dry skin or physical trauma.
For treatment, a topical antifungal medication may be adequate. If this fails or the nails are involved, an oral antifungal medication is needed.

Tinea barbae

Fungal infection occasionally affects the beard area. A specific form classically obtained from cattle and caused by T. verrucosum is called agminate folliculitis. Annular, red, scaly rings or aggregated follicular pustules may be seen (Fig.26.37). Sometimes, the inflammation is severe, resulting in a kerion (Figs 26.38 and 26.39). This condition is often misdiagnosed as a bacterial infection. A systemic antifungal (e.g. terbinafine) is usually needed.

Fig. 26.42 Tinea capitis, kerion. A large kerion is seen on this child.

Fig. 26.43 Tinea capitis, seborrheic dermatitis pattern. Seborrheic dermatitis is rare in a prepubertal black child. Tinea capitis is the diagnosis until proved otherwise.

Fig. 26.44 Tinea capitis, dry scale and no hair.

Fig. 26.45 Tinea capitis, black dot. The fungus may invade the hair (endothrix) and cause breakage at the base, resulting in multiple black dots.

Fig. 26.46 Tinea capitis, white dot. If the hair is white, multiple white dots may result from endothrix infection.

Fig. 26.47 Tinea capitis. Regional lymph nodes are often swollen.

Tinea faciei

Fungal infection of the face is called tinea faciei. Most cases are due to T. rubrum or to T. mentagrophytes var. mentagrophytes. The main reason to draw attention to this subset of fungal infections is that the diagnosis is often missed. The doctor often doesn’t consider a fungal infection when evaluating a rash on the face. Furthermore, the patient often has applied creams or lotions that can mask the scale. Often, the clinical clue is an annular, red border (Figs 26.40 and 26.41). In children, Microsporum canis (cat and dog ringworm) should also be considered, but this usually presents in a less subtle fashion.

Table 26.1 DIFFERENTIAL DIAGNOSIS OF TINEA CAPITIS

Disorder	Differentiating features
Psoriasis	Red skin with thick, uniform, silvery scale, sharply demarcated; often psoriasis at other body sites also.
Dermatitis	The main possibility is seborrheic dermatitis: usually more diffuse and has uniform fine scaling, rather than localized areas; doesn’t typically cause alopecia or significant inflammation. May also be present on the face, especially the nasolabial fold, or as otitis externa. Atopic dermatitis is generally diffuse on scalp and almost inevitably present at other sites, but may coexist with tinea capitis, especially in children.
Pityriasis amiantacea	Thick sheets of asbestos-like scale, very adherent, generally a solitary patch. This may occur in various dermatoses.
Lichen simplex	Usually nape of neck; cobblestoned or lichenified skin thickening, with broken hairs that are not coated with scale.
Alopecia areata	Usually not inflamed (may be mildly so), not scaly, usually sharply defined. ‘Exclamation mark’ hairs occur but are not coated with fungus; ‘cadaverized’ hairs especially cause difficulty, as they mimic black dot alopecia.
Scarring alopecias	For example discoid lupus erythematosus, lichen planus of scalp; cause perifollicular inflammation around intact hairs; usually associated with lesions at other sites also. Dissecting cellulitis of scalp is also in this differential.
Bacterial infections	Impetigo causes crusting but little inflammation, and hairs are intact; carbuncle is deeper and very tender but may be in the differential of kerion.
Trichotillomania	Broken hairs of unequal length, but hair shafts themselves and the scalp are normal.
Damage from hairdressing processes	Usually clear from the timescale.
Neoplasm	May be in the differential of kerion; usually slower-growing and mainly on elderly, balding scalp, whereas kerion is in children or young adults with previously intact hair.

Tinea capitis

Etiology and pathogenesis

Tinea capitis is a relatively common affliction of prepubertal children, particularly those from 4 to 6 years of age. There are three main patterns of infection that need to be considered.

•	Infection due to anthropophilic species (human types of ringworm). Currently in the USA and in some cities in the UK, T. tonsurans is by far the most common cause. Children living in crowded conditions and those of African American descent are particularly prone. Boys and girls are equally affected. Person-to-person and fomite-to-person transmission probably both occur. Hebert was able to culture fungi from hair of a doll, furniture, combs, brushes, and a telephone receiver. This organism also affects adults, and screening the whole family is valuable.
•	Infection from pets. In many countries, infection by M. canis is widely found. The infection is from dogs or cats but can be transmitted to other children.
•	Cattle ringworm-in some rural areas, cases of scalp ringworm seen by a dermatologist are most likely to be due to T. verrucosum, forming a kerion.

Clinical

Tinea capitis may present clinically in various ways, including a circumscribed area of alopecia with thick crust; a boggy mass of tissue (kerion, Fig.26.42); multiple hairs broken off at the level of the scalp (black dot ringworm, the typical pattern seen with T. tonsurans or T. violaceum); seborrheic dermatitis-like scaling without any alopecia; yellow, cup-shaped crusts (scutula), each pierced by a hair (also known as favus); and scattered, patchy areas of alopecia with slight scale (Figs 26.43-26.47). Some species, such as M. audouinii, typically cause little inflammation, whereas T. verrucosum typically causes a significant host response. The clinical patterns have been summarized as:

•	diffuse scale,
•	gray patch,
•	black dot,
•	diffuse pustular, and
•	kerion.

Prepubertal children are usually affected. In the case of T. tonsurans infection, a high percentage of siblings, parents, and grandparents of the index patient are asymptomatic carriers; in some areas, up to 41% of schoolchildren without symptoms and up to 30% of the mothers of affected children have positive cultures.
If alopecia and scale are present, a KOH examination may be positive. Otherwise, a culture is indicated. A sterile toothbrush or cotton-tipped applicator rubbed over various parts of the scalp, and then rubbed gently into a fungal culture plate, is an effective and painless technique that is able to sample large areas of the scalp. Wood’s light fluorescence is positive in some cases of Microsporum infection but not in the other types discussed earlier; in populations in which T. tonsurans is frequent, the predominance of a non-fluorescent organism makes screening with Wood’s light unhelpful, and family members should be screening by obtaining culture samples as described earlier.

Differential diagnosis

This is listed in Table 26.1.

Treatment

There are two main rules that apply.

•	The diagnosis for tinea capitis is usually presumptive. Although it is important to obtain specimens for culture before giving treatment, therapy should be started before the culture results come back, especially when there is significant inflammation.
•	A topical antifungal medication is not adequate.

Treatment options include griseofulvin, terbinafine, itraconazole, or fluconazole, depending on the likely organism.
    For T. tonsurans infection, griseofulvin (microsized 15mg/kg per day divided into two daily doses, or ultramicrosized 10-15mg/kg per day divided into two daily doses) should be used for 6-8 weeks. If no improvement is noted at approximately 3-4 weeks, the dose may be increased up to 20-25mg/kg per day. For significant inflammation, prednisone (1-2mg/kg per day) may be added. If the crusting is particularly severe, daily shampoo with frequent wet dressings may be necessary. Patients should be seen monthly and treated until clear. Laboratory monitoring is probably not necessary in a healthy child treated only for a few months. The patient and family members should be encouraged to use selenium sulfide shampoo (1 or 2.5%) or ketoconazole shampoo (2%) two or three times per week to eliminate the carrier state. Any hair beads, extensions, etc. must be removed immediately and discarded. Any head coverings should be washed or discarded. Terbinafine (62.5mg daily, age 6-12 years; 125mg daily, age 12-16 years), itraconazole (100mg daily), and fluconazole (6 mg/kg) have also been used.
    Tinea capitis caused by M. canis may resist treatment by terbinafine. Higher doses (e.g. 6-12.5mg/kg per day for 8 weeks in children) or the use of itraconazole is recommended. However, depending on the country of residence, use of terbinafine for children or for tinea capitis may currently be off-license.
    True drug eruptions to griseofulvin are rare, but the development of an intradermal reaction is common. It is papulosquamous in morphology and located typically on the face and upper torso. Therefore if a parent reports a drug eruption, the child should be seen.
    The diagnosis of tinea capitis should be presumed in the presence of a kerion, and an oral antifungal may be started immediately, although microscopy and culture from hairs or scale should be performed. Both gram-positive (e.g. staphylococci) and gram-negative (e.g. Proteus and Pseudomonas) bacteria may be cultured from kerions as secondary infection. Concomitant treatment with antibiotics is of unproven benefit, but it is likely to reduce inflammation and subsequent scarring. Terbinafine may be a better option than griseofulvin, as it is fungicidal rather than fungistatic and therefore faster to work, an issue of some importance when inflammation is severe and there is a risk of residual scarring alopecia.
    One value of culturing and identifying the dermatophyte is to determine whether an animal source is the likely cause. For example, if T. verrucosum (from cattle) or M. canis (from cat or dog) is found, then treatment of the animal(s) would be indicated.

PRACTICE POINTS

•	The diagnosis for tinea capitis is usually presumptive. Obtain specimens for culture before giving treatment, but therapy should be started before the culture results come back, especially when there is significant inflammation.
•	Tinea capitis is often erroneously thought to be excluded if a Wood’s light examination is negative; this test is only of value in Microsporum infections.
•	Tinea capitis is in the differential of any patchy alopecia, especially with scaling or inflammation.
•	A useful sign in kerion is that hairs can be pulled out with minimal traction and with no discomfort.
•	A topical antifungal medication is never adequate to treat tinea capitis.

Fig. 26.48 Candidiasis. The white, creamy lesions of candidiasis are commonly found on the tongue.

Fig. 26.49 Candida of the palate. Note the white, creamy lesions overlying the red, inflamed mucosa. The infection surrounds a mild torus palatine.

Fig. 26.50 Candida of the groin and paronychia. This woman had an acute infection of the groin (a), inframammary area (not shown), and the (b) paronychial area. (c) Close-up view showing satellite pustules.