Abstract: Fungi are numerous, ubiquitous, and diverse in their adaptations. Among thousands of fungal species are perhaps 100 to 200 species that regularly infect uncompromised humans and cause either superficial skin or mucous membrane infections, subcutaneous infection, or so-called “deep,” internal or visceral infection. Dermatophytes constitute a group of about 40 fungal species that are members of the Trichophyton, Microsporum, and Epidermophyton genera and cause superficial infections called dermatophytoses, ringworm, or tinea. The latter term is qualified by designation of the involved body area (eg, tinea capitis is tinea of the scalp). Dermatophytes invade keratin, the protein that forms the outermost epidermis, the nails, and hair. Tineas are among the most frequent reasons for visits to the pediatrician.Dermatophyte infection of the scalp (tinea capitis) is very common during childhood, as is infection of the general body surface (tinea corporis). Dermatophyte infection of the feet (tinea pedis) is much less common. Nail infection(onychomycosis) is unusual during the first two decades of life, with a prevalence of less than 1% that increases progressively with age.Prevalent dermatophyte species differ over time and with geographic location(Table 1). Causative species of tinea capitis are especially likely to shift to a different species over time. For example, in North America during the 1950s and 1960s, Microsporum sp caused most scalp and hair infections. Those infections were more often self-limited and less likely to be transmitted between individuals than those caused by the currently prevalent Trichophyton sp.Currently, T tonsurans dominates in the Americas. Throughout the 1980s and into the 1990s, this species became increasingly prevalent and now is overwhelmingly dominant, especially as a cause of tinea capitis. It has become more prevalent in Europe as well. T tonsuransinfection is more persistent than many other tineas and is spread easily and directly between humans; increasingly, it also is a cause of tinea corporis. Species of Trichophyton other than T tonsurans are prevalent in Africa.Because similar clinical presentations result from infection with various dermatophyte species, infections are named according to the body area affected and clinical presentation, using the general term tinea, rather than taking the name from the causative organism(s).Tinea capitis varies considerably in clinical appearance, depending on the immune response of the infected host. Differing fungal species usually alter the clinical presentation modestly. Impressions from physical examination of the patient can be misleading, and tinea capitis should be considered even when clinical changes are minimal.Dermatophyte species vary in their method of invasion and proliferation in hair. Microsporum sp that invade hair most typically produce spores on the exterior aspect of the hair shaft (exospores); species of Trichophyton usually fill the interior of the hair shaft with spores (endospores). Microsporum exospores often fluoresce, resulting in a positive Wood ultraviolet light examination, but T tonsurans endospores, which currently are more prevalent, do not fluoresce under Wood light, despite infection. In addition, Trichophyton endo-spores produce substantial hair fragility and breakage, often close to the scalp,which can result in a so-called “black-dot” appearance in which hairs are broken at the scalp or are short and stubby. The cardinal clinical feature of tinea capitis is the combination of inflammation with hair breakage and loss (Fig. 1). Hair breakage is especially evident with Trichophyton endospore infection and is seen most often with T tonsuransinfection. Because dermatophytes induce widely varied host immune responses,inflammatory changes can range from minimal scaling and redness that resembles mild seborrhea to a robust inflammatory response that includes tenderness, redness, edema, purulence, hair loss, and even formation of sinus tracts. This highly inflammatory presentation, often referred to as a kerion(Fig. 2),does not ordinarily indicate bacterial infection of the scalp;the latter is quite rare. Most patients who have any degree of inflammation ultimately develop retroauricular or posterior cervical lymphadenopathy. Rarely, patients even can exhibit an associated mild leukocytosis. Long-standing inflammatory tinea capitis, especially a kerion, can scar and result in permanent inability to grow hair. As tinea capitis progresses,especially after treatment begins, a hypersensitivity reaction to fungal antigen can develop, called a dermatophytid or “id” reaction(Fig. 3). Id reactions can present with either a dermatitis that includes redness,superficial edema involving the epidermis, and scaling or with a “pityriasis rosea-like” reaction that involves red, scaly papules and ovoid plaques on the face, neck, trunk, and proximal extremities, often with clustering on the upper body.Systemic treatment of tinea capitis is essential to allow antifungals to penetrate and become incorporated into growing hairs, thereby preventing the invasion of new fungal hyphae into hair. Topical antifungals are not effective for hair infection because they cannot penetrate or become incorporated into hair. Griseofulvin traditionally is preferred for initial treatment at a starting dose of about 20 mg/kg per day to enhance absorption and achieve sufficient levels in the blood and hair. There generally is no need for adjunctive antibacterial agents. Sporicidal shampoos such as 2.5% selenium sulfide are used in conjunction with oral antifungals to reduce contagion until the patient no longer is contagious, which usually is after about 2 weeks of effective systemic treatment. Infection can be spread via personal care objects, so sharing of towels, brushes, and combs should be avoided.Dermatophytid reactions can be treated with a short course (usually 1 to 2 weeks) of topical or systemic corticosteroids. Occasionally, 1 to 2 weeks of oral corticosteroid therapy is administered at the start of oral antifungal treatment to alleviate the discomfort and reduce the potential scarring of severe kerion.Dermatophyte infection of the general body surface that is not otherwise named more specifically is termed tinea corporis. Physical examination reveals individual and grouped red, scaly papules and small plaques (Fig. 4),sometimes with mild, superficial edema. These progressively enlarge and migrate to form expanding rings, arcs, or annular patterns. Often, clearing in previously affected areas produces the typical “ringworm” appearance. As redness and edema resolve or migrate outward, the skin becomes more scaly, generally on the edges of the papules or plaques. Less commonly, edema may lead to the development of vesicles, pustules, or larger blisters. Itching is often mild but can be bothersome, especially when there is substantial inflammation. These changes typically affect a small number of body regions. Topical therapy is the initial treatment approach (Table 2). Tinea corporis is similar in appearance virtually anywhere on the body, but slight regional variations have led to the use of specialized terms for infection of certain body regions. For example, tinea faciei connotes facial involvement and tinea cruris describes infection of the upper thigh and inguinal area. Although predominant species do have a tendency to vary by body location,the site of infection is often an unreliable indicator of species. Local conditions can alter the clinical appearance substantially. For example,with fungal infection of the genital area or feet, the area may become macerated and secondarily infected, most often with bacteria, due to moisture and increased heat at those body sites.Dermatophyte infections of the feet and of the hands, tinea pedis and tinea manuum, respectively, have overlapping clinical presentations, but differ in appearance from tineas of other body sites (Fig. 5). Initial infection is often interdigital in tinea pedis, usually involving the lateral toe webs, and is induced by the warmth and moisture of wearing shoes. The web spaces become red, scaly, and often macerated, occasionally with edema.Fungal infection frequently spreads to involve the soles of the feet or the palms, with dry scale and minimal-to-absent redness. Characteristically this scaling extends only to the side of the foot or hand,where the thicker ventral skin changes to the thinner skin found on the dorsum of the foot or hand. Scale often appears in small 1- to 3-mm circles. Vesicle and blister formation, frequently with increased redness and edema,is more common than with other types of tinea. Itching is common and often quite bothersome.Interdigital or plantar dermatophyte infection often leads to secondary bacterial infection and possible cellulitis or other deeper soft-tissue infections and even systemic infection through compromise of the skin of the feet. A vigorous immune response can rarely produce a dermatophytid reaction, as described for tinea capitis.Dermatophyte hand infection primarily involves the palm with dry scale,similar to that seen with tinea pedis, often including small circular areas of scale. For unknown reasons, infection of just one hand in conjunction with infection of both feet is the most common pattern. Topical therapy and keeping the involved areas as cool and as dry as possible is preferred for hand or foot tinea, with oral treatment when necessary.Dermatophyte infection of the nail plate is traditionally referred to as tinea unguium, but onychomycosis, a broader term referring to nail infection with any fungus, is used more often. Dermatophytes usually invade the nail plate from the skin beneath the distal underside of the nail to produce so-called distal subungual onychomycosis. The result is dystrophy of the nail, with discoloration, ridging, thickening,fragility, and possible breakage as well as accumulation of debris beneath the distal aspect of the nail and little or no inflammation (Fig. 6). Local care and topical treatment reduce thickening and allay discomfort. Oral treatment usually is required to clear infection, but eventual recurrence still is very common.A less common presentation is superficial growth of fungus on the surface of the nail plate through the dorsal aspect of the nail, called superficial white onychomycosis. The superficial nail plate becomes fragile and produces powdery white, off-white, or grayish opaque discoloration. There is no subungual thickening unless there also is a subungual infection. Superficial infection is asymptomatic, can be due to yeasts or dermatophytes, and unlike subungual infection, usually responds to topical treatment.Potassium hydroxide (KOH) examination of scale,hair, or nail is the most rapid and convenient diagnostic method. A sample of scale, hair, or nail from a possibly infected area is placed on a glass slide, covered with a few drops of 10% to 30% KOH, and left to digest for about 30 minutes or gently heated without boiling the solution. Adding dimethyl sulfoxide (DMSO) to the KOH solution usually renders heating unnecessary. The specimen is examined under moderate magnification (about 400× total magnification or 40× objective) and low light for spores and/or fungal hyphae that grow across cell membranes and branch (Fig. 7). Care must be taken to avoid false interpretation of the narrow spaces between overlapping cells as branching hyphae.Scale and affected hair or nail can be placed on the surface of Sabouraud or other appropriate agar for culture and incubated at room temperature for 2 to 3 weeks. Free air flow to the agar surface should be ensured by leaving the culture loosely covered. Antibiotics added to the agar inhibit bacterial growth, thereby facilitating fungal growth. Such media are commercially available for office use.At present, most dermatophyte hair infections (tinea capitis) can be attributed to species that do not produce fluorescence, so examination with ultraviolet light (Wood lamp) almost always is without benefit and should not be relied upon.Antifungal drugs have become increasingly effective,especially new orally administered systemic agents. However, experience with most of the newer drugs is limited among patients in the first decade of life. Therefore, drugs proven to be safe and effective, such as griseofulvin,often are preferred because of their long history of safe use and relatively low expense. On the other hand, newer agents allow less frequent dosing and shorter courses of treatment, thereby potentially enhancing compliance.Oral griseofulvin has a long-established history of effectiveness and low cost and a proven safety profile; it still is often the first choice for treatment of tinea capitis in children. However, its erratic oral absorption necessitates doses of about 20 mg/kg per day of the liquid preparation,always administered with a lipid-containing meal or beverage (such as milk)to ensure absorption and adequate blood levels. Ultramicrosize griseofulvin,available only as tablets, can be administered at the lower dose of 8 to 10 mg/kg per day because of enhanced absorption; the tablets can be crushed and placed into soft or ground food, such as applesauce.Because griseofulvin is fungistatic, treatment should be continued for at least 2 weeks after clinical resolution of inflammation and beginning regrowth of new hair in previously involved areas. Normal therapy requires a minimum duration of about 8 to 12 weeks. There is no need for routine laboratory evaluations or liver function testing when griseofulvin is used for 6 months or less in a healthy patient at routine doses. Failure to respond usually indicates inadequate griseofulvin absorption rather than drug resistance. Thus, treatment failure usually requires increased doses, better compliance, or preparations that are absorbed better, including newer agents.Common adverse effects associated with griseofulvin include headaches and gastrointestinal upset, especially nausea; these adverse effects are usually transient and can be alleviated by slightly lowering the dose and then increasing it again once the adverse symptoms have resolved. Occasional urticaria or morbilliform rashes can result from hypersensitivity, and photosensitivity can follow exposure to prolonged, intense sunlight. A dermatophytid reaction (see page 369) can be seen as therapy begins and should not be misinterpreted as griseofulvin allergy.Newer systemic agents include itraconazole and terbinafine. Ketoconazole appears to be less effective than griseofulvin for dermatophyte infection and is associated with a substantial risk of serious hepatotoxicity. Itraconazole is effective and can be given at 3 to 5 mg/kg per day for 4 to 6 weeks or until clearing,followed by a 4-week period off of therapy, with close observation for any recurrence and additional treatment as needed. A liquid formulation is now available. Oral terbinafine at 3 to 6 mg/kg per day for 4 to 6 weeks is effective, but experience with it in children is limited. One advantage of itraconazole and terbinafine is their rapid onset of action and a reservoir effect in the skin, hair, and nails, allowing antifungal activity to persist for weeks after cessation of drug administration. Shorter treatment durations and varying schedules with both itraconazole and terbenifine currently are being evaluated.Drug interactions should be considered;several oral antifungals, including griseofulvin, can augment the hepatic metabolism or hepatotoxic effects of other agents. Although the nature and magnitude of interactions with oral contraceptives and possible teratogenic effects are of uncertain magnitude, any systemic antifungal, including griseofulvin, should be prescribed cautiously to those who have liver disease or to sexually active females who could become pregnant.Many very effective topical antifungals are available (Table 2) and can be used once to twice daily to clear infections other than tinea capitis and onychomycosis. In general, the choice of antifungal can be based on cost and dosage schedule. Newer, more potent topical agents with once-daily dosing can aid compliance.Combining antifungals with topical mid- to high-potency cortico-steroids often causes adverse reactions and fails to clear infections because of the steroid effect; these agents should be avoided. Hydro-cortisone 1% or 2.5% can be added to antifungal therapy to reduce inflammation as needed. It is critical that affected areas be kept as cool and as dry as possible and that patients avoid discontinuing treatment too soon, which will lead to rapid recurrence of infection.
Publication Year: 1998
Publication Date: 1998-11-01
Language: en
Type: article
Indexed In: ['crossref']
Access and Citation
Cited By Count: 3
AI Researcher Chatbot
Get quick answers to your questions about the article from our AI researcher chatbot