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All cutaneous and mucosal surfaces can fall prey to fungi such as dermatophytes and yeasts. Here's how to recognize superficial fungal infections and initiate treatment.
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All cutaneous and mucosal surfaces can fall prey to fungi such as dermatophytes and yeasts. Here's how to recognize superficial fungal infections, discern the reasons for their occurrence, and then initiate treatment.
Monilial diaper dermatitis
Pityriasis (tinea) versicolor
Fungal infections of the skin, hair, nails, and mucous membranes, common in the pediatric and adolescent population, are on the rise.1 Fungi are plant-like organisms that have developed intricate strategies for survival in keratinaceous tissue. Diagnosing and treating superficial fungal infections is usually straightforward, but challenging cases occur that require us to play Sherlock Holmes and unlock the mystery behind a persistent or recurrent condition.
Among the fungi that are the most common cause of superficial skin infection are dermatophytes and yeasts such as Candida, Pityrosporum, and Malassezia furfur, the hyphal counterpart of Pityrosporum. Other pathogenic fungi and, occasionally, saprophytic molds are also culprits. All cutaneous and mucosal surfaces can fall prey to these invaders, especially when surface integrity has been changed by environmental factors such as moisture, heat, and friction, or by exposure to systemic or topical antibiotics, corticosteroids, and other immunosuppressants that shift the balance of nature in this microscopic ecosystem.
By definition, tinea corporis includes all dermatophyte infections involving glabrous skin with the exception of the groin, palms, and soles. Trichophyton, Microsporum, and Epidermophyton species can all cause tinea corporis, but Trichophyton tonsurans and Trichophyton rubrum are the most common isolates.2 Transmission can occur by direct contact with an infected human or animal, or by contact with an inanimate object such as clothing, furniture, and bed linen.
Classic tinea corporis appears as a pink-red, scaly, annular patch with an expanding border (tinea circinata) (Figure 1). Several variants exist, including bullous tinea (Figure 2), usually caused by T rubrum, as well as follicular variants such as Majocchi's granuloma (Figure 3), caused by the more inflammatory species (T rubrum, T mentagrophytes, T tonsurans, and T violaceum). Tinea corporis caused by an anthropophilic organism historically occurs in areas that are occluded or subject to trauma. Zoophilic species, such as Microsporum canis (Figure 4), tend to produce numerous lesions on exposed areas such as the face, neck, and arms, as might occur by cuddling an infected kitten or puppy. However, be suspicious when children who are at higher risk for tinea capitis, such as African-Americans, present with a few or many lesions of tinea corporis on the face, neck, upper chest, back, and arms. Fungal spores originating from the scalp can "shower" down from the scalp, producing this often overlooked pattern.
Tinea incognito (Figure 5) is the term for any superficial dermatophytic infection that has been treated with a corticosteroid, thereby reducing the degree of inflammation and scaling, but often resulting in a delay in treatment with an appropriate antifungal agent.
The diagnosis of tinea corporis usually is made clinically, but the old adage "if it scales, scrape it" can come in handy if the diagnosis is not obvious. A KOH examination is quick and easy to perform (Table 1), but if it is negative, a fungal culture may be helpful. In bullous tinea, the scraping should be done from the blister roof. With follicular infections such as Majocchi's granuloma, the KOH is frequently negative, and culture or biopsy may be necessary.
1. Place scales on a glass slide, add a coverslip, and add a few drops of 20% KOH in dimethyl sulfoxide (no heating necessary with DMSO). Gently press down on the coverslip.
2. Place the slide on the microscope stage, rack the condenser all the way down, and dim the light source.
3. Fungal spores, hyphae, and pseudohyphae will appear somewhat birefringent (doubly refractive). The latter two elements will be seen crossing over keratinocyte cell walls (see the figure).
Note: As of 1997, a Clinical Laboratory Improvement Amendments (CLIA) Certificate for Provider-Performed Microscopy Procedures is required to do in-office KOH exams.
Treatment of tinea corporis usually is accomplished with a topical antifungal agent. The majority of these agents are safe for children, and there are many from which to choose, including the imidazoles and allylamines37 (Table 2). The allylamines appear to have a slight edge over the azoles in terms of efficacy and require a shorter duration of treatment.8 Be careful when using combination antifungal-steroid preparations. Both nystatin and clotrimazole are available in combination with a medium-to-high-potency topical steroid. They may not be the best choice for areas that are particularly vulnerable to the side effects of topical steroids, such as the face and intertriginous areas,9 and some clinicians suggest not using them at all in children.10
An oral antifungal agent may be required if the tinea has not responded to an appropriate topical antifungal after the recommended length of treatment. If topical treatment failed, the pediatrician may wish to do a culture to identify the fungus or refer the patient to a dermatologist. An oral antifungal agent may also be required if lesions are extensive or involve hair follicles (as in Majocchi's granuloma11), or if the child is immunocompromised.9,12,13 When coexistent tinea capitis is detected, systemic therapy is the standard of care.
Inner city populations are at higher risk of tinea capitis, the most common fungal infection in young children. African-Americans have a 29-fold greater risk of this disease than the overall US population.14 Many practitioners have held that ethnic hair-care practices place African-Americans at higher risk; however, a recent controlled study of 66 patients with tinea capitis did not show an association between the incidence of infection and either braiding, frequency of shampooing, or use of a pomade.15
T tonsurans is the dermatophyte responsible for more than 90% of cases in the US.16 It is anthropophilic and spreads from person to person, either through direct contact or contact with spores present in hairs, shed scales, or inanimate objects (fomites). Viable spores have been found on toys, brushes, barber instruments, theater seats, and bed sheets, and can persist for a prolonged period.
Some people are colonized with the organism but remain asymptomatic. The prevalence of this carrier state is quite variable, but consistently higher in families of infected children. Approximately one third of families with an infected child have at least one carrier, and some carriers go on to develop overt disease. One study found that 14% of children in an urban school had positive cultures but were asymptomatic.17 The role that asymptomatic carriers play in the pathogenesis of tinea capitis is unclear, but they probably contribute to transmission and persistence of infection in the home and classroom.
Tinea capitis is a master of disguise (Tables 3 and 4). The majority of patients present with some degree of hair loss, scale, and pruritus. Classic signs include short, broken off "black-dot" hairs and discrete hair loss (Figure 6). Clinical findings may be more subtle, resembling seborrheic dermatitis or atopic dermatitis with diffuse scalp scaling and little or no hair loss. A more inflammatory response will produce papules, pustules, or crusting. Those with significant inflammatory disease may develop large, tender, boggy masses on the scalp that may form draining sinuses. Such lesions, called kerions (Figure 7), can be mistaken for bacterial abscesses and inappropriately treated with antibiotics. Lymphadenopathy, particularly of the posterior occipital nodes, is a common association with both inflammatory and noninflammatory tinea capitis.
Alopeciadiscrete, diffuse, severe, or subtle
Scalethick, fine, dry, or greasy
Papules, pustules, or crusts
Boggy, draining masses (kerion)
Systemic lupus erythematosus
Any child with scaling, hair loss, or erythema of the scalp should be evaluated for an underlying fungal infection. Rapid diagnosis of tinea capitis in the office was simple 50 years ago, when ectothrix infections were common and infected hairs fluoresced when the scalp was examined with a Wood's lamp; today, T tonsurans produces an endothrix infection that does not fluoresce. KOH is an option, but because it is more difficult to interpret in scalp disease, culture remains the gold standard. Although material for culture can be obtained by a number of means (hair plucking with forceps, or scalp scraping with blades or a toothbrush), the simplest and least expensive method utilizes a standard cotton swab18 (Table 5). This method has proved sensitive and specific, and requires little skill or expense.
1. Moisten a standard cotton swab with tap water.
Moisten a culturette transport swab with the enclosed media by crushing the bottom of the container.
2. Gently roll the moistened swab over all four quadrants of the scalp (this should take less than one minute!).
3. Return to the most involved site and roll the swab over this area again.
4. Immediately inoculate the sample on dermatophyte test medium (DTM) or Mycosel media, vigorously swabbing the surface several times.
Place the swab in the transport container and send to your local laboratory.
First-line therapy for tinea capitis is in a state of evolution. Standard care at the moment consists of oral griseofulvin (Grifulvin, Gris-PEG), 20 to 25 mg/kg/day of a microsize formulation for six to eight weeks (maximum, 1 g/day), and for at least two weeks following disappearance of symptoms. Such high dosing has been adopted because relative resistance of the pathogen has been noted in the last decade, with increased dosing leading to a higher cure rate.19 Response depends on the infecting pathogen; M canis is resistant to treatment and may require months of therapy before improvement is noted. Griseofulvin should be taken with a fatty meal to increase absorption. A topical agent, such as selenium sulfide or ketoconazole shampoo, is recommended for use on the scalp twice a week as a means of quickly reducing infectious risk by eliminating scalp spores. It should be kept in mind that many patients find such agents extremely drying and may not be compliant with this shampoo regimen.
Patients should be reevaluated after four weeks of treatment, and recultured at the end of treatment to determine if the organism has been eradicated. Family members and close contacts should be queried regarding signs and symptoms. Some practitioners recommend that all family members use a topical antifungal shampoo, given the high rate of the carrier state noted within affected families. It is important to emphasize the need for careful hygiene. Combs and brushes should not be shared, nor should hats, headgear, or pillows. As long as the child is being treated, we do not restrict him or her from returning to school.
Patients who cannot tolerate or do not respond appropriately to griseofulvin should be offered an alternative therapy. Several newer antifungal agents, including fluconazole (Diflucan), itraconazole (Sporanox), and terbinafine (Lamisil), have proved effective in the treatment of tinea capitis with a shorter course of therapy than what is required with griseofulvin. Consider the results of a multicenter, prospective, parallel-group trial of 200 children that compared the efficacy of these three agents with griseofulvin20 (most subjects were infected with T tonsurans). Griseofulvin, 20 mg/kg/day was given to 50 children for six weeks; 50 each were instead treated with two weeks of fluconazole, itraconazole, or terbinafine. All patients were reevaluated at four weeks, and those receiving one of the newer antifungals were given an additional week of therapy as deemed necessary.
At week 12, study participants were reevaluated, and complete cure was noted in 92% of the griseofulvin group, 94% of the terbinafine group, 86% of those on itraconazole, and 84% of the fluconazole-treated group. Adverse effects in all groups were minimal. Other investigators have not documented such high cure rates.21 With the exception of griseofulvin, these drugs are FDAapproved for children over 12 years of age only, and families must be advised of their off-label use. The optimal dosing for any of the newer agents has not been identified, but current dosing options are listed in Table 6.
Occasionally, kerions do not respond to systemic antifungal therapy. Several studies have shown that addition of a systemic corticosteroid does not significantly alter the outcome for kerions, so most experts will initiate therapy with standard antifungal treatment alone.22 A systemic steroid (for example, prednisone 1 to 2 mg/kg once daily for 10 to 14 days) is then added two weeks later if the patient has not responded to standard systemic antifungal therapy. An extensive, itchy eczema-like rash involving the trunk, extremities, and face (the "id," or autoeczematization, reaction) (Figure 8) that may represent a hypersensitivity reaction to the fungal microorganism can develop and is seen most commonly after institution of therapy. The id reaction usually responds to a mild- or moderate-strength topical corticosteroid applied twice daily to the skin (not the scalp) in conjunction with a systemic antihistamine. Severe cases may require the systemic corticosteroid therapy mentioned above for refractory kerions.
A dermatophyte infection of the beard and moustache area of males, tinea barbae presents as one of three clinical types: an annular form resembling tinea corporis, a superficial type resembling folliculitis or acne, and an inflammatory type that looks like a kerion. Diagnosis is by KOH or culture, or both. As with tinea capitis, treatment requires an oral antifungal.23
Tinea pedis (athlete's foot) is one of the most common dermatophyte infections, but rarely is it caused by dermatophytes alone. Many other types of skin flora, including micrococci, corynebacteria, and gram-negative bacteria, contribute to the presentation of this disorder. The most common dermatophytes causing tinea pedis are T rubrum, T mentagrophytes, and E floccosum. Four clinical varieties exist: interdigital, moccasin distribution, vesicular, and macerated. In the latter, it is important to exclude a secondary bacterial infection, and treat with a broad-spectrum topical antifungal, such as econazole (Spectazole) or ciclopirox (Loprox), that has antibacterial properties as well.24 These agents are applied twice daily. Gel formulations can be used to dry macerated areas.
Uncomplicated tinea pedis should respond to treatment with topical imidazole for four weeks, or topical allylamine for one to two weeks.3,25,26 The use of antifungal powders and sprays and absorbent socks can be helpful adjunctive and preventive measures. Recurrence of tinea pedis may be as high as 70%,9 which may be the result of incomplete treatment, persistence of fungal spores, or coexistence of onychomycosis. If toenails are the primary source of spores, systemic treatment is required.
Tinea cruristinea in the groin or perineal region that sometimes spreads to nearby areasalmost always occurs in males, is more common in summer months and in tropical areas, and can be associated with concomitant tinea pedis. The most common organisms are E floccosum, producing annular lesions that are less likely to spread to adjacent areas, and T rubrum, resulting in confluent patches that often spread to the abdomen, buttocks, and upper thighs. The latter can mimic seborrheic dermatitis, contact dermatitis, or even psoriasis. The diagnosis is made by clinical appearance, or by KOH or culture (or both). Treatment consists of a topical antifungalan imidazole for two weeks or an allylamine for one week5,25,26along with efforts to decrease moisture and occlusion in the area (absorbent powder and loose-fitting clothing).
Tinea gladiatorum is the term for tinea corporis infection in wrestlers. Outbreaks of tinea corporis have been documented on wrestling teams and in camp settings. A study of high school sports teams in the midwestern US noted that the increased risk of tinea corporis is limited to wrestlers, presumably because of close body contact during matches.27 Lesions are most often localized to the neck, upper back, and arms, and generally manifest a typical "ringworm" appearance, possessing scaling red papules and annular plaques. Trichophyton tonsurans is a common isolate from these lesions.
Athletes with tinea gladiatorum must be removed from competition unless the lesions are completely covered and the patient is undergoing treatment. Topical treatment usually is sufficient for localized lesions, with treatment continuing for one week after apparent clearing. Some practitioners now treat infected wrestlers and their at-risk teammates with systemic therapy such as itraconazole or fluconazole, but this regimen is not FDAapproved.27 When an outbreak occurs, effort should be made to identify and treat infected persons. Wrestling equipment should be cleaned as well as possible and headgear should not be shared.
Chronic infection of fingernails and toenails by fungal pathogens presents occasionally in the pediatric primary care office. Fungal infection of the nails is often accompanied by tinea pedis.28 Treatment traditionally has been long and difficult, but newer oral antifungal agents make the process easier and more successful.
Therapy should be aimed at specific pathogens: dermatophytes such as T rubrum, T mentagrophytes, and Epidermophyton floccosum, yeasts such as Candida species, and saprophytic fungi (molds). Commonly used topical antifungal preparations usually are ineffective in treating onychomycosis because the drugs do not adequately penetrate the nail plate. There may be a role for them if Candida is the culprit. Newer topicals, such as ciclopirox, in a lacquer form are very safe and more effective than other topicals, with a cure rate of about 30% when used over 48 weeks, according to the results of studies in the US.29 Antifungal nail lacquers may be useful in potentiating the cure rate when used in combination with an oral antifungal.30,31
Tinea unguiumtinea involving the nailsgenerally requires oral therapy. Both griseofulvin and ketoconazole (Nizoral) have proved unsatisfactory, with low cure and high relapse rateseven when treatment is administered for as long as 12 to 18 months.32 The newer antifungals are safer and more efficacious, but are not FDAapproved for treating nail infection in children under 12 years of age. Itraconazole in a pulse-regimen (daily treatment for one week followed by a three-week period without treatment) for three months has been shown to be highly effective (78% clinical cure, 61% mycologic cure) in adults.33 Patients age 12 and older are usually given 100 mg orally bid. Terbinafine seems to be superior when treating dermatophyte nail infections and better tolerated than itraconazole3335; it is given as a continuous 250 mg dose daily for three to four months. Itraconazole may be more effective against saprophytic fungi (nondermatophyte molds).36 Fluconazole, 150 mg once weekly for three to six months, is only one third as effective as terbinafine,37 but may be more effective against Candida than are other antifungals. Studies of these agents undertaken in the future in children younger than 12 years of age will help to define their safety and efficacy for use in pediatric onychomycosis.
In chronic paronychia, Candida species often are cultured from the nail of the involved digit. Whether this represents a true nail infection is the subject of debate. A recent study showed that topical steroids were more likely to prevent paronychia than systemic antifungals,38 lending support to the idea that this may be a chronic dermatitis with secondary monilial colonization, not true onychomycosis.
Pediatricians encounter Candida-associated infections of skin and mucous membranes almost daily.
Oral candidiasis (thrush), commonly seen in infants and immunocompromised patients, presents as scattered white patches on the oral and buccal mucosa, tongue, or palate, often progressing to esophagitis in the latter group. It may cause significant discomfort leading to poor oral intake. Nystatin oral suspension is the most commonly prescribed treatment, but fluconazole has been used in adults with HIV.39 It is important to remove or thoroughly clean any items that may be reservoirs of the yeast, such as pacifiers.40
Monilial diaper dermatitis is seen commonly in association with thrush. Stool cultures may be positive for Candida in 90% of children with oral candidiasis, and there is a 35% to 50% rate of co-existence of thrush and Candida diaper dermatitis.41 Antibiotic therapy, especially with penicillin derivatives, increases the incidence of monilial diaper dermatitis by changing the balance of perineal skin flora.42,43 Topical nystatin is the time-honored therapy, but other topicals, including miconazole,44 econazole, and oxiconazole (Oxistat), are effective. A recent study found that mupirocin was beneficial in treating perianal candidiasis.45
Intertrigo is an inflammatory dermatitis that develops at sites of friction on opposing skin surfaces, particularly body folds, in obese and, occasionally, diabetic patients (Figure 9). Candida may cause a secondary infection in these areas, and treatment with topical nystatin, one of the imidazoles, or terbinafine can be effective. It is important to maintain good hygiene and keep the areas as dry as possible to prevent maceration and additional skin breakdown.46 An antifungal powder can be used adjunctively.
This condition is caused by the growth of filamentous yeast forms within the stratum corneum. Although often referred to as tinea versicolor, this name is inappropriate because tinea refers to a dermatophyte infection. Pityriasis versicolor is an extremely common skin condition, especially in tropical climates. The yeast responsible for this infection, Malassezia furfur, is a dimorphic, lipid-loving yeast that lives on the skin as a member of the normal skin flora. Under appropriate conditions (warmth, humidity, and immunosuppression) this benign yeast can transform into an invasive hyphal phase. It is the definitive pathogen in pityriasis versicolor, pityrosporum folliculitis, and some cases of catheter-line sepsis.47 It has also been implicated in several other conditions, including seborrheic dermatitis, flares of atopic dermatitis, and a neonatal rash termed neonatal cephalic pustulosis.48 Although most cases of pityrosporum versicolor occur in healthy adolescents and adults, 5% to 7% of confirmed cases have been documented in children under 13 years of age.49 Heredity may play a role; some families show a predilection for the disease.
Most patients complain of unsightly spots on the trunk that may itch (Figure 10). Lesions favor sebum-rich areas such as the upper chest and back. One third of children will exhibit facial involvement, particularly the forehead and temples (Figure 11). The upper arms, neck, and axillae are less commonly involved; rarely, the ear canal.50 Most lesions are ovoid and hypopigmented. Versicolor is an appropriate name, as white, brown, pink, or tan coloration may be present. The lesions are discrete and coalescent, and possess a fine faint scale that is more noticeable upon scraping the site. When such scrapings are viewed microscopically with the KOH prep, short hyphae and spores ("macaroni and meatballs") are apparent.
Pityriasis versicolor may be confused with pityriasis alba, vitiligo, pityriasis rosea, seborrheic dermatitis, and tinea infections. KOH evaluation is very helpful in confirming the diagnosis. Culture is not usually helpful; because the organism is a normal commensal on skin, growth from that site is not diagnostic of infection. In addition, Pityrosporum requires a lipid-enriched medium and cannot be isolated by standard fungal culture.
A number of topical agents are effective against pityriasis versicolor, but none of them is uniformly curative: Recurrence is common. A simple, cosmetically appealing treatment consists of the application of ketoconazole shampoo to wet skin for three to five minutes for three consecutive days.51 Systemic treatment is appropriate for extensive or recurrent disease, and several therapies are now available. Oral griseofulvin and terbinafine are ineffective, but oral itraconazole, ketoconazole, and fluconazole all are effective, as is terbinafine topical spray. Various dosing regimens are available; perhaps the simplest is one dose of 400 mg of fluconazole.52 Relapse is common even with systemic treatment, and patients must be told of the utility of monthly prophylactic topical treatment.
Piedra is a fungal infection of hair that is characterized by nodules that adhere to the hair shaft, resulting in weakening and breakage. Black piedra, caused by Piedraia hortae, is common in tropical climates. Small dark nodules are firmly attached, primarily to scalp hair. White piedra, caused by Trichosporon beigelii, involves facial and pubic hair more commonly than scalp hair, and is seen in more temperate climates. These white to tan nodules are softer and less adherent to the hair shaft. Piedra infection is asymptomatic and transmission from person to person is rare. Treatment involves cutting or shaving the hair, although use of adjunctive topical or oral antifungals (including ketoconazole) has been reported.
Tinea nigra, caused by Exophiala werneckii, is a superficial infection of the stratum corneum, usually on the palm or sole (Figure 12), resulting in brown-black macules that can be confused with melanocytic lesions such as nevi, lentigines, or melanoma.53 This entity is more common in the tropics, but can be found in the southern US. Topical antifungals (ketoconazole and terbinafine) as well as keratolytics (urea or tretinoin) are usually effective.
Recognizing these disorders and the circumstances surrounding their appearance or persistence is half the battle in the ongoing turf war between flora and fauna. New treatments, both topical and oral, are under investigation that should ease the frustrations of caregivers as well as patients and parents dealing with this jungle of fungal infections.
The authors dedicate this article to the memory of their friend and colleague, Walter W. Tunnessen, MD, an "honorary" pediatric dermatologist and member of the editorial board of Contemporary Pediatrics who, before his untimely death in 2001, invited them to write this article.
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