Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Residents and travelers experience a variety of fungal infections of the skin. Many are not unique to the travel location, but the heat and humidity of the tropical environment increases susceptibility to these infections. In addition, inoculation with endemic fungal pathogens can result in deep fungal infections of the skin and subcutaneous tissues. In some cases presentation is delayed until travelers have returned to their home country.
Fungal infections of the skin (mycoses) are broadly divided into superficial and subcutaneous, based on the depth of involvement in the skin. Etiologies vary by presentation.
Superficial cutaneous mycoses invade the outer layer of skin (stratum corneum), hair, or nails. Dermatophytes and Candida species are the primary organisms responsible for the superficial mycoses, and immune response of the host may be minimal.
Dermatophyte infections are due to fungal species in three genera: Trichophyton , Microsporum , and Epidermophyton. Worldwide, Trichophyton rubrum is the most common cause of dermatophyte infection, but in many instances the same clinical presentation can be caused by dermatophytes from different genera.
The epidemiology of dermatophyte infection is different for each clinical presentation and geographic area. For example, tinea pedis and nail infections are uncommon before puberty, whereas tinea capitis is primarily a disease of childhood. Dermatophyte infections are enhanced by heat and humidity, and travelers to the tropics may note an exacerbation of a pre-existing infection. Sources of dermatophyte infection include soil, animal reservoirs, and human-to-human transmission.
Tinea capitis , or “ringworm” of the scalp, is mainly a disease of children caused by Microsporum or Trichophyton species. Trichophyton tonsurans , Microsporum canis , and Microsporum audouinii are most common.
The condition presents with hair loss (alopecia), usually with scale. Patchy areas of broken hairs covered by white scales can resemble seborrheic dermatitis. When tinea capitis invades the hair shaft the scalp shows a characteristic “black-dot” pattern, in which hairs broken off at scalp level resemble comedones within patches of alopecia. Lymphadenopathy is frequently present and can help differentiate from non-infectious causes of hair loss.
Inflammatory tinea capitis occurs in the setting of tinea infection coupled with a brisk host inflammatory response. A boggy inflamed plaque (kerion) may form, which is associated with systemic symptoms, including fever, pain, and regional lymphadenopathy. Permanent hair loss may occur.
Tinea favosa ( favus ) is a special type of chronic and progressive inflammatory infection on the scalp most frequently caused by Trichophyton schoenleinii . This variant is seen in Asia, Africa, the Middle East, and South America. It is characterized by permanent hair loss and inflammation of the scalp, which becomes covered by matted hair with dense, yellow, follicular, cup-shaped crusts (scutula) that have an unpleasant odor.
Tinea corporis , or “ringworm,” affects all ages and is recognized by annular, thin plaques, with erythema and scale most prominent at the advancing border ( Fig. 38.1 ). Lesions spread outward with central clearing. There may be multiple areas involved, but widespread involvement is unusual. The plaques vary in size from a few millimeters to many centimeters in diameter. Pruritus is variable. In some cases there is follicular involvement presenting with papules and pustules, especially at the advancing border. Differential diagnosis of tinea corporis includes psoriasis, nummular eczema, pityriasis rosea, subacute cutaneous lupus, and secondary syphilis.
Tinea imbricata is an unusual variant of tinea corporis caused by Trichophyton concentricum that is endemic in the South Pacific, Southeast Asia, and Central and South America. This presentation is chronic and results in the development of multiple large, loosely adherent scales covering large areas of the body that coalesce to form lacy concentric patterns similar to wood grain.
Tinea cruris , or “jock itch,” usually occurs in adult males and may be accompanied by tinea pedis. It is caused by Epidermophyton floccosum , Trichophyton rubrum , or Trichophyton mentagrophytes. The infection begins as an erythematous scaling patch involving intertriginous areas of the groin folds and inner thighs. Although it may extend on the lower abdomen and gluteal region, the scrotum is usually spared. There is mild erythema, with a well-demarcated scaly border. Differential diagnosis includes seborrheic dermatitis, erythrasma, intertrigo, candidiasis, and psoriasis.
Tinea pedis , or “athlete's foot,” is the most common location for dermatophyte infections. Clinical variants of tinea pedis include maceration and scale of the interdigital spaces and mild diffuse erythema and scale of the foot in a moccasin distribution. A vesicular presentation with 1-2 mm dried vesicles of the plantar surface, commonly on the mid foot, may occur. Differential diagnosis includes contact dermatitis and psoriasis.
Onychomycosis , or dermatophyte infection of the nail, results in nail plate thickening, dystrophy, and subungual debris of one or several nails. Toenails are affected more often than fingernails. Many organisms may cause onychomycosis, including nondermatophytes. When dermatophytes are the culprit, then concurrent tinea pedis is usually the source of the nail infection. Differential diagnosis includes psoriasis, lichen planus, candidiasis, and hereditary nail dystrophies. In diabetic individuals dermatophyte infections of the nails and feet create a portal of entry for bacterial infections, putting them at risk for cellulitis, especially due to streptococci.
In all forms of dermatophyte infection, diagnosis rests on demonstrating the fungus, either by KOH examination of scrapings or by culture. The KOH examination is a simple, rapid diagnostic tool. A sample is taken of scale at the active border of skin lesions, of subungual debris in onychomycosis, or of hairs in tinea capitis. The sample is placed on a microscope slide, covered with a few drops of 10-20% KOH and a coverslip, then heated briefly to lyse keratinocytes and reveal the KOH-resistant fungal structures. The specimen is examined for hyphae using the ×10 objective with the condenser lowered. Culture for dermatophytes often requires 2-6 weeks' growth to identify the fungal species.
Topical therapy is usually adequate for tinea pedis, tinea cruris, and limited forms of tinea corporis. Topical agents include imidazoles (clotrimazole, miconazole, ketoconazole, and econazole), the allylamine terbinafine, and other agents (ciclopirox, naftifine, and tolnaftate). These agents are usually applied as creams twice daily until clearing occurs. Avoid topical steroid use in these conditions, as it can worsen infection.
For tinea capitis, oral treatment is required; griseofulvin is effective therapy. The newer antifungals terbinafine, itraconazole, and fluconazole have been shown to be efficacious and safe alternatives to griseofulvin.
Griseofulvin single or divided daily dose, 20 mg/kg/day for 6-12 weeks
Terbinafine: patient weight >35 kg, 250 mg/day for 2-4 weeks; patient weight <25 kg, 125 mg/day for 6 weeks
Itraconazole: 5 mg/kg per day for 4-6 weeks or pulse dosing of 5 mg/kg per day for 1 week each month for 2-3 months.
Duration of therapy with these agents is adjusted based on clinical response. Adjunctive use of antifungal shampoos (selenium sulfide or ketoconazole) often hastens the clinical response and may help prevent spread of infection to others.
Systemic therapy is indicated for recalcitrant or widespread tinea corporis, cruris, and pedis. The following regimens (adult doses) have been used:
Terbinafine: 250 mg daily for 2 weeks
Fluconazole: 50-100 mg daily or 150 mg once a week for 2-3 weeks
Itraconazole: 100 mg daily for 2 weeks or 200 mg daily for 7 days.
Onychomycosis is treated systemically. The following regimens have been used:
Terbinafine: 250 mg/day for 6 weeks in fingernails and 12 weeks in toenails
Itraconazole: 200 mg orally twice a day for 7 days/month for 3 months for toenails (two pulses for fingernails) or 200 mg orally daily for 12 weeks
Fluconazole: 150-200 mg orally weekly for 9 months for toenails (6 months for fingernails).
The imidazole antifungals (ketoconazole, itraconazole, and fluconazole) have significant drug interactions; review the patient's medications for conflicts before prescribing.
Tinea nigra is an uncommon superficial mycosis, often grouped with the dermatophytes, but caused by the melanin-producing dimorphic yeast Hortaea werneckii . The organism lives in soil, sewage, decaying vegetation, and also has been found on shower stalls in humid environments.
Tinea nigra is a rare condition found in warm and humid climates, thought to be contracted from soil or decaying vegetation. The disease has been reported mainly in Central and South America, although cases have been identified in the southern United States, Africa, and Southeast Asia. Inoculating the organism into the skin with minor trauma has produced experimental infections, and this is believed to be the probable mechanism for natural infection. Lesions slowly develop over years and have been observed in travelers to endemic areas.
The typical lesion is a well-demarcated, asymptomatic, brown to black patch of the palmar or plantar skin, resembling a stain. The lesions may resemble junctional nevi or acral lentiginous melanoma; however, the pigment may be partly removed by shaving off the most superficial stratum corneum layer of the skin. It occurs most commonly on the palms, but feet and other areas can be involved.
KOH preparation of skin scrapings reveals hyphae. If a skin biopsy is done, the pigmented organisms can be seen in the stratum corneum.
Tinea nigra is effectively treated with twice daily applications of imidazole or ciclopirox. Topical tolnaftate and oral griseofulvin are reported to be ineffective.
Malassezia furfur and Malassezia globosa are lipophilic fungi and part of the normal human microbiome. It is believed they play a pathogenic role in several dermatologic conditions, including seborrheic dermatitis, tinea (pityriasis) versicolor, and Malassezia ( Pityrosporum ) folliculitis. The latter two conditions are discussed here.
Tinea versicolor (pityriasis versicolor) is a common, usually asymptomatic superficial fungal infection that thrives under conditions of warmth and increased moisture.
It is primarily a condition of adolescents and young adults, although those of any age may be affected. In some tropical populations, prevalence may exceed 50% among young adults. Infection is believed to reflect changes in host flora, and therefore person-to-person transmission is thought not to occur. Travelers to the tropics may experience their first episode of tinea versicolor.
The lesions of tinea versicolor are round or oval macules that coalesce into larger patches. They have a fine scale that sometimes is evident only when the lesion is scraped during the physical examination. In untanned Caucasians lesions may be subtly fawn brown and go unnoticed. The yeast blocks melanin synthesis in the skin and also produces a skin bleaching agent. With ultraviolet exposure a hypopigmented spotted appearance is enhanced due to contrast with the darkened surrounding skin ( Fig. 38.2 ). Lesions are typically distributed over the shoulders, chest, and back, and occasionally on the neck. Pruritus is usually absent.
In tinea versicolor, the clinical presentation is often sufficient to make the diagnosis. A KOH examination of scale scraped from lesions invariably shows the organisms and confirms the clinical suspicion. They are seen as short, curved hyphae and spherical yeast, giving a characteristic “spaghetti and meatballs” appearance.
The ease of confirming the diagnosis makes differential diagnosis less important. However, the appearance of hypopigmented lesions in the tropics may raise concerns of Hansen's disease ( Chapter 40 ), in which hypopigmented lesions are anesthetic, or vitiligo, in which the lighter areas are not covered by scale and are completely depigmented rather than merely lighter in color.
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here