Cutaneous fungal infections are categorized as follows:
Superficial: infecting the stratum corneum, hair, and nails.
The three major genera are Trichophyton, Microsporum, and Epidermophyton. The term “tinea” is used to denote fungal infection and is typically modified by body site (e.g., tinea capitis, tinea corporis).
Candida is a normal inhabitant of the oropharynx and gastrointestinal tract. Moist, wet conditions favor Candida overgrowth and can lead to superficial infection of the skin or mucosal surfaces.
Deep: involving the dermis and subcutaneous tissues.
Subcutaneous mycoses are the result of implantation and include chromoblastomycosis, mycetoma, sporotrichosis, basidiobolomycosis, and lobomycosis.
Deep mycoses are the result of hematogenous spread or extension from an underlying structure. True pathogens infect hosts with normal immunity and include histoplasmosis, coccidioidomycosis, and paracoccidioidomycosis. Opportunistic pathogens infect immunocompromised hosts and include disseminated candidiasis and aspergillosis.
Tinea capitis is a fungal infection (Microsporum or Trichophyton) of the scalp and hair characterized by follicular inflammation with painful, boggy nodules that drain pus and result in hair loss.
INSIGHT 
If there is any doubt about the diagnosis, a fungal culture of affected hairs and scale can be very helpful. If systemic treatment is given without improvement, the initial diagnosis is called into question, but culture after treatment is extremely low-yield.
SYNONYMS Scalp ringworm, tinea tonsurans, herpes tonsurans, hair ringworm.
AGE Children: 2 to 10 years; rarely seen in infants or adults.
GENDER M > F, >2:1.
RACE Blacks > whites.
INCIDENCE Most common fungal infection in childhood. Up to 8% of the pediatric population affected.
ETIOLOGY Trichophyton tonsurans (90%) in the United States and West Europe > Microsporum canis > M. audouinii > T. verrucosum. T. violaceum > T. tonsurans in Southeast Europe and North Africa.
Two to four days after exposure, scaly pruritic patches appear in the scalp with hair loss. Untreated, the lesions enlarge and boggy papular lesions may develop within the alopecic patches. Systemic symptoms may include cervical lymphadenopathy, malaise, or fever. Additionally, a systemic allergy to fungal elements can be seen (see “Tinea and Id Reaction”).
Ectothrix (infection on the outside of the hair shaft).
Gray patch ringworm. Brittle hair; shafts break off 1 to 2 mm above the scalp surface. Broken hairs give patch a grayish appearance. Caused by M. audouinii and M. canis (Fig. 21-1).
Endothrix (infection on the inside of the hair shaft).
Black dot ringworm. Broken-off hair shafts flush with the level of the scalp give the appearance of black dots, caused by T. tonsurans and T. violaceum (Fig. 21-2). Easily spread via fomites.
Kerion. Boggy, purulent, inflamed painful nodule drains pus. Hairs do not break but fall out easily. Heals with residual hair loss (Fig. 21-3).
Favus. Scutula (yellowish crusts) are present on the scalp infected with T. schoenleinii (Fig. 21-4). Favus is endemic in Asia, the Middle East, and South Africa.
FIGURE 21-2
Tinea capitis, “black-dot” type
Asymptomatic patch of alopecia on the frontal scalp of a 4-year-old child with a Trichophyton tonsurans infection. (Reproduced with permission from Fitzpatrick TB, Wolff K, Johnson RA. Color Atlas and Synopsis of Clinical Dermatology. 4th ed. New York, NY: McGraw-Hill; 2001.)
WOOD’S LAMP Wood’s lamp reveals bright green hair shafts in scalp infections caused by M. audouinii and M. canis. T. schoenleinii fluorescence is grayish green. T. tonsurans, however, does not exhibit fluorescence.
DIRECT MICROSCOPIC EXAMINATION WITH 10% KOH Spores within (T. tonsurans and T. violaceum, Fig. 21-5) or surrounding (Microsporum) the hair shaft, consistent with endothrix or ectothrix tinea capitis, respectively.
FUNGAL CULTURE Infected hair or scalp scale can be inoculated on Sabouraud’s agar or other Dermatophyte Test Medium (DTM) and the causative organism can be identified in several weeks’ time.
Tinea capitis spreads on brushes, combs, towels, pillowcases, and hats. Children with scalp ringworm should not share these items. Tinea capitis can also be spread by close contact with infected children. The current recommendation is that infected children may attend school once treatment has begun.
Antifungal shampoos (ketoconazole 2% or selenium sulfide 2.5%) decrease shedding fungal elements and thus decrease spread of infection. Patients should be instructed to lather the shampoo and let it sit on the scalp for 5 to 10 minutes before rinsing 2 to 3 times per week. Household contacts can also shampoo daily or every other day until the patient is disease-free. Pets including cats and dogs are reservoirs of M. canis and veterinary treatment of household pets should be considered if they are suspected to be the source of infection or reinfection.
SYSTEMIC THERAPIES Topical treatments are not effective in treating the hair bulb; thus oral antifungal treatment is needed. Oral griseofulvin is the gold standard for tinea capitis in children, and refractory cases may need higher doses or fluconazole. Known side effects include headaches and gastrointestinal upset. Newer antifungal agents (itraconazole, terbinafine) are efficacious, but none of these agents have the long-term safety profile of griseofulvin.
Tinea faciei is a superficial fungal infection on the face, characterized by a well-circumscribed erythematous enlarging plaque.
SYNONYMS Tinea faciale, tinea facialis, ringworm of the face.
AGE Most common in children.
INCIDENCE Common.
ETIOLOGY T. mentagrophytes, T. rubrum > M. audouinii, M. canis.
Tinea faciei is most commonly caused by a child’s exposure to an infected animal, especially puppies or kittens. By hugging or playing with the animal, the dermatophyte is transferred by fur to skin contact.
An asymptomatic papule slowly enlarges to a plaque. The lesion is asymptomatic or mildly pruritic. Multiple discrete lesions may be present. No systemic symptoms are present.
TYPE Macule, plaque, scale (Fig. 21-6).
COLOR Pink to red, hyperpigmentation.
DISTRIBUTION Any area of face; cheeks are most common.
Tinea faciei is the most commonly misdiagnosed fungal infection. It is often mistaken for seborrheic dermatitis, contact dermatitis, erythema chronicum migrans, lupus erythematosus, polymorphic light eruption, or a photoinduced drug eruption.
KOH Examination of scraping shows hyphae. Scrapings from patients who have used topical antifungals may be falsely negative. Patients who have used topical corticosteroids show massive numbers of hyphae.
FUNGAL CULTURE Skin scrapings taken from the area and inoculated on Sabouraud’s agar or other DTM media will grow the causative dermatophyte in a few weeks.
For the treatment of tinea faciei, topical antifungals such as substituted pyridine (ciclopirox), naphthiomates (tolnaftate), imidazoles (clotrimazole, econazole, miconazole, ketoconazole, oxiconazole), allylamines (terbinafine, naftifine) are effective if applied BID at least 2 cm beyond the advancing edge of the skin lesion until the lesion clears (typically 6 weeks). It is recommended to continue the topical medication for one more week after clinical clearing to ensure clinical cure.
Affected household members or pets should also be treated. In severe refractory or recurrent cases, systemic fluconazole, griseofulvin, itraconazole, or terbinafine may be necessary.
Tinea corporis is a superficial fungal infection characterized by scaling papular lesions occurring in an annular arrangement with peripheral enlargement and central clearing on the trunk, limbs, or face.
SYNONYMS “Ringworm,” tinea corporis gladiatorum.
AGE All ages.
INCIDENCE Common.
ETIOLOGY T. rubrum > T. mentagrophytes > M. canis > M. audouinii.
Tinea corporis can result from human-to-human, animal-to-human, or soil-to-human spread. Kittens and puppies are an important risk factor in the transmission of organisms, as are gymnasiums, crowded housing, locker rooms, wrestling, outdoor occupations, and immunosuppressive states.
One to three weeks after inoculation, the infection spreads centrifugally resulting in annular scaly plaques with pustules at the active border. Lesions may be asymptomatic, pruritic, or with a burning sensation. Systemic symptoms are not present.
TYPE Plaques with or without pustules or vesicles.
SIZE 1 to 10 cm.
COLOR Pink to red.
ARRANGEMENT Enlargement, central clearing, annular configuration (Fig. 21-7).
DISTRIBUTION Exposed skin of forearm, neck most common; found on all locations on trunk.
Tinea corporis is often mistaken for annular erythemas, psoriasis, contact dermatitis, eczema, pityriasis rosea, seborrhea, granuloma annulare, or lupus erythematosus.
KOH Scales from the edge demonstrate hyphae, arthrospores, or budding yeasts. The type of dermatophyte cannot be determined, but rather its presence or absence.
FUNGAL CULTURE Skin lesion scrapings can be inoculated on Sabouraud’s agar or other media, and dermatophyte types will grow and can be identified in a matter of weeks.
For the treatment of tinea corporis, topical antifungals such as substituted pyridine (ciclopirox), naphthiomates (tolnaftate), imidazoles (clotrimazole, econazole, miconazole, ketoconazole, oxiconazole), and allylamines (terbinafine, naftifine) are effective if applied BID at least 2 cm beyond the advancing edge of the skin lesion until the lesion clears (typically 6 weeks). It is recommended to continue the topical medication for one more week after clinical clearing to ensure clinical cure. Affected household members or pets should also be treated.
In severe refractory or recurrent cases, systemic fluconazole, griseofulvin, itraconazole or terbinafine may be necessary.
Tinea cruris is a subacute or chronic fungal infection of the upper thigh or groin area, usually caused by Epidermophyton floccosum , T. rubrum, or T. mentagrophytes.
SYNONYM Jock itch.
AGE Adolescents and young adults.
GENDER M > F.
ETIOLOGY T. rubrum > T. mentagrophytes > E. floccosum.
Most patients with tinea cruris have concomitant tinea pedis. The fungal infection on the feet typically precedes the groin infection. The fungal elements are spread when underclothes are dragged over the infected feet up to the groin area. Other predisposing factors include warm, humid environment, tight clothing, obesity, diabetes, and immunosuppression.
Often seen in athletes, tinea cruris begins as erythema and mild pruritus in the groin area. Occlusive, wet clothing (tight clothes, exercise outfits, bathing suits) aggravates the condition.
TYPE Plaques, papules, scale, pustules.
COLOR Dull red to brown.
DISTRIBUTION Bilateral intertriginous areas, upper thighs, and buttock (Fig. 21-8). Scrotum is rarely involved (in contrast to candidiasis).
The differential diagnosis for tinea cruris includes candidiasis, erythrasma, intertrigo, seborrheic dermatitis, psoriasis, irritant dermatitis, and contact dermatitis.
KOH Scrapings will show hyphae, arthrospores, or budding yeasts.
FUNGAL CULTURE Skin scrapings taken from the area and inoculated on Sabouraud’s agar or other DTM media will grow causative dermatophyte in a few weeks.
Measures to prevent tinea cruris include less occlusive clothing, shower shoes in public or home bathroom floor, antifungal foot powder, and concomitant treatment of tinea pedis (athlete’s foot) if present. Patients should be instructed to put on their socks before their underwear to avoid dragging the fungal elements from the floor or their infected feet up to their groin area.
For the treatment of tinea cruris, topical antifungals such as substituted pyridine (ciclopirox), naphthiomates (tolnaftate), imidazoles (clotrimazole, econazole, miconazole, ketoconazole, oxiconazole), allylamines (terbinafine, naftifine) are effective if applied BID at least 2 cm beyond the advancing edge of the skin lesion until the lesion clears (typically 6 weeks). It is recommended to continue the topical medication for one more week after clinical clearing to ensure clinical cure.
In severe refractory or recurrent cases, systemic fluconazole, griseofulvin, itraconazole, or terbinafine may be necessary.
Tinea pedis is an itchy, scaly fungal infection of the feet seen in adolescents or adults, but rarely in young children.
SYNONYM Athlete’s foot.
AGE Adolescents and adults; rare in children.
GENDER M = F.
INCIDENCE Most common fungal infection in adolescents and adults.
ETIOLOGY T. rubrum, T. mentagrophytes > E. floccosum, T. tonsurans.
Tinea pedis is caused by T. rubrum, T. mentagrophytes, E. floccosum, or T. tonsurans growing in humid weather with occlusive footwear. The fungal organisms are likely contracted from going barefoot in locker rooms, gymnasiums, or public facilities, but host susceptibility also plays a role in that some people never get tinea pedis despite exposure and others always have recurrences despite treatment. Prevalence is more common with increasing age.
Tinea pedis usually begins as interdigital scaling and fissuring, especially between the fourth and fifth toes. It can then spread to affect both plantar aspects of the feet (“moccasin distribution”) and palmar aspects of the hands. Inflammation and/or ulceration may be present. Also, a systemic autoeczematization response can be seen (see “Tinea and Id Reaction”).
TYPE Scale, maceration, vesicles, bullae (Fig. 21-9).
COLOR Pink to red; opaque white scales.
DISTRIBUTION Webspace between third/fourth toes, plantar surface, especially arch.
Tinea pedis, although common in adolescents and adults, is uncommon in children. Most instances of “athlete’s foot” in children are actually atopic dermatitis, contact dermatitis, psoriasis, juvenile plantar dermatosis, erythrasma, or a bacterial infection.
KOH Webspace or scaly areas reveal hyphae, arthrospores, or budding yeasts.
FUNGAL CULTURE Skin scrapings inoculated on Sabouraud’s agar or DTM media will show fungal growth in a few weeks.
Tinea pedis tends to be chronic and recurrent with exacerbations in hot weather or with exercise. Macerated skin may lead to lymphangitis or cellulitis.
Tinea pedis is difficult to treat and is prone to recurrences. Acute episodes can be treated with open wet compresses (Burow’s solution, 1:80 dilution) and topical antifungal creams such as substituted pyridine (ciclopirox), naphthiomates (tolnaftate), imidazoles (clotrimazole, econazole, miconazole, ketoconazole, oxiconazole), or allylamines (terbinafine, naftifine). They should be applied BID over both feet up to the ankles bilaterally until the lesions clear (typically 2–6 weeks). It is recommended to continue the topical medication for one more week after clinical clearing to ensure clinical cure. The addition of keratolytic creams (glycolic acid, lactic acid, or urea) can help reduce hyperkeratosis. Keeping the feet dry will help prevent relapses and can be achieved with open footwear or absorbent socks/antifungal foot powder.
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