Section 21. Cutaneous Fungal Infections

Cutaneous fungal infections are categorized as follows:

1. 1. 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 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.

1. 2. Deep: involving the dermis and subcutaneous tissues.

• Subcutaneous mycoses are the result of implantation and include chromoblastomycoses, 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

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.

Synonym Scalp ringworm.

Epidemiology

Age Children: 2 to 10 years; rarely seen in infants or adults.

Gender M > F, 5:1.

Race Blacks > whites.

Incidence Most common fungal infection in childhood. Eight percent of the pediatric population.

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.

History

Two to four days after exposure, scaly pruritic patches appear in the scalp with hair loss. Untreated, the lesions enlarge. Systemic symptoms may include cervical lymphadenopathy, malaise, or fever. Additionally, a systemic allergy to fungal elements can be seen (see “Tinea and Id Reaction”).

Physical Examination

Skin Lesions

1. 1. Ectothrix (infection on the outside of the hair shaft).

   a. Gray patch ringworm. Brittle hair; shafts break off close to scalp surface. Caused by M. audouinii and M. canis (Fig. 21-1).

   2. Endothrix (infection on the inside of the hair shaft).

   a. Black dot ringworm. Broken-off hairs give appearance of black dots, caused by T. tonsurans and T. violaceum (Fig. 21-2).

   b. Kerion. Boggy, purulent, inflamed painful nodule drains pus. Hairs do not break but fall out easily. Heals with residual hair loss (Fig. 21-3).

   c. Favus. Scutula (yellowish crusts) are present on the scalp infected with (Fig. 21-4) T. schoenleinii. Favus is endemic in the Middle East and South Africa.

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.

Laboratory Examinations

Direct Microscopic Examination with 10% KOH Spores within (T. tonsurans and T. violaceum, Fig. 21-5) or surrounding (Microsporum) the hair shaft.

Fungal Culture Infected hair or scalp scale can be inoculated on Sabouraud’s agar or other DTM media and the causative organism can be identified in several weeks time.

Management

Tinea spreads on brushes, combs, towels, pillowcases, and hats. Children with scalp ringworm should not share these items. Tinea 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×/wk. Household contacts can also shampoo daily or every other day until the patient is disease-free.

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, terbenifine) are efficacious, but none of these agents have the long-term safety profile of griseofulvin.

Tinea Faciei

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.

Epidemiology

Age Most common in children.

Incidence Common.

Etiology T. mentagrophytes, T. rubrum > M. audouinii, M. canis.

Pathophysiology

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.

History

An asymptomatic papule slowly enlarges to a plaque. The lesion is asymptomatic or mildly pruritic. No systemic symptoms are present.

Physical Examination

Skin Findings

Type Macule, plaque, scale (Fig. 21-6).

Color Pink to red, hyperpigmentation.

Distribution Any area of face.

Differential Diagnosis

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 photodrug eruption.

Laboratory Examinations

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.

Management

For the treatment of tinea faciei, topical antifungals such as substituted pyridine (ciclopirox), naphthiomates (tolnaftate), imidazoles (clotrimazole, econazole, miconazole, ketoconazole, oxiconizole), 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 1 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 terbenifine may be necessary.

Tinea Corporis

Tinea corporis is a superficial fungal infection characterized by scaling papular lesions occur in an annular arrangement with peripheral enlargement and central clearing on the trunk, limbs, or face.

Synonyms “Ringworm,” tinea corporis gladiatorum.

Epidemiology

Age All ages.

Incidence Common.

Etiology T. rubrum > T. mentagrophytes > M. canis > M. audouinii.

Pathophysiology

Tinea corporis can result from human-to-human, animal-to-human, or soil-to-human spread. Kittens and puppies are an important factor in the transmission of organisms as are gymnasiums, crowded housing, locker rooms, wrestling, and outdoor occupations.

History

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 burn. Systemic symptoms are not present.

Physical Examination

Skin Findings

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.

Differential Diagnosis

Tinea corporis is often mistaken for annular erythemas, psoriasis, contact dermatitis, eczema, pityriasis rosea, seborrhea, granuloma annulare, or lupus erythematosus.

Laboratory Examinations

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.

Management

For the treatment of tinea corporis, topical antifungals such as substituted pyridine (ciclopirox), naphthiomates (tolnaftate), imidazoles (clotrimazole, econazole, miconazole, ketoconazole, oxiconizole), 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 terbenifine may be necessary.

Tinea Cruris

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.

Epidemiology

Age Adolescents and young adults.

Gender M > F.

Etiology T. rubrum > T. mentagrophytes > E. floccosum.

Pathophysiology

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, and obesity.

History

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.

Physical Examination

Skin Findings

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).

Differential Diagnosis

The differential diagnosis for tinea cruris includes candidiasis, erythrasma, intertrigo, seborrheic dermatitis, psoriasis, irritant dermatitis, and contact dermatitis.

Laboratory Examinations

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.

Management

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, oxiconizole), 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 terbenifine may be necessary.

Tinea Pedis

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.

Epidemiology

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.

Pathophysiology

Tinea pedis is cause 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.

History

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 and palms. Also, a systemic allergic response can be seen (see “Tinea and Id Reaction”).

Physical Examination

Skin Findings

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.

Differential Diagnosis

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.

Laboratory Examinations

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.

Course and Prognosis

Tinea pedis tends to be chronic and recurrent with exacerbations in hot weather or with exercise. Macerated skin may lead to lymphangitis or cellulitis.

Management

Tinea pedis is difficult to treat and is prone to recurrences. Acute episodes can be treated with open wet compresses (Burrow’s solution 1:80) and topical antifungal creams such as substituted pyridine (ciclopirox), naphthiomates (tolnaftate), imidazoles (clotrimazole, econazole, miconazole, ketoconazole, oxiconizole), 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.

Tinea Manuum

Tinea manuum is a chronic dermatophytosis of the hand(s), often unilateral, and most commonly on the dominant hand. There is almost invariably a preexisting tinea pedis, with or without nail involvement (onychomycosis).

Synonym Tinea manus.

Epidemiology

Age Adolescents and adults. Uncommon in children.

Gender M = F.

Incidence Common.

Etiology T. rubrum, T. mentagrophytes > E. floccosum.

Pathophysiology

Tinea manuum is a dermatophyte infection of the palm and interdigital spaces often seen in patients with concomitant moccasin-type tinea pedis, and is thought to spread from the feet.

History

Tinea manuum usually presents as unilateral (usually dominant hand) palmar scaling in an individual with chronic or intermittent preexisting tinea pedis or onychomycosis. Like tinea pedis, it tends to have a chronic and relapsing course.

Physical Examination

Skin Findings

Type Papules, vesicles (Fig. 21-10).

Color Pink to red.

Distribution Diffuse hyperkeratosis of the palms or patchy scaling on sides of fingers; 50% of patients have unilateral involvement.

Differential Diagnosis

Tinea manuum is often mistaken for psoriasis, lichen planus, allergic contact or irritant dermatitis, or dyshidrotic eczema.

Laboratory Examinations

KOH Scales taken from the advancing edge will show hyphae elements.

Fungal Culture Skin scrapings can be inoculated on Sabouraud’s agar or DTM media and will grow the causative dermatophyte in several weeks time.

Course and Prognosis

When combined with tinea capitis, onychomycosis, tinea pedis, or tinea corporis, tinea manuum may recur following treatment, and this can be a frustrating problem.

Management

Acute episodes of tinea manuum can be treated with open wet compresses (Burrow’s solution 1:80) and topical antifungal creams such as substituted pyridine (ciclopirox), naphthiomates (tolnaftate), imidazoles (clotrimazole, econazole, miconazole, ketoconazole, oxiconizole), or allylamines (terbinafine, naftifine). It is recommended to continue the topical medication for one more week after clinical clearing to ensure clinical cure. Eradication of other concomitant tinea infections (e.g., tinea capitis, onychomycosis) needs to occur to prevent further recurrences.

Onychomycosis

Onychomycosis is a common, unsightly fungal infection of the toenails and/or fingernails.

Synonym Tinea unguium.

Epidemiology

Age Adolescents and adults, rarely children.

Gender M > F

Incidence Common.

Etiology T. rubrum, T. mentagrophytes > E. floccosum.

Pathophysiology

Onychomycosis is associated with tinea pedis and trauma helps inoculate the nail with fungus. Host susceptibility to tinea pedis predisposes the patient to onychomycosis. However, onychomycosis can also superinfect diseased nails (psoriasis or eczema).

History

Onychomycosis typically is seen in individuals with chronic tinea pedis or tinea manuum. The onset is slow and insidious, and typically affects the toenails more often than the fingernails. Topical treatments are ineffective and oral regimens, while efficacious, do not prevent relapses.

Physical Examination

Nail Lesions

• Distal Subungual Onychomycosis: Whitish-yellow discoloration of the free edge with separation of nail plate/nail bed and subungual accumulation of debris.
• White Superficial Onychomycosis: White area on the nail plate, occurs relatively commonly in HIV-infected patients in both toenails and fingernails.
• Proximal Subungual Onychomycosis: Rare. Starts as whitish-brown area on the proximal part of the nail plate. May enlarge to affect the whole nail plate.
• Candida Onychomycosis: Toenails/fingernails in chronic mucocutaneous candidiasis are thickened, rough, furrowed, and eventually disintegrates into a brittle mass.

Distribution Infected nails coexist with nor mal-appearing nails (Fig. 21-11). Toenails > fingernails. Twenty nails involved in immuno suppressed patients (seen in chronic mucocuta neous candidiasis and acrodermatitis entero pathica).

Differential Diagnosis

The differential diagnosis of onychomycosis includes nail psoriasis, eczema, trauma, photo-onycholysis, pachyonychia congenital and other inherited nail disorders.

Laboratory Examinations

KOH Examination of nail scrapings reveals hyphae.

Fungal Culture Nail clippings taken and inoculated on Sabouraud’s agar or other DTM media will grow the causative dermatophyte in a few weeks.

Dermatopathology A PAS stain of an infected nail clipping will reveal hyphae.

Management

Topical treatment for onychomycosis is not successful, but topical preparations (ciclopirox) are safer in children and with chronic use can eliminate tinea pedis, which in turn may clear onychomycosis slowly. Oral antifungals are the treatment of choice in adolescents and adults. Oral griseofulvin is slow and not as effective as oral fluconazole, itraconazole, or terbinafine for toenail clearance, which have an 80% cure rate, but a significant relapse rate. Old shoes should be discarded, proper footwear, cotton socks, and absorbent powders may be helpful.

Tinea and Id Reaction

An “id” reaction is a generalized acute cutaneous reaction to an infection (e.g., tinea) or inflammatory skin condition (e.g., contact dermatitis) characterized by a vesicular eruption on the trunk and extremities.

Insight

The word “id” comes from the Greek suffix ides, meaning “son or daughter of” and is not related to the psychoanalytic term.

Synonym Dermatophytid reaction, autoeczematization.

Epidemiology

Age Any age.

Gender M = F.

Incidence 5% of tinea infections.

Etiology Unclear.

Pathophysiology

An id reaction may be caused by an abnormal immune recognition of autologous skin antigens, increased stimulation of T cells, a lower irritation threshold, disseminated infectious antigen with a secondary response, or hematogenous cytokines.

History

An id reaction is an uncommon generalized vesicular eruption that appears after the primary focus of infection (tinea capitis, faciei, corporis, pedis or manuum) has been present for a while and clearance has started. Symptomatically, the rash can be very pruritic and systemically the patients may have mild fever or lymphadenopathy.

Physical Examination

Skin Findings

Type Diffuse papules and vesicles, edema (Fig. 21-12).

Color Pink to red.

Size 2 to 5 mm.

Distribution Trunk, extremities (Fig. 21-13), face.

General Findings

Fever

LAD Mild lymphadenopathy may be present.

Differential Diagnosis

An id reaction can be confused with a drug reaction, viral exanthem, dyshidrotic eczema, contact dermatitis, cutaneous T-cell lymphoma (CTCL), follicultis, scabies, or generalized tinea infection.

Laboratory Examinations

Dermatopathology Epidermal spongiotic vesicles, a few dermal eosinophils.

Course and Prognosis

Once the primary infection or inflammatory condition has been cleared, the id reaction will self-resolve. Unfortunately, recurrences are common, especially if the primary source is not fully eradicated.

Management

Eradication of the primary infection or inflammatory condition is the best way to treat an id reaction. Symptomatic relief can be obtained with a short course of topical steroids, wet compresses, and systemic antihistamines (diphenhydramine, loratadine).

Oral Candidiasis

Oral candidiasis is characterized by the presence of painful, white, milk-like removable plaques on the oral mucosa.

Synonyms Moniliasis, thrush, mycotic stomatitis, Candida leukoplakia.

Epidemiology

Age Newborns, 8 or 9 days old.

Gender M = F.

Incidence Common in newborns and infants. Uncommon in adults: may be a marker for immunodeficiency.

Etiology Candida albicans, most commonly.

Pathophysiology

Candida is present in the mouth and intestinal tract in up to 50% of the normal population and > 20% of the genital tract in normal women. Candida is transmitted to the infant at the time of delivery during passage through the vaginal canal.

History

In newborns and infants, the white curd-like plaques appear at day of life 8 to 9 and are usually asymptomatic. Mechanical removal with a dry gauze pad leaves an erythematous or bleeding mucosal surface.

Physical Examination

Mucous Membrane Findings

Type Plaques.

Size Few millimeter to several centimeter.

Color White to creamy.

Palpation Plaques are friable and removable with dry gauze.

Distribution Tongue, buccal mucosa, hard/soft palate, and pharynx (Fig. 21-14).

Differential Diagnosis

The differential diagnosis for oral candidiasis includes oral hairy leukoplakia, condyloma acuminatum, geographic tongue, hairy tongue, lichen planus, and a bite irritation.

Laboratory Examinations

KOH Scraping shows Candida pseudohyphae as well as budding yeast forms.

Cultures Buccal or tongue plaques scraped and cultured will grow species of Candida.

Course and Prognosis

Oral candidiasis is benign and usually asymptomatic. It responds nicely to topical treatment, but may intermittently recur. In adults, chronic recurrent oral candidiasis may be a sign of immunosuppression.

Management

For mild cases, nystatin suspension can be used until clinical clearing is noted. Refractory or recurrent cases may require topical clotrimazole, systemic itraconazole, or fluconazole.

Cutaneous Candidiasis

Cutaneous candidiasis is a superficial infection occurring on moist cutaneous sites and mucosal surfaces; many patients have predisposing factors such as occluded moist skin sites, diabetes, antibiotic therapy, or alteration in systemic immunity.

Classification

1. 1. Intertrigo:

   • a. Body folds (neck, groin, intergluteal, axilla, inframammary).
   • b. Webspaces: fingers, toes may be associated with candidal paronychia.

   2. Genital: Balanoposthitis, balanitis, vulvitis.

   3. Occluded skin: diaper (Fig. 21-15), surgical cast, immobilized patient, etc.

   4. Chronic Mucocutaneous Candidiasis: Rare immunologic (e.g., T-cell defects) or endocrinologic disorders (e.g., hypoparathyroidism, hypoadrenalism, hypothyroidism, diabetes) that lead to chronic mucosal, cutaneous, or nail C. albicans infections.

Synonyms Moniliasis, candidosis, erosio interdigitalis blastomycetica.

Epidemiology

Age Any age. Infants (diaper area, mouth).

Gender M = F.

Incidence Common.

Etiology C. albicans; normal in oropharynx and GI tract, not on the skin.

Pathophysiology

Abnormal C. albicans overgrowth on the skin can occur in the setting of diabetes, obesity, hyperhidrosis, heat, maceration, immunologic defects (depressed T-cell function), polyendocrinopathies, systemic antibacterial agents, systemic and topical corticosteroids, chronic debilitation (carcinoma, leukemia), chemotherapy.

History

Areas of candida overgrowth tend to be moist and warm with frequent episodes of wetness (from sweating, water exposure). The lesions begin as pink, slightly pruritic areas that progress to red, macerated, sore, painful, irritated skin.

Physical Examination

Skin Findings

Type Papules, pustules, plaques, erosions.

Color Beefy red skin, white exudates.

Distribution Body folds, webspaces between fingers (Fig. 21-16) and toes.

Differential Diagnosis

The differential diagnosis for candidiasis includes psoriasis, erythrasma, atopic dermatitis, an irritant dermatitis, seborrheic dermatitis, or other fungal infections.

Laboratory Examinations

KOH Gram stain or 10% KOH of skin scraping shows pseudohyphae and yeast forms.

Fungal Culture Skin scrapings inoculated on Sabouraud’s agar will grow Candida.

Course and Prognosis

Unless a precipitating causative agent can be removed (a diaper, a surgical cast), most cases of candidiasis [intertrigo, chronic mucocutaneous candidiasis (CMC)] are chronic and recurrent.

Management

Preventatively, keeping intertriginous areas dry and open to air as much as possible will help. Daily application of drying topical powders or antifungal creams can help. Useful topical antifungal preparations include polyenes (nystatin, amphotericin B), substituted pyridine (ciclopirox), imidazoles (clotrimazole, econazole, miconazole, ketoconazole, oxiconizole or sulconazole). They should be applied bid to the affected areas 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. Topical antifungals + steroid combinations (1% clotrimazole +  betamethasone dipropionate, nystatin +  triamcinolone) are effective for Candida treatment, but have a strong steroid component and thus should be used sparingly for a limited time.

If extensive or resistant to topical treatment, oral antifungal treatment (fluconazole, ketoconazole, itraconazole) for 2 to 3 weeks may be needed. Side effects include nausea, vomiting, and LFT abnormalities.

For fluconazole-resistant candidiasis, amphotericin B may be necessary. Side effects include renal tubular acidosis, hypokalemia, hypomagnesemia, fever, chills, delirium, phlebitis, nausea, vomiting, hypotension, hypertension, renal failure, and bone marrow depression

Pityriasis versicolor is a common asymptomatic superficial fungal infection of the trunk, characterized by white or brown scaling macule and associated with the overgrowth of Pityrosporum ovale.

Synonym Tinea versicolor, dermatomycosis furfuracea, tinea flava.

Epidemiology

Age Any age. Most common in young adults.

Gender M = F.

Incidence Common.

Prevalence Temperate zones: 2% of population during summer; tropical zones: 40% of the population. In athletes, rash may persist year round.

Etiology P. ovale (also known as P. orbiculare and Malassezia furfur).

Pathophysiology

P. ovale is a lipophilic yeast that is a normal inhabitant of skin. Pityrosporum infections are not contagious, but an overgrowth of resident cutaneous form under certain favorable conditions. Seborrheic dermatitis and Pityrosporum folliculitis are thought to be other cutaneous manifestations of P. ovale overgrowth, and all three conditions can be seen concomitantly. High humidity, sweat, sebum, occlusion, poor nutrition, pregnancy, topical steroids, and application of oils (e.g., cocoa butter, bath oil) on the skin can lead to P. ovale overgrowth. The pigmentary changes are caused by dicarboxylic acids formed by enzymatic oxidation of fatty acids in skin surface lipids inhibiting tyrosinase in epidermal melanocytes.

History

The rash of pityriasis versicolor begins insidiously and spreads over months to years. It is typically asymptomatic or mildly pruritic. There are no systemic symptoms and the resultant blotchy pigmentation is what usually brings the patient into the office.

Physical Examination

Skin Findings

Type Macules, patches, scale.

Color Light skin: hyperpigmentation. Dark skin: hypopigmentation (Fig. 21-17).

Size 5 mm to several centimeters.

Shape Round or oval.

Distribution Sebaceous areas: trunk, arms, neck, axillae, groin, thighs, genitalia. Rarely on the face.

Differential Diagnosis

The differential diagnosis for pityriasis versicolor includes vitiligo, pityriasis rosea, pityriasis alba, postinflammatory hypopigmentation, tinea corporis, seborrheic dermatitis, guttate psoriasis, secondary syphilis, and nummular eczema.

Laboratory Examinations

Dermatopathology Budding yeast and hyphae forms in the most superficial layers of the stratum corneum. PAS stain will stain P. ovale very bright pink.

KOH 10% KOH of skin scrapings will show filamentous hyphae and spores (a so-called spaghetti-and-meatballs appearance; Fig. 21-18).

Wood’s Lamp Faint yellow-green fluorescence of scales may be detected.

Course and Prognosis

Pityriasis versicolor has a benign but chronic/ relapsing course. Skin or systemic symptoms are rare, but the pigmentary changes can be very noticeable, persist for months and is cosmetically unappealing to the patient.

Management

Pityriasis versicolor responds well to topical agents such as antimycotic (selenium sulfide 2.5%, ketoconazole 2%) shampoos which can be lathered on the body and left on for 15 minutes followed by a bath/shower 2×/wk for 2 to 4 weeks. Imidazole creams (clotrimazole, econazole, miconazole, oxiconazole, sulconazole) can be used to small, localized areas for 1 to 2 week.

For chronic, recurrent, or severe involvement, oral antifungals (ketoconazole, fluconazole, itraconazole) may be warranted. Side effects include nausea, vomiting, and LFT abnormalities.

All patients should be counseled regarding likely recurrences and predisposing factors (sweat, topical oils). In athletes, prophylactic weekly shampoo with selenium sulfide may be helpful. Additionally, even when P. ovale is cleared, the pigmentary changes of pityriasis versicolor can persist for months and do not represent therapeutic failure.

Sporotrichosis

Sporotrichosis is a deep fungal infection that follows accidental inoculation of the skin and is characterized by ulceration and/or nodule formation at the inoculation site, followed by subcutaneous nodule formation along the course of lymphatic drainage.

Classification

1. 1. Lymphocutaneous sporotrichosis: most common, seen in 25% of cases. Proximal to local cutaneous lesion, intervening lymphatics become indurated, nodular, thickened, with occasional ulcer formation.

   2. Fixed cutaneous sporotrichosis: 20% of cases, subcutaneous papule at inoculation. The patient is previously sensitized to sporotrichosis; no lymphatic spread.

   3. Chancriform form of sporotrichosis: rare, < 8% of cases with associated lymphadenopathy proximally.

   4. Disseminated sporotrichosis: < 1% of cases. Hematogenous spread to lungs, liver, spleen, pancreas, thyroid, myocardium, or CNS in immunocompromised host.

Synonyms Sporotrichum infection, rose gardener’s disease

Epidemiology

Age Any age. More common in adults.

Gender M > F.

Etiology Sporothrix schenckii, a dimorphic fungus commonly found in soil, rose and barberry thorns, wood splinters, sphagnum moss, straw, and marsh hay.

Geography Ubiquitous, worldwide. More common in temperate and tropical zones.

Pathophysiology

Commonly, sporotrichosis begins with a subcutaneous inoculation by a contaminated thorn, rock, glass, barb, splinter, cat scratch, or other sharp item. Following subcutaneous inoculation, S. schenckii grows locally and slowly spreads along the draining lymphatics. Secondary skin lesions develop along the lymphatic chain. Rarely inhalation, aspiration, or ingestion causes systemic infection.

History

Three days to 12 weeks after inoculation of the fungal organism, an asymptomatic or slightly painful nodule will appear at the inoculation site followed by erythematous nodule formation extended proximally along the path of lymphatic drainage.

Physical Examination

Skin Findings

Type Papules, nodules, ulcers (Fig. 21-19).

Color Pink, red.

Size 1 to 2 cm.

Arrangement Linear described as “sporotrichoid” spread (Fig. 21-20).

Distribution Upper extremity > face, trunk.

Differential Diagnosis

The differential diagnosis for sporotrichosis includes tuberculosis, atypical mycobacterial infection (particularly M. marinum), anthrax, tularemia, cat-scratch disease, primary syphilis, leishmaniasis, herpes simplex virus infection, staphylococcal lymphangitis, histoplasmosis, coccidioidomycosis, blastomycosis, and cryptococcosis.

Laboratory Examinations

Dermatopathology Granulomatous, Langerhans’-type giant cells, pyogenic microabscesses. Organisms rare, difficult to visualize. Yeast, if visible, appear as 1 to 3 μm by 3 to 10 μm cigar-shaped forms and will stain with PAS or silver stains. Fluorescent antibody or PCR can help detect the S. schenckii organism in vitro.

Culture Organism isolated few days after culture of aspirate of skin lesion.

Course and Prognosis

Sporotrichosis shows little tendency to resolve spontaneously. The deep fungal infections respond well to systemic therapy, but relapses are possible.

Management

Topical therapy for sporotrichosis is not effective. Oral antifungal agents (fluconazole, ketoconazole, itraconazole) work, but should be taken 4 to 6 weeks beyond resolution of the lesions. Side effects include nausea, vomiting, and LFT abnormalities. There has also been reported success with saturated solution of potassium iodide (oral SSKI), which enhances the host’s immune system. It should also given for 4 to 6 weeks beyond clinical resolution of cutaneous lesions. Side effects include iododerma, GI upset, and thyroids suppression.

For severe or systemic disease, especially in immunocompromised hosts, IV amphotericin B may be needed for 2 to 3 weeks. Side effects include renal tubular acidosis, hypokalemia, hypomagnesemia, fever, chills, delirium, phlebitis, nausea, vomiting, hypotension, hypertension, renal failure, and bone marrow depression.

Cryptococcosis

Cryptococcosis is a deep fungal infection acquired by the inhalation of Cryptococcus neoformans, causing a primary pulmonary infection that can lead to hematogenous dissemination, and spread of infectionges, kidneys, and/or skin.

Synonyms Torulosis, European blastomycosis.

Epidemiology

Age All ages. Mort commonly: 30 to 60 years.

Gender M > F, 3:1.

Incidence Rare.

Etiology C. neoformans, a yeast.

Geography Worldwide, ubiquitous. Europe, South America > United States.

Pathophysiology

C. neoformans, is an opportunistic pathogen that is accidentally inhaled from infected dust of avian feces (pigeons, parakeets, and canaries). Serotypes A, B, C, and D can cause disease in humans. After inhalation, Cryptococcus causes a pulmonary infection. Immunodeficient hosts may have a subsequent hematogenous dissemination of the organism to meninges, kidneys, and skin. Transplacental transmission is possible and Cryptococcus may also inhabit the female genital tract leading to inoculation of the infant as it passes through the birth canal.

History

Often, cryptococcal disease remains localized to the lungs with absent or minimal symptoms. In immunosuppressed individuals, hematogenous dissemination leads to CNS infection with headache (80%), mental confusion, and visual disturbances for months. Thirty percent of disseminated cases are associated with malignancy (usually Hodgkin’s disease).

Physical Examination

Skin Findings

Seen in 15% of systemic cases.

Type Papules, pustules, plaques, nodules, ulcers (Fig. 21-21).

Color Pink to red, blue.

Distribution Any site.

Site of Predilection Face (especially around nose and mouth), scalp.

General Findings

CNS Headache, behavioral disturbance, seizures.

Pulmonary Cough, pneumonia, pleural effusions.

Other Hepatomegaly, splenomegaly, lymphadenopathy.

Differential Diagnosis

The differential diagnosis for Cryptococcus includes blastomycosis, histoplasmosis, molluscum contagiosum, HSV, and other bacterial or systemic fungal infections.

Laboratory Examinations

Dermatopathology Thick-walled organisms 5 by 20 μm in the skin biopsy. Methylene blue, alcian blue, or mucicarmine will brightly stain the polysaccharide capsule.

Indirect Immunofluorescence Anitbodies available to detect cryptococcal organism in body fluids of tissue specimens.

Culture Cryptococcus from body fluids or tissues can be grown on Sabouraud’s agar.

CXR Pneumonia, infiltrates, nodules, abscesses, or pleural effusions may be present.

Course and Prognosis

Untreated, secondary cutaneous cryptococcosis is fatal in 80% of cases. Appropriate antifungal treatment leads to an 80% cure rate. And a dramatic decrease in the incidence of Cryptococcal infection in the HIV population has been seen with the use of fluconazole and highly active antiretroviral therapy.

Management

Prevention of Cryptococcus in high-risk patients (on chemotherapy, high-dose steroids, neutropenia) and antifungal prophylaxis (fluconazole, voriconazole, moconazole, ketoconazole, itraconazole) is recommended. The treatment of choice for Cryptococcus used to be amphotericin B for 2 months. Side effects include renal tubular acidosis, hypokalemia, hypomagnesemia, fever, chills, delirium, phlebitis, nausea, vomiting, hypotension, hypertension, renal failure, and bone marrow depression. It is now recommended to use voriconazole or one of the echinocandins (caspofungin).

Histoplasmosis

Histoplasmosis is a common, highly infectious systemic fungal infection caused by Histoplasma capsulatum and characterized by an asymptomatic pulmonary infection that occasionally disseminates.

Synonyms Darling’s disease, cave disease, Ohio Valley disease, reticuloendotheliosis.

Epidemiology

Age All ages.

Gender M = F.

Incidence Common.

Etiology H. capsulatum exists in the soil in warm moist climates

Geography Endemic in SE and central US.

Pathophysiology

Birds, fowl, or bats are reservoirs for histoplasmosis. The feces of these animals contain the organism, thus their habitats (caves, chicken coops, construction sites) are high-risk areas for contracting the disease.

History

Humans acquire H. capsulatum by inhaling the aerosolized spores from contaminated soil. Histoplasmosis exists as self-limited pulmonary infection in 75% of cases, which are asymptomatic. Flu-like pulmonary symptoms (fever, malaise, cough, and chest pain) develop in 25% of cases and < 1% of patients progress to disseminated histoplasmosis (fever, hepatosplenomegaly, anemia, and weight loss), especially in the setting of immunosuppression.

Physical Examination

Skin Findings

Type Papules, plaques, pustules (Fig. 21-22), nodules, abscesses, or ulcers.

Color Pink, red, purple.

Distribution Any site, mucosa surface.

General Findings

Fever

Pulmonary Cough, dyspnea, chest pain

Other Hepatosplenomegaly, and weight loss.

Differential Diagnosis

The differential diagnosis of histoplasmosis includes miliary tuberculosis, coccidioidomycosis, paracoccidioidomycosis, cryptococcosis, leishmaniasis, and lymphoma.

Laboratory Examinations

Dermatopathology Skin biopsy may show small intracellular yeast-like forms with a rim of clearing within histiocytes and giant cells. PAS or Gomori methenamine silver stains will make yeast more visible.

Touch Preparation Lesional skin touched to glass slide and stained with Giemsa stain will show H. capsulatum.

Culture Tissue or blood inoculated on Sabouraud’s agar may grow H. capsulatum.

Histoplasmosis Skin Test In infants, a positive reaction 2 to 3 weeks after infection indicates active, current infection; but in endemic populations, up to 90% of children and adults react positively, signifying past or present infection.

Serology Immunodiffusion, agar gel precipitin, yeast phase complement fixation, collodion, or latex particle agglutination can be performed on blood samples. Titers greater than 1:32 are highly suggestive of active histoplasmosis disease.

CXR Interstitial infiltrates and/or hilar adenopathy.

Course and Prognosis

In 99% of cases, asymptomatic pulmonary histoplasmosis is a benign and self-limited disease, and treatment is not necessary. In symptomatic or disseminated form, untreated histoplasmosis has a high mortality rate.

Management

If bird or bat droppings are to be cleared in an endemic area for H. capsulatum, protective equipment (respirators, goggles, and so forth) should be worn. Most cases of histoplasmosis do not require therapy. In severe systemic cases or disseminated disease, systemic antifungals (amphotericin B, itraconazole, voriconazole) may be necessary. Side effects include renal tubular acidosis, hypokalemia, hypomagnesemia, fever, chills, delirium, phlebitis, nausea, vomiting, hypotension, hypertension, renal failure, and bone marrow depression.