Superficial Fungal Infections. Caused by fungi that are capable of colonizing (cutaneous microbiome) and superficially invading skin and mucosal sites:
Deeper, Chronic Cutaneous Fungal Infections. Occur after percutaneous inoculation:
Phaeohyphomycosis (eumycetoma, chromoblastomycosis)
Systemic Fungal Infections with Cutaneous Dissemination. Occur most often with host defense defects. Primary lung infection disseminates hematogenously to multiple organ systems, including the skin: Cryptococcosis, histoplasmosis, North American blastomycosis, coccidioidomycosis, and penicillinosis.
Superficial Fungal Infections ICD-9: 111 ICD-10: B36
Superficial fungal infections are the most common of all mucocutaneous infections, often caused by overgrowth of mucocutaneous microbiome.
Candida Species. Require a warm humid microenvironment.
Malassezia Species. Require a humid microenvironment and lipids for growth.
Dermatophytes. Infect keratinized epithelium, hair follicles, and nail apparatus Trichosporon species Hortaea (Exophiala or Phaeoannellomyces) werneckii: Tinea nigra
Candidiasis ICD-9: 112 ICD-10: B37.0
Etiology. Most commonly caused by the yeast Candida albicans. Less often by other Candida species.
Mucosal Candidiasis. Otherwise healthy individuals: oropharynx and genitalia. Host defense defects: in the esophagus and tracheobronchial tree.
Cutaneous Candidiasis. Intertriginous and occluded skin.
Disseminated Candidemia. Host defense defects, especially neutropenia. Usually after invasion of the gastrointestinal (GI) tract.
Epidemiology and Etiology
Etiology. C. albicans, C. tropicalis, C. parapsilosis, C. guilliermondii, C. krusei, C. pseudotropicalis, C. lusitaniae, C. glabrata.
Ecology. Candida spp. frequently colonize the GI tract and can be transmitted via the birth canal. Approximately 20% of healthy individals are colonized. Antibiotic therapy increases the incidence of colonization.
Ten percent of women are colonized vaginally; antibiotic therapy, pregnancy, oral contraception, and intrauterine devices increase incidence. C. albicans may transiently be present on the skin and infection is usually endogenous. Candida balanitis may be transmitted from sexual partner. The young and old are more likely to be colonized.
Host Factors. Host defense defects, diabetes mellitus, obesity; hyperhidrosis, warm climate, maceration; polyendocrinopathies; glucocorticoids; chronic debilitation.
Direct Microscopy. KOH preparation visualizes pseudohyphae and yeast forms (Fig. 26-1).
Figure 26-1. Candida albicans: KOH preparation Budding yeast forms and sausage-like pseudohyphal forms.
Culture. Identifies species of Candida; however, the presence in culture of C. albicans does not make the diagnosis of candidiasis. Sensitivities to antifungal agents can be performed on isolate in cases of recurrent infection. Rule out bacterial secondary infection.
Cutaneous candidiasis occurs in moist, occluded sites.
Many patients have predisposing factors.
See Section 32 for candidiasis of the nail.
Candidai Intertrigo. Pruritus, tenderness, pain. Initial pustules on erythematous base become eroded and confluent. Subsequently, fairly sharply demarcated, polycyclic, erythematous, eroded patches with small pustular lesions at the periphery (satellite pustulosis). Distribution: Inframammary or submammary Fig. 26-2, axillae, groins (Fig. 26-3, perineal, and intergluteal cleft.
Figure 26-2. Cutaneous candidiasis: intertrigo Small peripheral “satellite” papules and pustules that have become confluent centrally, creating a large eroded area in the submammary region.
Figure 26-3. Cutaneous candidiasis: intertrigo Erythematous papules with a few pustules, becoming confluent in the inguinal area and medial thigh. The lesions occurred during a holiday trip to the Caribbean.
Interdigital. Most common in obese elderly. Initial pustule becomes eroded, with formation of superficial erosion or fissure (Fig. 26-4). May be associated with Candida paronychia. Distribution: webspace usually between third and fourth fingers (Fig. 26-4); feet: maceration in webspace.
Figure 26-4. Cutaneous candidiasis: interdigital intertrigo An 80-year-old male with painful site in the webspace of the hand. Erosion with erythema is seen in the webspace between two fingers.
Diaper Dermatitis. Irritability, discomfort with urination, defecation, changing diapers. Erythema, edema with papular, and pustular lesions; erosions, collarette-like scaling at the margins of lesions. Distribution: genital and perianal skin, inner aspects of thighs and buttocks (Fig. 26-5).
Figure 26-5. Candidiasis: diaper dermatitis Confluent erosions, marginal scaling, and “satellite pustules” in the area covered by a diaper in an infant. Atopic dermatitis or psoriasis also occurs in this distribution and may be concurrent.
Occluded Skin. Under occlusive dressing, under cast, on back in hospitalized patient.
Follicular Candidiasis. Small, discrete pustules in ostia of hair follicles. Usually in occluded skin.
Intertrigo/Occluded Skin. Intertriginous psoriasis, erythrasma, dermatophytosis, pityriasis versicolor, streptococcal intertrigo,
Diaper Dermatitis. Atopic dermatitis, psoriasis, irritant dermatitis, seborrheic dermatitis.
Folliculitis. Bacterial (Staphylococcus aureus, Pseudomonas aeruginosa) folliculitis, Pityrosporum folliculitis, acne.
Clinical findings confirmed by direct microscopy or culture.
Prevention. Keep intertriginous areas dry, wash with benzoyl peroxide bar and use imidazole powder.
Topical Antifungals. Nystatin, azole, or imidazole cream.
Oral Antifungals. Nystatin (suspension, tablet, pastille.) Eradicates bowel colonization. May be effective in recurrent candidiasis of diaper area, genitals, or intertrigo.
Systemic Antifungal Agents. Fluconazole tablets (50, 100, 150, 200 mg), oral suspension (50 mg/ml); parenteral for IV infusion. Itroconazole capsules (100 mg), oral solution 10 mg/ml), ketoconazole tablets (200 mg), amphotericin B IV for severe disease.
ICD-9: 112.0 ICO-10: B38.0
Occurs with minor variations in host factors. Antibiotic therapy; glucocorticoid therapy (topical or systemic); age (very young, very old); host defense defects.
Incidence. Often mucosal candidiasis occurs in otherwise healthy individuals. In advanced HIV disease: oropharyngeal candidiasis is common, relapses after treatment, and may be associated with esophageal and tracheobronchial candidiasis.
Classification of Mucosal Candidiasis
• Pseudomembranous candidiasis or thrush
• Erythematous or atrophic candidiasis
• Candidal leukoplakia or hyperplastic candidiasis
• Angular cheilitis
Esophageal and Tracheobronchial Candidiasis. Occurs in states of severe host defense defects. AIDS-defining conditions.
Oropharyngeal Candidiasis. Often asymptomatic. Burning or pain on eating spices/acidic foods, diminished taste sensation. Cosmetic concern about white curds on tongue. Odynophagia. In HIV disease, may be the initial presentation.
• Pseudomembranous Candidiasis. See Figs. 26-6 through 26-8. White cottage cheese-like flecks (colonies of Candida) on any mucosal surface; vary in size from 1–2 mm to extensive and widespread. Removal with a dry gauze pad leaves an erythematous mucosal surface. Distribution: Dorsum of tongue, buccal mucosa, hard/soft palate, pharynx extending down into esophagus and tracheobronchial tree.
Figure 26-6. Oral candidiasis: thrush White curd-like material on the mucosal surface of the lower lip of a child; the material can be abraded with gauze (pseudomembranous), revealing underlying erythema.
Figure 26-7. Oral candidiasis: thrush Extensive cottage cheese-like plaques, colonies of Candida that can be removed by rubbing with gauze (pseudomembranous), on the palate and uvula of an individual with advanced HIV/AIDS. Patches of erythema between the white plaques represent erythematous (atrophic) candidiasis. Involvement may extend into the esophagus and become associated with dysphagia.
Figure 26-8. Oral candidiasis: atrophic and pseudomembranous A 48-year-old male with HIV disease. The surface of the tongue is shiny and red; posterior tongue has a white coating (thrush).
• Erythematous or Atrophic Candidiasis. Dorsum of tongue is smooth, red, atrophic (Fig. 26-8). Areas of thrush may also be present.
• Candidal Leukoplakia. White plaques that cannot be wiped off but regress with anticandidal therapy. Distribution: buccal mucosa, tongue, hard palate.
• Angular Cheilitis. Intertrigo at the angles of lips (Fig. 26-9). Erythema; slight erosion. White colonies of Candida in some cases. Usually associated with oropharyngeal colonization with Candida.
Figure 26-9. Angular cheilitis A 55-year-old male. The angle of the lips is moist and red. KOH preparation revealed candida pseudohyphae. Oral candidiasis was also present.
Esophageal and Tracheobronchial Candidiasis. Occurs in HIV disease when CD4+ cell count is low and is an AIDS-defining condition. Odynophagia, resulting in difficulty eating and malnutrition. Pseudomembranous lesions are seen on endoscopy.
Invasive Disseminated Candidiasis. In individuals with severe prolonged neutropenia. Portal of entry of Candida: GI tract, invading submucosa, and blood vessels; intravascular catheter. Candidemia: hematogenous dissemination to skin and viscera. Disseminated red papules (Fig. 26-14)
Pseudomembranous Candidiasis. Oral hairy leukoplakia, condyloma acuminatum, geographic tongue, hairy tongue, lichen planus, bite irritation.
Atrophic Candidiasis. Lichen planus, poor nutrition, vitamin deficiency
Clinical suspicion confirmed by KOH preparation of scraping from mucosal surface. Endoscopy to document esophageal and/or tracheobronchial candidiasis.
Most cases respond to correction of the precipitating cause such as use of inhaled glucocorticoids. Topical agents effective in most cases. Clinical resistance to antifungal agents may be related to patient noncompliance, severe immunocompromised, drug–drug interaction (rifampin–fluconazole).
Topical Therapy. Nystatin or clotrimazole.
Systemic Therapy. Oral fluconazole, itraconazole, ketoconazole. Amphotericin B for severe resistant disease.
ICD-9: 112.1/112.2 ICD-10: B37.3/B37.4
Occurs on the nonkeratinized genital mucosa
Preputial sac of the penis
Usually represents overgrowth of Candida in mucocutaneous microbiome.
More than 20% of women have vaginal colonization by Candida. C. albicans accounts for 80–90% of genital isolates.
Incidence. Most vaginal candidiasis occurs in the healthy population. Seventy-five percent of women experience at least one episode; 40–45% experience two or more episodes. Often associated with vulvar candidiasis, i.e., vulvovaginal candidiasis.
Risk Factors. Diabetes mellitus, HIV disease. Females: Often none; pregnancy. Males; uncircumcised.
Vulvitis/Vulvovaginitis. Onset often abrupt, usually the week before menstruation. Symptoms may recur before each menstruation. Pruritus, vaginal discharge, vaginal soreness, vulvar burning, dyspareunia, and external dysuria.
Vulvitis. Erosions, edema, erythema (Fig. 26-10), swelling, removable curd-like material. Pustule on lateral vulva and adjacent skin
Figure 26-10. Candidiasis: vulvitis and intertrigo Psoriasiform, erythematous lesions becoming confluent on the vulva with erosions and satellite pustules on the thighs.
Vulvovaginitis. Vaginal erythema and edema; white plaques that can be wiped off vaginal and/or cervical mucosa. May be associated with candidal intertrigo of inguinal folds and perineum. Subcorneal pustules at periphery with fringed, irregular margins. In chronic cases, vaginal mucosa glazed and atrophic.
Balanoposthitis, balanitis glans, and preputial sac: papules, pustules, erosions (Fig. 26-11). Maculopapular lesions with diffuse erythema. Edema, ulcerations, and fissuring of prepuce, usually in diabetic men; white plaques under foreskin.
Figure 26-11. Candidiasis: balanoposthitis A 52-year-old uncircumcised male. Erythema and a curd-like matter is seen on the glans penis and foreskin.
Vulvovaginal Candidiasis. Trichomoniasis (caused by T. vaginalis), bacterial vaginosis (caused by replacement of normal vaginal flora by an overgrowth of anaerobic microorganisms and Gardnerella vaginalis), lichen planus, lichen sclerosus et atrophicus.
Balanoposthitis. Psoriasis, eczema, lichen planus
Clinical suspicion confirmed by KOH preparation of scraping from mucosal surface.
Azole Creams or Suppository. Treat sexual partners and consider systemic therapy (as for mucocutaneous candidiasis p. 596) if recurrent.
Chronic Mucocutaneous Candidiasis
ICD-9: 112.3 ICD-10: B37.7
Characterized by persistent or recurrent Candida infections of the oropharynx, skin, and nail apparatus.
Inheritance. Usually autosomal recessive or sporadic.
Host Defense Defect. Various specific and global defects in cell-mediated immunity.
Onset. Usually in infancy or early childhood.
Oropharyngeal Candidiasis. Refractory to conventional therapy. Relapsing after successful therapy. Chronic infection results in hypertrophic (leukoplakic) candidiasis.
Cutaneous candidiasis manifests as: Intertrigo. Widespread infection (Figs. 26-12 and 26-13) of the face, trunk, and/or extremities, Lesions become hypertrophic in chronic untreated cases. Infection of the nail apparatus is universal: Chronic paronychia; nail plate infection and dystrophy; eventually total nail dystrophy.
Figure 26-12. Mucocutaneous candidiasis Persistent candidiasis in an immunocompromised infant manifesting as erosions covered by scales and crusts, oropharyngeal candidiasis, and widespread infection of the trunk.
Figure 26-13. Mucocutaneous candidiasis A 3-year-old child with hypothyroidism had thrush, intertriginous candidiasis, warty hyperkeratoses, and crusts on the scalp and face; and also, candidal onychomycosis.
Many patients also have dermatophytosis and cutaneous warts.
Six Types of Chronic Mucocutaneous Candidiasis
• Chronic oral candidiasis
• Chronic candidiasis with endocrinopathy
• Chronic candidiasis without endocrinopathy
• Chronic localized mucocutaneous candidiasis
• Chronic diffuse candidiasis
• Chronic candidiasis with thymoma.
Disseminated Candidiasis ICD-9: 112.5 ICD-10: B37
Etiology. C. albicans, C. tropicalis, and other non-albicans species.
Incidence. Fifth most common cause of nosocomial bloodstream infections in the United States.
Risk Factors. Neutropenia. Venous access catheters. Hospitalization.
Pathogenesis. Candida enters the blood stream having colonized venous access catheters or penetrated the intestinal mucosa. Candidemia seeds the skin and internal organs, i.e., hepatosplenic candidiasis.
Cutaneous Lesions. Small disseminated erythematous cutaneous papules (Fig. 26-14). Lesions may occur acutely or chronically.
Figure 26-14. Invasive candidiasis with candidemia Multiple, erythematous papules on the hand of a febrile patient with granulocytopenia associated with treatment of acute myelogenous leukemia. The usual source of the infection is the gastrointestinal tract. C. tropicalis was isolated on blood culture; candidal forms were seen on lesional skin biopsy.
Systemic Dissemination. Eye with retinal changes. Liver, spleen, CNS
Malassezia folliculitis, which occurs on the trunk of healthy individuals.
Lesional biopsy specimen: Candida yeast forms are visualized in the dermis; Candida species isolated on culture.
Candidemia has high associated morbidity and mortality.
Fluconazole in nonneutropenic patients; triazoles echinocandins, caspofungin, micafungin, anidulafungin, voriconazole and posaconazole, as well as lipid formulations of amphotericin B.
Tinea Versicolor ICD-9: 111.0 ICD-10: B36.0
Etiology. Associated with the superficial overgrowth of the mycelial form of Malassezia furfur. Lipophilic yeast that normally resides in the keratin of skin (Fig. 26-15) and hair follicles of individuals at puberty and beyond. An opportunistic organism, causing tinea or pityriasis versicolor (TV) and Malassezia folliculitis; it is implicated in the pathogenesis of seborrheic dermatitis. Malassezia infections are not contagious; overgrowth of resident cutaneous flora (cutaneous microbiome) occurs under certain favorable conditions.
Clinical Findings. Chronic. Well-demarcated scaling patches. Variable pigmentation: hypo- and hyperpigmented; pink. Most commonly on the trunk.
Demography. Young adults. Less common when sebum production is reduced or absent; tapers off during fifth and sixth decades.
Predisposing Factors. Sweating. Warm season or climates; tropical climate. Hyperhidrosis; aerobic exercise. Oily skin. Temperate zones: more common in summertime; 2% prevalence in temperate climates; 20% in tropics. Application of lipids such as cocoa butter predisposes young children.
Pathogenesis. Malassezia changes from blastospore form to mycelial form under the influence of predisposing factors. Dicarboxylic acid formed by enzymatic oxidation of fatty acids in skin surface lipids inhibits tyrosinase in epidermal melanocytes and lead to hypomelanosis; the enzyme is present in M. furfur.
Figure 26-15. Malassezia furfur: KOH preparation Round yeast and elongated pseudohyphal forms, so-called “spaghetti and meatballs.”
Usually asymptomatic. Cosmetic concerns about dyspigmentation. Lesions present for months or years.
Macules, sharply marginated (Figs. 26-16 to 26-19) round or oval in shape, varying in size. Fine scaling is best appreciated by gently abrading lesions. Treated or resolved lesions lack scale. Some patients have findings of Malassezia folliculitis and seborrheic dermatitis.
Figure 26-16. Pityriasis versicolor A 43-year-old white female with orange-tan lesions of the lateral neck. Sharply marginated scaling macules.
Figure 26-17. Pityriasis versicolor: neck A 23-year-old obese black female with discoloration of the neck for 1 year. Sharply marginated brown scaling macules on the left side of the neck. The velvety texture and hyperpigmentation of the skin of the neck is acanthosis nigricans associated with obesity.
Figure 26-18. Pityriasis versicolor: chest and arm A 36-year-old male with pigmented patches on chest and arms for several years. Multiple pink, well-demarcated scaling macules becoming confluent on the neck, chest, flank, and arm.
Figure 26-19. Pityriasis versicolor: back Multiple, small-to-medium-sized, well-demarcated hypopigmented macules on the back of a tanned individual with white skin.
Color. In nontanned skin, lesions are light brown (Fig. 26-18) or pink. On tanned skin, hypopigmented (Fig. 26-19). In brown- or black-skinned persons, dark brown macules (Figs. 26-17 and 26-20). Brown of varying intensities and hues (Fig. 26-18). In time, individual lesions may enlarge and merge, forming extensive geographic areas.
Figure 26-20. Pityriasis versicolor: face A 18-year-old black female hypopigmented scaling macule on chin. She had been applying cocoa butter to face since childhood.
Distribution. Upper trunk, upper arms, neck, abdomen, axillae, groins, thighs, genitalia. Facial, neck, or scalp lesions occur in persons applying creams or ointments or topical glucocorticoid preparations.
Hypopigmented Macules. Vitiligo, pityriasis alba, postinflammatory hypopigmentation.
Scaling Lesions. Tinea corporis, seborrheic dermatitis, cutaneous T cell lymphoma.
Direct Microscopic Examination of Scales Prepared with KOH. Filamentous hyphae and globose yeast forms, termed spaghetti and meatballs are seen (Fig. 26-15).
Wood’s Lamp. Blue-green fluorescence of scales; may be negative in individuals who have showered recently because the fluorescent chemical is water soluble. Vitiligo appears as depigmented, white, and has no scale.
Dermatopathology. Budding yeast and hyphal forms in the most superficial layers of the stratum corneum, seen best with periodic acid–Schiff (PAS) stain. Variable hyperkeratosis, psoriasiform hyperplasia, chronic inflammation with blood vessel dilatation.
Clinical findings confirmed by positive KOH preparation findings.
Infection persists for years if predisposing conditions persist. Dyspigmentation persists for months after infection has been eradicated.
Topitcal agents. Selenium sulfide (2.5%) lotion or shampoo. Ketoconazole shampoo. Azole creams (ketoconazole, econazole, micronazole, clotrimazole). Terbinafine 1% solution.
Systemic therapy Ketoconazole 400 mg stat, 1 hour before exercise. Fluconazole 400 mg stat. Itraconazole 400 mg stat (drugs not approved for use in TV in the United States).
Secondary prophylaxis. Topical agents weekly or systemic agents monthly.
Malassezia Folliculitis. See “Infectious Folliculitis” Section 31.
Seborrheic Dermatitis. See “Seborrheic Dermatitis” Section 2.
Etiology. Trichosporon species of yeasts. Soil inhabitants. Microbiome of skin, respiratory and GI tracts.
Treatment. Topical or systemic azoles.
Piedra: Asymptomatic superficial fungal biofilm/colonization on hair shaft. Incidence high in tropical regions with high temperature and humidity.
• White piedra. White to beige nodules on hair shaft; soft; easily removed. Pubic, axillary, beard, and eyebrow/eyelash hair.
• Black piedra. Darkly pigmented, firmly attached nodules (up to a few millimeters) on the hair shaft; weakens hair shaft with hair breakage. Scalp hair.
Disseminated Trichosporonosis. Emerging opportunistic infection. Associated with neutropenia. Dissemination occurs to skin (erythematous or purpuric tender papules), lungs, kidneys, and spleen. Similar to disseminated candidiasis.
Tinea Nigra ICD-10: B36.1
Superficial fungal colonization of the stratum corneum
Etiology. Hortaea werneckii, a dematiaceous or pigmented fungus.
Epidemiology. More common in tropical climates. Transmitted by direct inoculation onto the skin from contact with decaying vegetation, wood, or soil seems to be the mode of acquisition.
Clinical Manifestation. Brown to black macule(s) with well-defined borders (Fig. 26-21) that resemble silver nitrate stains. Distribution: Palm: tinea nigra palmaris. Sole: tinea nigra plantaris
Diagnosis. Direct microscopy, visualizing abundant branching septate hyphae.
Management. Topical azole or alcohol gel sanitizer.
Figure 26-21. Tinea nigra Uniformly tan macule on the plantar foot, present for several years. KOH preparation showed hyphae.
Dermatophytoses ICD-9: 110 ICD-10: B35.0-B36
Dermatophytes are a unique group of fungi capable of infecting nonviable keratinized cutaneous structures including stratum corneum, nails, and hair. Arthrospores can survive in human scales for 12 months. Dermatophytosis denotes an infection caused by dermatophytes.
Clinical Infection by Structure Involved. Epidermal dermatophytosis. Dermatophytosis of hair and hair follicles. Onychomycosis or tinea unguium: dermatophytosis of the nail apparatus.
Pathogenesis of dermatophytosis leading to different clinical manifestations is schematically depicted in Figs. 26-22 and 26-23.
The term tinea is best used for dermatophytoses and is modified according to the anatomic site of infection, e.g., tinea pedis.
“Tinea” versicolor is referred to as pityriasis versicolor except in the United States; it is not a dermatophytosis but rather an infection caused by the yeast Malassezia.
Tinea nigra is caused by a pigmented or dematiaceous fungus, not a dermatophyte.
Figure 26-22. Epidermal dermatophyte infections Dermatophytes (red dots and lines) within the stratum corneum disrupt the horny layer and thus lead to scaling; also elicit an inflammatory response (black dots symbolize inflammatory cells), which may then manifest as erythema, papulation, and vesiculation.
Figure 26-23. Hair follicle dermatophyte infections Hair shaft is involved (red dots) resulting in the destruction and breaking off of the hair. If the dermatophyte infection extends farther down into the hair follicle, it will elicit a deeper inflammatory response (black dots) and this manifest as deeper inflammatory nodules, follicular pustulation, and abscess formation.
TABLE 26-1 CLASSIFICATION OF TINEA PEDIS
Epidemiology and Etiology
Etiology. Three genera of dermatophytes (“skin plants”): Trichophyton, Microsporum, Epidermophyton. More than 40 species are currently recognized; approximately 10 spp. are common causes of human infection.
• Trichophyton rubrum is the most common cause of epidermal dermatophytosis and onychomycosis in industrialized nations. Currently, 70% of the U.S. population experience at least one episode of T. rubrum infection (usually tinea pedis). Soldiers wearing occlusive boots in tropical climates developed “jungle rot”—extensive tinea pedis with secondary bacterial infection. In U.S. adults, T. rubrum is the most common cause of dermatophytic folliculitis.
• Tinea capitis. Etiology in children varies geographically. Trichophyton tonsurans: Most common cause in North America and Europe. Previously, M. audouinii, T. violaceum: Europe, Asia, and Africa.
Age of Onset. Children have scalp infections (Trichophyton, Microsporum). Young and older adults have intertriginous infections. The incidence of onychomycosis is correlated directly with age; in the United States, up to 50% of individuals aged 75 years have onychomycosis.
Demography. Adult blacks may have a lower incidence of dermatophytosis. Tinea capitis is more common in black children.
Geography. Some species have a worldwide distribution; others are restricted to particular continents or regions. However, T.concentricum, the cause of tinea imbricata, is endemic to the South Pacific and parts of South America. T. rubrum was endemic to Southeast Asia, Western Africa, and Australia but now occurs commonly in North America and Europe.
Transmission. Dermatophyte infections can be acquired from three sources:
• Most commonly from another person [usually by fomites, less so by direct skin-to-skin contact (tinea gladiatorum)]
• From animals such as puppies or kittens.
• Least commonly from soil.
Classification of Dermatophytes. Based on their ecology, dermatophytes classified:
• Anthropophilic: Person-to-person transmission by fomites and by direct contact.
• Zoophilic: Animal-to-human by direct contact or by fomites.
• Geophilic: Environmental.
Predisposing factors. Atopic diathesis: Cell-mediated immune deficiency for T. rubrum. Topical immunosuppression by application of glucocorticoids: tinea incognito. Systemic immunocompromised: Patients have a higher incidence and more intractable dermatophytoses; follicular abscesses and granulomas may occur (Majocchi granuloma).
In vivo, dermatophytes grow only on or within keratinized structures and, as such, involve the following:
• Epidermal dermatophytosis. Tinea facialis, tinea corporis, tinea cruris, tinea manus, tinea pedis.
• Dermatophytoses of nail apparatus. Tinea unguium (toenails, fingernails). Onychomycosis (more inclusive term, including nail infections caused by dermatophytes, yeasts, and molds).
• Dermatophytoses of hair and hair follicle. Dermatophytic folliculitis, Majocchi granuloma, tinea capitis, tinea barbae.
Dermatophytes synthesize keratinases that digest keratin and sustain existence of fungi in keratinized structures. Cell-mediated immunity and antimicrobial activity of polymorphonuclear leukocytes restrict dermatophyte pathogenicity. Host factors that facilitate dermatophyte infections: atopy, topical and systemic glucocorticoids, ichthyosis, collagen vascular disease. Local factors favoring dermatophyte infection: sweating, occlusion, occupational exposure, geographic location, high humidity (tropical or semitropical climates). The clinical presentation of dermatophytoses depends on several factors: site of infection, immunologic response of the host, and species of fungus. Dermatophytes (e.g., T. rubrum) that initiate little inflammatory response are better able to establish chronic infection. Organisms such as Microsporum canis cause an acute infection associated with a brisk inflammatory response and spontaneous resolution. In some individuals, infection can involve the dermis, as in kerion and Majocchi granuloma.
See Fig. 26-24.
Figure 26-24. Dermatophytes: KOH preparation Multiple, septated, tubelike structures (hyphae or mycelia) and spore formation in scales from an individual with tinea pedis.
• Skin: Collect scale with a no. 15 scalpel blade, edge of a glass microscope slide, brush (tooth or cervical brush). Scales are placed on center of microscope slide, swept into a small pile, and covered with a coverslip. Recent application of cream/ointment or powder often makes identification of fungal element difficult/impossible.
• Nails: Keratinaceous debris is collected with a no. 15 scalpel blade or small curette. Distal lateral subungual onychomycosis (DLSO): debride from the undersurface of nail of most proximally involved site or nail bed; avoid nail plate. Superficial white onychomycosis: superficial nail plate. Proximal subungual onychomycosis (PSO): undersurface of proximal nail plate; obtain sample by using a small punch biopsy tool, boring through involved nail plate to undersurface; obtain keratin from undersurface of the involved nail plate.
• Hair: Remove hairs by epilation of broken hairs with a needle holder or forceps. Place on microscope slide and cover with glass coverslip. Skin scales from involved hairy site can be obtained with a brush (tooth or cervical).
Preparation of sample potassium hydroxide 5–20% solution is applied at the edge of coverslip. Capillary action draws solution under coverslip. The preparation is gently heated with a match or lighter until bubbles begin to expand, clarifying the preparation. Excess KOH solution is blotted out with bibulous or lens paper. Condenser should be “racked down.” Epidermal dermatophytosis: positive unless patient has been effectively treated. 90% of cases positive. Variations in KOH with fungal stains: Swartz–Lamkin stain and chlorazol black E stain.
Microscopy Dermatophytes are recognized as septated, tubelike structures (hyphae or mycelia; Fig. 26-24).
Wood’s lamp examination: Hairs infected with Microsporum spp. fluoresce greenish. Coral red fluorescence of intertriginous site confirms diagnosis of erythrasma.
Fungal Cultures. Specimens collected from scaling skin lesions, hair, and nails. Scale and hair from the scalp are best harvested with tooth or cervical brush; the involved scalp is brushed vigorously; keratinaceous debris and hairs then placed into fungal culture plate. Culture on Sabouraud’s glucose medium. Repeat cultures recommended monthly.
Dermatopathology DLSO. PAS or methenamine silver stains are more sensitive than KOH preparation or fungal culture in identification of fungal elements in DLSO.
Topical agents for epidermal dermatophytoses: Imidazoles (clotrimazole, miconazole, ketoconazole, econazole, oxiconazole, sulconazole, sertaconazole); allylamines (naftifine, terbinafine); naphthionates (tolnaftate); substituted pyridine (ciclopirox olamine).
Systemic Antifungal Agents
• Terbinafine 250-mg tablet. Allylamine. Most effective oral antidermatophyte antifungal; low efficacy against other fungi. Approved for onychomycosis in the United States.
• Itraconazole 100-mg capsules; oral solution (10 mg/mL): Intravenous. Triazole. Needs acid gastric pH for dissolution of capsule. Raises levels of digoxin and cyclosporine. Approved for onychomycosis in the United States.
• Fluconazole 100-, 150-, 200-mg tablets; oral suspension (10 or 40 mg/mL); 400 mg IV.
• Ketoconazole 200-mg tablets. Needs acid gastric pH for dissolution of tablet. Take with food or cola beverage; antacids and H2 blockers reduce absorption. The most hepatotoxic of azole drugs; hepatotoxicity occurs in an estimated one of every 10,000–15,000 exposed persons. Not approved for treatment of dermatophyte infections in the United States.
Dermatophytoses of Epidermis
Epidermal dermatophytoses are the most common dermatophytic infection. May be associated with dermatophytic infection of hair/hair follicles and/or the nail apparatus. Synonym: Ringworm.
Tinea Pedis ICD-9: 110.4 ICD-10: B35.3
Dermatophytic infection of the feet.
Clinical Findings. Erythema, scaling, maceration, and/or bulla formation. Infections at other sites such as tinea cruris usually associate initial tinea pedis.
Course. Provides breaks in the integrity of the epidermis through which bacteria such as S. aureus or group A streptococcus (GAS) can invade, causing skin or soft-tissue infection.
Synonyms. Athlete’s foot. Jungle rot.
Age of Onset. Late childhood or young adult life. Most common, 20–50 years.
Predisposing Factors. Hot, humid climate; occlusive footwear; hyperhidrosis.
Duration: months to years to lifetime. Often, prior history of tinea pedis, and tinea unguium of toenails. Usually asymptomatic. Pruritus. Pain with secondary bacterial infection (Fig. 25-30).
Interdigital Type. Two patterns: dry scaling (Fig. 26-26); maceration, scaling, fissuring of toe webs (Fig. 26-27). Hyperhidrosis common. Most common site: between fourth and fifth toes. Infection may spread to adjacent areas of feet.
Figure 26-25. Tinea pedis and onychomycosis in father and son The foot of a 5-year-old male with tinea pedis (ringworm lesion) and toenail dystrophy shown with his father’s foot with similar, but more advanced, findings. The son most likely became infected with dermatophyte from fomite in his home. Both father and son had atopic diathesis with history of atopic dermatitis.
Figure 26-26. Tinea pedis: interdigital dry type The interdigital space between the toes shows erythema and scaling; the toenail is thickened, indicative of associated distal subungual onychomycosis.
Figure 26-27. Tinea pedis: interdigital macerated type A 48-year-old male with athlete’s foot and hyperhidrosis for years. The skin of the webspace between the fourth and fifth toes is hyperkeratotic and macerated (hydration of the stratum corneum). The KOH+ preparation shows septated hyphae, confirming the diagnosis of dermatophytosis. Wood’s lamp demonstrated coral-red fluorescence confirming concomitant erythrasma. P. aeruginosa was isolated on bacterial culture.
Moccasin Type. Well-demarcated scaling with erythema with minute papules on margin, fine white scaling, and hyperkeratosis (Figs. 26-28 and 26-29) (confined to heels, soles, lateral borders of feet). Distribution: Sole, involving area covered by a ballet slipper. One or both feet may be involved with any pattern; bilateral involvement more common.
Figure 26-28. Tinea pedis: moccasin type A 65-year-old female with scaling feet for years. Sharply marginated erythema of the foot with a mild keratoderma associated with distal/lateral subungual onychomycosis, typical of T. rubrum infection.
Figure 26-29. Tinea pedis: moccasin type A 63-year-old male with scaling feet for years. Sharply marginated erythema of the medial foot with a mild keratoderma. Tinea corporis was also present on the forearms and dorsum of hands.
Inflammatory/Bullous Type. Vesicles or bullae filled with clear fluid (Fig. 26-30). Pus usually indicates secondary infection with S. aureus infection or GAS. After rupturing, erosions with ragged ringlike border. May be associated with “id” reaction (autosensitization or dermatophytid). Distribution: Sole, instep, webspaces.
Figure 26-30. Tinea pedis: bullous and ulcerative types A 34-year-old female with painful blisters in the webspaces and on the plantar foot. Tinea pedis was secondarily infected with S. aureus. A dermatophytid reaction was present on the hands with small vesicle on the fingers.
Ulcerative Type. Extension of interdigital tinea pedis onto plantar and lateral foot (Fig. 26-30). May be secondarily by S. aureus.
Interdigital Type. Erythrasma, pitted keratolysis
Moccasin Type. Psoriasis, eczematous dermatitis (dyshidrotic, atopic, allergic contact), pitted keratolysis.
Inflammatory/bullous type. Bullous impetigo, allergic contact dermatitis, dyshidrotic eczema, bullous disease.
Direct Microscopy (Fig. 26-24). In bullous type, examine scraping from the inner aspect of bulla roof for detection of hyphae.
Wood’s Lamp. Negative fluorescence usually rules out erythrasma in interdigital infection. Erythrasma and interdigital tinea pedis may coexist.
Culture. Dermatophytes can be isolated in 11% of normal-appearing interspaces and 31% of macerated toe webs. Candida spp. may be copathogens in webspaces. In individuals with macerated interdigital space, S. aureus, P. aeruginosa, and diphtheroids are commonly isolated. S. aureus causes secondary infection.
Demonstration of hyphae on direct microscopy, isolation of dermatophyte on culture.
Tends to be chronic. May provide portal of entry for soft-tissue infections, especially in patient’s venous stasis. Without secondary prophylaxis, recurrence is the rule.
See p. 609.
Tinea Manuum ICD-9: 110.2 ICD-10: B35.2
Chronic dermatophytosis of the hand(s).
Often unilateral, most commonly on the dominant hand.
Usually associated with tinea pedis.
Frequently symptomatic. Pruritus. Dyshidrotic type: Episodic symptoms of pruritus.
Well-demarcated scaling patches, hyperkeratosis, fissures on palmar hand (Fig. 26-31). Borders well demarcated; central clearing. May extend onto dorsum of hand with follicular papules, nodules, and pustules with dermatophytic folliculitis. Dyshidrotic type: Papules, vesicles, bullae (uncommon on the margin of lesion) on palms and lateral fingers, similar to lesions of bullous tinea pedis. Secondary changes: Lichen simplex chronicus, prurigo nodules, secondary S. aureus infection. Distribution: Diffuse hyperkeratosis of the palms with pronounced involvement of palmar creases or patchy scaling on the dorsa and sides of fingers; 50% of patients have unilateral involvement. Usually associated with tinea pedis (Fig. 26-32) and tinea cruris. If chronic, often associated with tinea unguium of fingernails and toenails (Fig. 26-32).
Figure 26-31. Tinea manuum Erythema and scaling of the right hand, which was associated with bilateral tinea pedis; the “one-hand, two-feet” distribution is typical of epidermal dermatophytosis of the hands and feet. In time, distal/lateral subungual onychomycosis occurs on the fingernails.
Figure 26-32. Tinea manuum, tinea pedis, and onychomycosis A 57-year-old male immunosuppressed renal transplant recipient with extensive epidermal dermatophytosis of hands, feet, and nail. The feet are initially infected; infection spreads to hands, arms, and nails.
Atopic dermatitis, lichen simplex chronicus, allergic contact dermatitis, irritant contact dermatitis, psoriasis vulgaris.
Chronic, does not resolve spontaneously. After treatment, recurs unless onychomycosis of fingernails, feet, and toenails is eradicated. Fissures and erosions provide portal of entry for bacterial infections.
Must eradicate tinea unguium of fingernails as well as toenails; also tinea pedis and tinea cruris, otherwise, tinea manuum will recur.
Oral agents eradicate dermatophytoses of hands, feet, and nails: Terbinafine: 250 mg daily for 14 days. Itraconazole: 200 mg daily for 7 days. Fluconazole: 150–200 mg daily for 2–4 weeks. Note: Eradication of fingernail onychomycosis requires longer use.
Tinea Cruris ICD-9: 110.3 ICD-10: B35.6
Subacute or chronic dermatophytosis of the upper thigh and adjacent inguinal and pubic regions. A better name is tinea inguinalis (groin); cruris refers to the lower leg. “Always” associated with tinea pedis, the source of the infection.
Months to years duration. Often, history of long-standing tinea pedis and prior history of tinea cruris.
Large, scaling, well-demarcated dull red/tan/brown plaques (Fig. 26-33). Central clearing. Papules, pustules may be present at margins: dermatophytic folliculitis. Treated lesions: lack scale; postinflammatory hyperpigmentation in darker-skinned persons. In atopics, chronic scratching may produce secondary changes of lichen simplex chronicus. Distribution. Groins and thighs; may extend to buttocks (Figs. 26-34 and 26-35). Scrotum and penis are rarely involved.
Figure 26-33. Tinea cruris (inguinalis): acute A 80-year-old female with pruritic inguinal rash for several weeks. She was being treated with prednisone for polymyalgia rheumatica. Typical inflamed rings and arcs are seen on the proximal thigh and adjacent inguinal area.
Figure 26-34. Tinea cruris (inguinalis): subacute A 20-year-old male with pruritic inguinal rash for several months. He was a college wrestler. Concomitant dermatophyte infection was also present on the feet, trunk, and face. He was treated with oral terbinafine.
Figure 26-35. Tinea cruris (inguinalis): chronic A 65-year-old male with pruritic inguinal rash for many months. The skin of the proximal thigh is lichenified from chronic rubbing and scratching. He had applied topical corticosteroid to the site. He also had tinea pedis and onychomycosis.
Erythrasma, Candida intertrigo, intertriginous psoriasis, tinea, or pityriasis versicolor.
Prevention. After eradication minimize reinfection with shower shoes and antifungal powders;
Antifungal Agents. See p. 609
Tinea Corporis ICD-9: 110.5 ICD-10: B35.4
Dermatophyte infections of the trunk, legs, arms, and/or neck, excluding the feet, hands, and groin.
Etiology. Most commonly caused by T. rubrum. M. canis lesions are often inflammatory or bullous. T. tonsurans caused tinea corporis in parents of black children with tinea capitis.
Scaling, sharply marginated plaques. Peripheral enlargement and central clearing (Figs. 26-36 through 26-39) produce annular configuration with concentric rings or arcuate lesions; fusion of lesions produces gyrate patterns. Single and occasionally scattered multiple lesions. Psoriasiform plaques. Lesions of zoophilic infection (contracted from animals) are more inflammatory, with marked vesicles, pustules, crusting at margins. Papules, nodules, pustules: dermatophytic folliculitis, i.e., Majocchi granuloma.
Figure 26-36. Tinea corporis: tinea incognito An 80-year-old male with a rash on buttocks for 1 year. Erythematous patches on the buttocks, some with sharp margination, others with clearing, and excoriations. He had been treating the pruritus with topical corticosteroid. Tinea cruris, tinea pedis, and onychomycosis were also present.
Allergic contact dermatitis, atopic dermatitis, annular erythemas, psoriasis, seborrheic dermatitis, pityriasis rosea, pityriasis alba, tinea versicolor, erythema migrans, subacute lupus erythematosus, cutaneous T cell lymphoma.
See “Direct Microscopy (Fig. 26-24),” and culture.
See p. 609
Figure 26-37. Tinea corporis A 80-year-old female with red, scaling lesions on the lower leg. Lesions were present under a foot brace that occluded the skin. Corticosteroid has been applied to the site. Tinea corporis was associated with tinea pedis and onychomycosis (see inset).
Figure 26-38. Tinea corporis: tinea incognito A 60-year-old renal transplant recipient has been treating thigh rash with topical corticosteroid for several months. Blotchy erythema with areas of atrophy and scale on the right medial upper thigh bordering the inguinal area. Tinea pedis and onychomycosis were also present. KOH preparation showed septated hyphae. Topical steroid facilitates dermatophyte growth, suppressing the immune response, creating an undiagnosed infection, tinea incognito.
Figure 26-39. Tinea corporis: inflammatory A 13-year-old female with inflammatory lesion on the arm for 1 week. A younger sibling had tinea capitis. Acutely inflamed edematous exudative annular plaque on the upper arm.
Dermatophytosis of the glabrous facial skin. Well-circumscribed erythematous patch. More commonly misdiagnosed than any other dermatophytosis.
Synonym: Tinea faciei
Etiology. T. tonsurans associated with tinea capitis in black children and their parents. T. mentagrophytes, T. rubrum most commonly; also M. audouinii, M. canis.
Well-circumscribed macule to plaque of variable size; elevated border and central regression (Figs. 26-40 and 26-41). Scaling is often minimal. Pink to red; in black patients, hyperpigmentation. Any area of face but usually not symmetric.
Figure 26-40. Tinea facialis A 5-year-old girl with inflammatory lesion on the periorbital skin. Papules are dermatophytic folliculitis of vellus hairs. The site has previously been treated with hydrocortisone cream.
Figure 26-41. Tinea facialis A 83-year-old immunosuppressed male with a history of prednisone treatment for polymyalgia rheumatica and chronic lymphatic leukemia. Note a facial lesions and a new nodule. Well-demarcated erythema and scaling in the beard area. SCC in situ is present on the left eyebrow. The tumor on the left neck is B-cell lymphoma; this lesion regressed when prednisone was tapered.
Seborrheic dermatitis, contact dermatitis, erythema migrans, lupus erythematosus, polymorphous light eruption, phototoxic drug eruption, lymphocytic infiltrate.
See “Direct Microscopy,” and culture.
See p. 609
Epidermal dermatophytosis, often associated with dermatophytic folliculitis.
Occurs after the topical application of a glucocorticoid preparation to a site colonized or infected by dermatophyte.
Variably inflamed patches. Occurs when an inflammatory dermatophytosis is mistaken for psoriasis or an eczematous dermatitis (Figs. 26-35–26-38 and 26-40). Involved sites often have exaggerated features of epidermal dermatophytoses, being a deep red or violaceous. Scaling often not apparent. Papules or pustule within involved sites is dermatophytic folliculitis. Epidermal atrophy caused by chronic glucocorticoid application may be present.
Systemic antifungal therapy may be indicated due to deep involvement of the hair apparatus. See p. 609.
Dermatophytoses of Hair
Dermatophytes are capable of invading hair follicles and hair shafts, causing:
Two types of hair involvement are seen (see Fig. 26-42).
Figure 26-42. Dermatophytic folliculitis. Ectothrix type: mycelia and arthroconidia are seen on the surface of the hair follicle (extrapilary). Endothrix type: hyphae and arthroconidia occur within the hair shaft (intrapilary).
Tinea Capitis ICD-9: 110.5 ICD-10: B35.0
Dermatophytic trichomycosis of the scalp, predominantly in preadolescent children.
Clinical presentations vary widely:
Scaling and broken-off hairs
Severe, painful inflammation with painful, boggy nodules that drain pus (kerion) and result in scarring alopecia
Synonyms: Ringworm of the scalp, tinea tonsurans
Epidemiology and Etiology
Toddlers and school-age children (6–10 years of age) most commonly affected. Much more common in blacks than in whites in the United States. Etiology varies from country to country and from region to region. Species change in time due to immigration. Infections can become epidemic in schools and institutions, especially with overcrowding. United States: Random fungal cultures in urban study detected a 4% infection rate and a 12.7% colonization rate among black children.
• United States and Western Europe. 90% of cases of tinea capitis caused by T. tonsurans. Less commonly, M. canis.
• Eastern and Southern Europe, North Africa. T. violaceum
Transmission. Person-to-person, animal-to-person, via fomites. Spores are present on asymptomatic carriers, animals, or inanimate objects.
Pathogenesis. Scalp hair traps fungi from the environment or fomites. Asymptomatic colonization is common. Trauma assists inoculation. Dermatophytes initially invade stratum corneum of scalp, which may be followed by hair shaft infection. Spread to other hair follicles then occurs.
• Ectothrix infection. Occurs outside hair shaft. Hyphae fragment into arthroconidia, leading to cuticle destruction. Caused by Microsporum spp. (M. audouinii and M. canis) (Fig. 26-42).
• Endothrix infection. Occurs within hair shaft without cuticle destruction (Fig. 26-42). Arthroconidia found within hair shaft. Caused by Trichophyton spp. (T. tonsurans in North America; T. violaceum in Europe, Asia, parts of Africa).
• “Black dot” tinea capitis. Variant of endothrix resembling seborrheic dermatitis.
• Kerion. Variant of endothrix with boggy inflammatory plaques.
• Favus. Variant of endothrix with arthroconidia and airspaces within hair shaft. Very uncommon in Western Europe and North America. In some parts of the world (Middle East, South Africa), however, it is still endemic.
Noninflammatory Infection. Scaling. Diffuse or circumscribed alopecia. Occipital or posterior auricular adenopathy.
“Gray patch” tinea capitis (Fig. 26-43). Partial alopecia, often circular in shape, showing numerous broken-off hairs, dull gray from their coating of arthrospores. Fine scaling with fairly sharp margin. Hair shaft becomes brittle, breaking off at or slightly above scalp. Small patches coalesce, forming larger patches. Inflammatory response minimal, but massive scaling. Several or many patches, randomly arranged, may be present. Microsporumspecies may show green fluorescence with Wood’s lamp. Differential diagnosis: Seborrheic dermatitis, psoriasis, atopic dermatitis, lichen simplex chronicus, and alopecia areata.
Figure 26-43. Tinea capitis: “gray patch” type A large, round, hyperkeratotic plaque of alopecia due to breaking off of hair shafts close to the surface, giving the appearance of a mowed wheat field on the scalp of a child. Remaining hair shafts and scales exhibit a green fluorescence when examined with Wood’s lamp. M. canis was isolated on culture.
“Black Dot” Tinea Capitis. Broken-off hairs near the scalp give appearance of “dots” (Fig. 26-44) (swollen hair shafts) in dark-haired patients. Dots occur as affected hair breaks at surface of scalp. Tends to be diffuse and poorly circumscribed. Low-grade folliculitis may be present. Resembles seborrheic dermatitis. Usually caused by T. tonsurans, T. violaceum. Differential diagnosis: Seborrheic dermatitis, psoriasis, atopic dermatitis, lichen simplex chronicus, chronic cutaneous lupus erythematosus, alopecia areata.
Figure 26-44. Tinea capitis: “black dot” variant A subtle, asymptomatic patch of alopecia due to breaking off of hairs on the frontal scalp in a 4-year-old black child. The lesion was detected because her infant sister presented with tinea corporis. T. tonsurans was isolated on culture.
Kerion. Inflammatory mass in which remaining hairs are loose. Characterized by boggy, purulent, inflamed nodules, and plaques (Fig. 26-45). Usually painful; drains pus from multiple openings, like honeycomb. Hairs do not break off but fall out and can be pulled without pain. Follicles may discharge pus; sinus formation; mycetoma-like grains. Thick crusting with matting of adjacent hairs. A single plaque is usual, but multiple lesions may occur with involvement of entire scalp. Frequently, associated lymphadenopathy is present. Usually caused by zoophilic (T. verrucosum, T. mentagrophytes var. mentagrophytes) or geophilic species. Heals with scarring alopecia.
Figure 26-45. Kerion A 5-year-old black boy with an inflammatory mass on the scalp unresponsive to oral antibiotics. The bobby swelling with multiple pustules and postauricular lymphadenopathy. T. tonsurans was isolated on fungal culture. He was successfully treated with oral terbinafine for 4 weeks. (From Proudfoot LE, Morris-Jones R. Kerion celsi. N Engl J Med 2012;366:1142. Used with permission.)
Favus. Latin for honeycomb. Early cases show perifollicular erythema and matting of hair. Later, thick yellow adherent crusts (scutula) composed of skin debris and hyphae that are pierced by remaining hair shafts (Fig. 26-46). Fetid odor. Shows little tendency to clear spontaneously. Often results in scarring alopecia. Differential diagnosis: Impetigo, ecthyma, crusted scabies.
Figure 26-46. Tinea capitis: favus Extensive hair loss with atrophy, scarring, and so-called scutula, i.e., yellowish adherent crusts present on the scalp; remaining hairs pierce the scutula. T. schoenleinii was isolated on culture.
Wood’s Lamp. T. tonsurans does not fluoresce.
Direct Microscopy. Skin scales contain hyphae and arthrospores. Ectothrix: arthrospores can be seen surrounding the hair shaft in cuticle. Endothrix: spores within hair shaft. Favus: loose chains of arthrospores and airspaces in hair shaft (Fig. 26-42).
Fungal Culture. Growth of dermatophytes usually seen in 10–14 days.
Bacterial Culture. Rule out bacterial infection, usually S. aureus or GAS.
Course and Treatment
Chronic untreated kerion and favus, especially if secondarily infected with S. aureus, result in scarring alopecia. Regrowth of hair is the rule if treated with systemic antifungal agents (see p. 609).
Tinea Barbae ICD-9: 110.0 ICD-10: B35.0
Dermatophytic folliculitis involving the androgen-sensitive beard and moustache areas. Resembles tinea capitis, with invasion of the hair shaft.
T. verrucosum, T. mentagrophytes var. mentagrophytes, most commonly. May be acquired through animal exposure. T. rubrum an uncommon cause.
Pustular folliculitis (Fig. 26-47), i.e., hair follicles surrounded by red inflammatory papules, pustules, nodules, or plaques. Involved hairs are loose and easily removed. With less follicular involvement, there are scaling, circular, reddish patches (tinea facialis) in which hair is broken off at the surface. Papules may coalesce to inflammatory plaques topped by pustules.
Figure 26-47. Tinea barbae A 63-year-old male with pustules in beard area for several months. A large pustule in an inflammatory nodule is seen on the moustache area. Extensive subtle tinea facialis was also present. Tinea pedis, onychomycosis, and tinea cruris were present as well. KOH preparation was positive; T. rubrum was detected on dermatophyte culture. Bacterial culture was negative for pathogens. Facial lesions resolved with oral terbinafine.
Kerion: boggy purulent nodules and plaques as with tinea capitis (Fig. 26-48). Beard and moustache areas, rarely, eyelashes, eyebrows.
Figure 26-48. Tinea barbae with kerion and tinea facialis Confluent, painful papules, nodules, and pustules on the upper lip (kerion). Epidermal dermatophytosis (tinea facialis) with sharply marginated erythema and scaling is present on the cheeks, eyelids, eyebrows, and forehead. T. mentagrophytes was isolated on culture. In this case, the organism caused two distinct clinical patterns (epidermal involvement, tinea facialis versus follicular inflammation, tinea barbae), depending on whether glabrous skin or hairy skin was infected (see also Fig. 26-23).
Regional lymphadenopathy, especially if of long duration and if superinfected.
S. aureus folliculitis, furuncle, carbuncle, acne vulgaris, rosacea, pseudofolliculitis.
Laboratory Examinations. See p. 608.
Topical agents ineffective. Systemic antifungal therapy required (see p. 609).
Dermatophytic Folliculitis. See “Infectious Folliculitis” in Section 31.
Dermatophytic folliculitis with foreign-body granuloma occurring in response to keratin in dermis and immune reaction to dermatophyte.
Etiology. Most commonly T. rubrum, T. tonsurans
Risk Factors. Topical glucocorticoid application. Host defense defects
Follicular type with local immunosuppression (topical glucocorticoid use)
Subcutaneous nodular type with systemic immunocompromised (Fig. 26-49). Solitary or multiple
Figure 26-49. Majocchi granuloma A 55-year-old diabetic male renal transplant recipient with painful nodules on left lower thigh. Eroded papules with crusting above the knee. Tinea pedis and onychomycosis were also present. T. rubrum was isolated on dermatophyte culture. He was treated with voriconazole.
• Folliculocentric papules and pustules arise within an area of epidermal dermatophytosis such as tinea incognito (Fig. 26-38).
Distribution: Any hair-bearing area; scalp, face, forearms (Fig. 26-50), dorsum of hands/feet, shaved legs.
Figure 26-50. Majocchi granuloma A 87-year-old male with two nodules on the L-forearm for 6 weeks. Initial impression was cutaneous malignancies. Diagnosis of Majocchi granuloma was made on lesional biopsy. Systemic terbinafine was given.
Invasive and Disseminated Fungal Infections
These topics are covered in Appendix C (p. 875).