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- Essentials of Diagnosis
- General Considerations
- Clinical Findings
- Prevention & Control
- Table 1. Differential diagnosis for dermatophytoses.
- BOX 1 . Treatment of Dermatophytoses
- BOX 2. Prevention & Control of Dermatophytoses
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Essentials of Diagnosis
• Characteristic pattern of inflammation on glabrous skin surfaces. The active border of infection is scaly, red, and slightly elevated.
• Wet mount preparation with potassium hydroxide (10-20%). Skin scraping of the active border shows branching, translucent, rod-shaped filaments (hyphae) in keratinized material under low-power microscopy (10-40×). Hyphae are uniformly wide and regularly septated.
• Wood’s light examination (UV light at 365 nm) shows blue-green fluorescence for Microsporum canis and Microsporum audouinii. Trichophyton schoenleinii is pale green, and tinea versicolor shows white-yellow fluorescence.
• Culture should be performed with hair, nail, and skin specimens from particularly inflammatory lesions, to make a definitive mycologic diagnosis.
Dermatophytes are molds that infect keratinized tissues including skin, hair, and nails. Whereas 40 dermatophyte species are known to infect humans, only about 15 of these are common causes of disease. These organisms belong to three genera, Microsporum, Trichophyton, and Epidermophyton. Because these fungi have such similar infectivity, morphology, and pathogenicity, they are often categorized according to the clinical syndrome and the preferred anatomic site with which they are associated, such as tinea capitis, tinea pedis, etc. “Tinea” comes from the Latin word meaning worm or moth. These superficial mycoses often create serpiginous skin markings.
Although tinea versicolor (caused by Malassezia furfur or Pityrosporum spp.) is not formally considered a dermatophytosis, it is also discussed in this chapter, as it also affects superficial skin layers.
A. Epidemiology. Dermatophytes are found in three distinct environmental niches and display specific adaptation to these sites: animals, humans, and soil. Therefore, they are classified as anthropophilic, zoophilic, or geophilic organisms. As these names imply, infection occurs following exposure to either infected humans, animals (such as cats, dogs, or cattle), or soil.
Dermatophytoses occur worldwide, and vary in their presentation according to the site of infection. Improved living standards in the United States since the end of World War II have decreased the incidence of tinea capitis. On the other hand, dramatic increases in the incidence of tinea pedis and tinea cruris due to Trichophyton rubrum, an anthropophilic dermatophyte, have been observed in recent years in developed nations. T rubrum is the most common dermatophyte pathogen worldwide, affecting up to one-third of the population of industrialized countries. Tinea pedis occurs almost exclusively among people who wear shoes, because the latter provide warmth and moisture, conditions that are preferred by the causative organisms.
Transmission of zoophilic dermatophytes occurs through direct contact with infected animals or fomites, such as via troughs and stalls used by infected animals. Geophilic dermatophyte infections occur from direct contact with soil and are seen in greenhouse workers, but infections with these organisms are relatively less common than those caused by anthropophilic dermatophytes.
B. Microbiology. The dermatophytes belong to three anamorphic (asexual or imperfect) genera, Epidermophyton, Microsporum, and Trichophyton of the Deuteromycota (Fungi Imperfecti). Members of the Epidermophyton genus have macroconidia that are smooth-walled and either single or in clusters, but these fungi have no microconidia. Members of the Microsporum genus have macroconidia with fusiform or cylindrical and roughened walls. There are fewer microconidia, and they are found alone along the hyphae as pear-shaped structures. Trichophyton species have macroconidia with smooth cylindrical walls. Their microconidia are numerous, and spherical or pear shaped; they appear in clusters along the hyphae.
Conidia are used as the basis for dermatophyte speciation. Because dermatophytes form only hyphae and arthrospores in the nonviable keratinized tissue of infected humans, they must be cultivated in the laboratory to develop conidia for purposes of identification. Colonies form at room temperature on Sabouraud’s agar, and their color, texture and morphology are also useful in species identification.
C. Pathogenesis. Host factors that enhance the development of dermatophytoses include genetic-susceptibility markers; abraded skin; occlusive clothing, footwear, or dressings; and the presence of other cutaneous diseases like atopic dermatitis. The dermatophytes invade the keratinized layers of skin by producing keratinases, enzymes that digest keratin. While adhering to and invading host skin, the dermatophytes elicit a diverse set of clinical responses. Most lesions are contained within a certain anatomic boundary and may even be self-limited, but widespread dermatophyte infection has been observed in patients with AIDS, patients on immunosuppressive drug regimens, and those who have endocrinopathies such as Cushing’s disease. The pathogenic features of superficial dermatophyte infections of the skin.
Trichophyton is also the name of a crude extract from certain dermatophytes that produces a tuberculinlike response in most adults. There are two moieties of the galactomannan peptide responsible for antigenic response. The carbohydrate portion is responsible for an immediate response, and the peptide portion is associated with a delayed response and probably immunity as well. Resistance to infection is T cell mediated and may be acquired after infection, but it varies in duration and degree, depending on host factors, species of the fungus, and site of infection.
The superficial mycoses are named according to the site of infection, which usually corresponds to the site of local inoculation. The degree of inflammation is often dictated by the nature of the environment from which the fungus originates. For example, anthropophilic dermatophytes elicit a milder immune response in humans than do the zoophilic fungi. The anthropophilic M audouinii causes minimal inflammation as compared with the zoophilic M canis. Table 1 lists the microbiological differential diagnosis for each clinical syndrome discussed below.
A. Tinea Capitis. Tinea capitis or scalp ringworm mainly affects prepubertal children ages 4-14. It is most commonly observed in crowded living conditions and in areas of poverty. Infection of the hair shaft distinguishes this disease from other dermatophytoses that involve the glabrous skin. Tinea capitis is often classified according to one of three patterns of fungal invasion noted microscopically: endothrix, ectothrix, or favus. Endothrix infections invade the inside of the hair shaft, and the cuticle is not destroyed; thus, clinically it appears as simple scaling of the scalp. It may resemble seborrheic dermatitis or dandruff. There may be gray patches of alopecia with minimal or no inflammation or “black dot” alopecia, in which hairs break off at the roots.
The ectothrix infections present with gray or scaling patches of alopecia with minimal or no inflammation. The “black dot” appearance is also seen. Kerions and prominent inflammatory lesions may be observed, as the dermatophytes that cause ectothrix infections invade both the inside and the outside of the hair shaft and follicles. Kerions are boggy, suppurative, and usually painful. Kerions are most commonly seen with M canis and rarely with Trichophyton mentagrophytes or Trichophyton verrucosum.
Favus infection leads to crusting and matted hair on the scalp with such severe invasion that permanent alopecia often results. It is primarily seen in Eastern Europe and Africa.
B. Tinea Barbae. Tinea barbae, like tinea capitis, affects the hair follicles and shafts but in the facial area, and it is often diagnosed only after it fails to respond to several courses of antibacterial agents. Affected hairs are easily removed, unlike those in bacterial folliculitis, which resist removal. The zoophilic dermatophytes T mentagrophytes and T verrucosum are the most common causes of tinea barbae. The condition often begins with a small clump of follicular pustules, then develops into a boggy, erythematous tumorlike abscess.
C. Tinea Corporis. Tinea corporis or ringworm refers primarily to lesions affecting the nonhairy or glabrous skin, but this condition may also result from extensions of scalp or groin infections. Lesions are usually sharply demarcated and ringlike with a raised border. The infections can range from mildly to highly inflammatory with pustules, vesicles, and marked erythema. The central area may become brown or hypopigmented and less scaly as the active border progresses.
D. Tinea Cruris. Tinea cruris or jock itch is more common in men and may involve the perineum and the perianal and thigh areas, but it rarely affects the scrotum. (Candida infections, in contrast, typically involve the scrotum.) Tinea cruris typically presents with bilateral asymmetric erythematous plaques that spread distally from the groin. There is often central clearing and an active erythematous border, which may have vesicles or papules. Pruritis and burning are common complaints.
This infection is usually transmitted from the patient’s foot to the groin. Tinea cruris often occurs in the summer months after sweating or wearing wet clothing or in the winter months after wearing many layers of clothing, leading to the predisposing warm moist conditions conducive to fungal growth.
E. Tinea Pedis. Tinea pedis, also known as athlete’s foot, is the most common dermatophyte infection diagnosed overall, and it is usually caused by the anthropophilic organism T rubrum. Occlusive footwear promotes warmth and sweating which provide an ideal environment for fungal growth. Tinea pedis presents in four general fashions (a) interdigital infection with erythema, maceration, and scale formation; (b) “moccasin foot” with erythema and thick hyperkeratotic scales; (c) inflammatory infection with vesicles usually on the medial foot; and (d) a less common ulcerative infection affecting the web spaces of the toes, sometimes superinfected with bacteria, and often seen in immunocompromised patients. If tinea unguium is present, tinea pedis may persist because of constant reinfection from the nails.
F. Tinea Unguium. Tinea unguium or onychomycosis is an infection of the fingernails or toenails. Infections typically begin along the leading edge of the nail or the lateral border and involve the nail plate; the result is opaque, chalky or yellow nail discoloration. The nail may also become thickened and brittle. Inflammatory changes of the skin around the nail including paronychia are not seen with tinea unguium. Toenails are more frequently involved than fingernails, and the incidence of this infection increases with age.
The nondermatophytic molds such as Scopulariopsis and Scytalidium spp., Acremonium fusarium, and Candida spp. cause ~ 5% of fungal nail diseases. This prevalence varies by geography, and these molds may account for = 50% of fungal nail infections in Southeast Asia. These fungi are important to distinguish, because not all respond to the same therapy.
G. Tinea Incognito. Tinea incognito refers to dermatophyte infections that are disguised, often because they are treated with topical steroids and then lose some of their characteristic clinical features. Steroids may temporarily reduce inflammation, but the fungus is able to grow unchecked by the impaired immune response. The rash changes such that scaling margins disappear, borders become irregular, and a once localized process may expand. The diagnosis is easily made once steroids are stopped for a few days and scaling reappears and hyphae can be seen on microscopy. Tinea incognito is most often observed in the groin, face, and hands.
H. Dermatophytid. Dermatophytid or the “id” reaction is an allergic response to tinea processes that causes sterile dermatitis at distant sites. The most common presentation is a patient with tinea pedis who develops itching and burning on the hands, usually on the sides of the fingers near the crease. Vesicles may appear that enlarge to bullae. Desquamation of the palms and soles occurs less commonly, without inflammation. The lesions persist until the primary process resolves.
I. Tinea Versicolor. Tinea versicolor is a common fungal infection of the superficial layer of skin caused by members of the Malassezia genus, especially Malassezia furfur, formerly known as both Pityrosporum orbiculare and Pityrosporum ovale. These organisms are lipophilic and make use of medium-chain-length fatty acids. They are members of the normal skin flora, but certain conditions promote proliferation, such as excess heat, humidity, pregnancy, oral contraceptives, malnutrition, burns, Cushing’s disease, corticosteroid therapy, or other forms of immunosuppression.
Clinically, tinea versicolor has a characteristic distribution and lesions; it begins as small circular macules of various colors (thus the name “versicolor”), such as white, pink, or brown, that expand radially. The varied color with this rash stems from the pathologic response of the host. For example, reddish macules or patches are related to a hyperemic inflammatory response; the hypopigmented lesions are caused by alterations in melanosome formation and transfer of pigment to keratinocytes; the tan or dark macules or patches are also related to alterations in melanosome formation. The color of the lesions is uniform in each individual. The upper trunk is the area that is most commonly affected, because the organism is found in highest numbers in areas of increased sebaceous activity. The lesions often become more obvious in summer, when the hypopigmented areas contrast more sharply with the unaffected tanned skin. The lesions are usually asymptomatic, but they may itch if there is inflammation.
In addition to clinical recognition and diagnosis on clinical grounds, there are three specific techniques that are useful in the work-up and more definitive diagnosis of superficial mycoses: UV light examination, direct microscopy, and culture. Direct examination of the patient’s skin in a darkened room by using UV light (a Wood’s lamp) is useful only for infections — primarily tinea capitis or corporis — caused by certain species, including M. audouinii, M canis, and T schoenleinii. These infections give off a blue-green color.
Specimens for diagnosis by microscope or culture can be collected using a razor or scalpel to scrape keratinized or flaking material from the leading edge of the newest lesion. Nail scrapings are ideal if the nail is scraped underneath the nail plate, initially to clean it and then to collect a specimen onto a microscope slide or to inoculate culture. A few drops of 10-20% KOH solution is placed on the slide to dissolve keratin. Heating accelerates the process. This enables visualization of hyphae seen with dermatophytes or of hyphae and spores seen in candidal and tinea versicolor infections.
Because KOH wet mounts cannot differentiate among dermatophyte species, the organisms should be cultivated to reveal the distinguishing forms of conidia. From a clinical perspective, it is usually not necessary to identify the dermatophyte species, because topical and oral agents are active against all of them. Species identification is important for scalp infections, severe or inflammatory skin infections, and certain nail infections, because systemic treatment is necessary for scalp infections, treatment may be prolonged and expensive, and species identification may enable prevention of zoophilic infections. Some nail infections may be caused by a mold (eg, Scopulariopsis spp.), which, despite being indistinguishable from dermatophytoses on a gross visual basis, will not respond to the same therapy. Culture is usually performed using Sabouraud’s agar slants, which are incubated at room temperature for 1-3 weeks. The specific dermatophyte is then identified by colony color and texture, as well as by light microscopy, which reveals the specific morphologic patterns.
Diagnosis of tinea versicolor is made by Wood’s light examination, which shows irregular whitish-yellow areas of fluorescence, although some lesions do not fluoresce. Potassium hydroxide wet mount preparations show short, broad hyphae and clusters of budding cells, which are often described as having the appearance of “spaghetti and meatballs”. Cultivation is possible but rarely indicated and requires the addition of oil to the fungal culture media because the organism is lipophilic.
The principles of treatment are outlined in Box 1, according to the specific clinical presentation. Most tinea infections involving the skin can be treated with topical agents such as an imidazole twice a day for 2 or 3 weeks. Terbinafine is also available both in topical and oral formulations and appears to be a more potent drug, requiring shorter dosing with longer lasting clinical responses. Terbinafine and newer related drugs block ergosterol synthesis at an earlier step than do the azole drugs.
If the infection is widespread, involving a large surface area, or if it is particularly inflammatory, systemic drugs are indicated. For infections of the hair and nails, debridement is important prior to systemic treatment. Several oral medications including itraconazole, fluconazole, and terbinafine can be dosed on a daily basis or in so-called “pulsed” regimens for effective treatment of infections of the keratinized tissues. The concept underlying pulse dosing takes advantage of drug deposition in the nail so that the total dose can be reduced; elevated amounts of drug are given repeatedly for short intervals corresponding to the length of time for a finger or toenail to grow. For example, a slightly higher daily dose is given for 1 week each month for the length of time estimated for the infected nail to grow again.
Treatment of tinea versicolor is with a 2.5% selenium sulfide suspension applied to the entire skin surface from the lower posterior scalp area down to the thighs for 10 min every day for 7 days. Another common regimen is to apply the lotion and wash it off after 24 h, repeating once a week for a month. Antifungal creams are useful. Single dose oral treatment with ketoconazole, itraconazole, or fluconazole has also been shown to be effective. Other important adjunctive measures to minimize reinfection include discarding or boiling frequently worn garments that are in contact with the skin. The lesions may take months to clear as they result from depigmentation, which persists despite eradication of the fungus.
Prevention & Control
Several interventions have been shown useful in the prevention and control of dermatophytes, depending on their type and anatomic location (Box 2). In general, ensuring a clean and dry body surface; avoiding occlusive gloves or shoes that may promote tinea unguium, manus, or pedis; and avoiding sweat-dampened clothing that enables tinea versicolor to thrive all control this infection. Regular cleaning of showers and changing areas at public pools with bleach is thought to control some infection, as is the use of chemicals on an individual basis, such as foot powders.
Table 1. Differential diagnosis for dermatophytoses.
Tinea capitis (ringworm of the scalp)
Circular bald patches, short hair stubs, pruritic, advancing red border
Alopecia areata, psoriasis, seborrheic dermatitis, bacterial infections
UV light for M canis and M audouinii
KOH mount of hair follicles and scrapings
Tinea barbae (ringworm of the facial hair
Inflammatory lesions, follicular pustules, pruritic
KOH mounts of exfoliated skin
Tinea corporis (ringworm of the smooth nonhairy skin)
Circular scaly patches, advancing red borders, pruritic
Eczema, psoriasis, pityriasis rosea, ery thema annulare centrifigum, and sub acute cutaneus lupus, drug allergy
KOH mount of skin scraping from leading edge
Culture if indicated
Tinea cruris (ringworm of the groin)
Well-demarcated, scaling circinate lesions with erythematous raised borders; scrotum is rarely involved
Cutaneous Candida, erythrasma, eczematous dermatitis, psoriasis
Vesicle from eczematous lesion: KOH and culture if indicated
Tinea pedis (ringworm of the feet)
Interdigital: erythema, maceration and scale
Moccasin foot: erythema, thick hyperkeratotic scales Inflammatory: vesicles on medial foot
Ulcerative: especially in web spaces and secondary bacterial infection
Other fungi: Scytalidium hyalinum or S cytalidium dimidiatum, erythrasma, candidiasis, psoriasis, and dyshidrosis
KOH mount of skin scraping from leading edge and culture if indicated
Tinea unguium (onychomycosis)
Small yellow spot begins at nail base; nail becomes brittle, friable, thickened
Nail bed tumors, yellow-nail syndrome, pachyonychia congenita, traumatic onychodystrophy
KOH mount of nail shaving or nail bed detritus and culture if indicated
P orbiculare (also called Malassezia furfur)
Not formally a dermatophyte
Begins as multiple small circular macules (white, pink or brown) that enlarge radially
Vitiligo, pityriasis alba, seborrheic dermatitis, secondary syphilis, and pityriasis rosea
KOH mount of skin scraping
Wood’s light = irregular pale yellow-white fluorescence; fades with treatment (some lesions do not fluoresce)
Fungal “id” reaction
Not a dermatophyte at the local site but associated with certain tinea infestations
Adults: vesicular eruption of the palms
Children: erythematous lichenoid papules
Adults: associated with tinea pedis
Children: associated with kerions of the scalp
Look for and diagnose the primary offending dermatophyte
BOX 1 . Treatment of Dermatophytoses
• Terbinafine 250 mg orally per d (× 2-3 weeks for T tonsurans; × 4-8 weeks for M canis)
• Pediatric considerations: safe
• Griseofulvin, 500 mg orally per d (adults × 4-6 weeks; children, 10-20 mg/kg/d × 6-8 weeks)
• Selenium sulfate shampoo may hasten eradication of the organism
• For highly inflamed kerions, a short course of prednisone should be considered
• Antibiotics as indicated
• Same as for tinea capitis
• Same as for tinea capitis
Each cream is applied twice daily to the affected area for 2-3 weeks (use for 1 week beyond resolution)
• Pediatric considerations: these are safe in children dosed twice daily
• Terbinafine, 250 mg orally once per d × 2-3 weeks
If highly inflammatory zoophilic infection, extended oral therapy may be indicated
• For highly inflamed kerions, a short course of prednisone should be considered
Tinea Cruris or Pedis
• Same as tine corporis
• Undecylenic acid or tolnaftate or haloprogin topical cream twice per d for 2-3 weeks
• Avoid tight clothing
• Avoid occlusive shoes
• Dry feet thoroughly
• Selenium sulfide lotion 2.5% (Selsun or Exsel) applied from base of scalp to knees for 10 min each day for 7 d (topical treatment used only for limited disease, but with high recurrence rates)
• Pediatric considerations:selenium sulfide lotion safe with same schedule of application
• Itraconazole, 200 mg orally once daily for 5-7 d
• Ketoconazole, 400 mg oral single dose or 200 mg orally for 7 d
• Fluconazole, 400 mg oral single dose (repeat in 1 week)
• Hot laundering of clothing may reduce recurrence rate
Tinea Unguium (Onychomycosis)
• Terbinafine, 250 mg orally daily ×6 weeks for fingers and ×12 weeks for toes
• Pulse dosing: 500 mg daily ×1 week/month for 4 months for toes and 2 months for fingers
• Pediatric considerations: safe in children
• Fluconazole, 150-300 mg orally each week ×3-6 months for fingers or ×6-12 months for toes
• Itraconazole, 200 orally four times per d ×3 months for toes
• Pulse dosing: 200 mg orally twice daily ×1 week per month ×2 months for fingers
• Keep nails short and clean, clipped straight
• Use cotton gloves for dry manual work and vinyl gloves for wet work
• Change instruments between care of normal and infected nails
• Use antifungal foot and shoe powder
BOX 2. Prevention & Control of Dermatophytoses
• Identify and avoid exposures to animals or fomites suspected of harboring dermatophytes
• Boil or wash clothing using a commercial facility
• Disinfect public shower and bathing areas
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