Superficial fungal infections attack the epidermis, mucosa, nails, and hair, and are divided into two groups: molds (e.g. dermatophytes) and yeasts (e.g. Candida). Superficial dermatophyte infections are named according to the body site affected: tinea capitis (scalp), tinea corporis (body), tinea cruris (groin) and tinea pedis (feet). Fungal infections invariably cause itching; the skin may be dry and scaly or in flexural areas, softening of the skin can occur.
Diagnosis of Tinea infection is done by the following methods:
Although microscopic evaluation of skin samples of scale does not allow for the identification of the species or characterization of the susceptibility profile, it is used as a quick and inexpensive bedside tool to provide evidence of dermatophyte infection. In infections involving the skin, hair or nails, specific fungal structures (septa and hyphae) are visualized under microscopic examination with 10%–20% Potassium Hydroxide preparation. All superficially infecting dermatophytes appear identical when visualized in this manner. Because Potassium Hydroxide examination may not be able to give a positive result in up to 15% of cases, patients suspected of having dermatophyte infection on clinical impressions are usually treated. Culture confirmation is considered whenever systemic treatment is warranted, such as in the case of tinea capitis.
Scale from the skin is collected by scraping the involved area with a dull edge outward from the advancing margins. Full-thickness nail clippings involve as much of the destroyed portion as possible without causing injury. Hairs are plucked (not cut), placed on a glass slide and prepared with 10%–20% Potassium Hydroxide and covered with a coverslip.
The identification of species of superficial fungi is based on macroscopic, microscopic and metabolic characteristics of the organism. While some dermatophytes are readily identified on the basis of their primary isolation cultures, most require further differentiation through sub-cultures on specific media (identification culture) or through specific biochemical tests.
Sabouraud’s dextrose agar (SDA) is the most commonly used isolation medium for dermatophytes and it serves as the medium on which most morphologic descriptions are based. Elimination of contaminant molds, yeast and bacteria are achieved by the addition of specific antibiotics to the medium making it highly selective for the isolation of dermatophytes. Cultures are incubated at room temperature (20°C–25°C) for at least 4 weeks before being finalized as no growth.
Identification of isolated fungi is facilitated by subculture on specific media such as potato dextrose agar (PDA) that stimulate spore formation, production of pigment and development of typical shapes. Finally, dermatophytes may be differentiated further by their ability to grow on specialized mediums or require nutritional supplementation for growth.
Skin biopsy is not often employed in the workup of typical dermatophyte infection. Localized eruptions suspected to represent dermatophyte infection with equivocal Potassium Hydroxide examination are often treated despite the lack of confirmation. A biopsy may confirm the diagnosis when a systemic agent is being considered for the treatment of a recalcitrant or a more widespread eruption. The biopsy may be used to aid in the diagnosis of Majocchi’s granuloma in which Potassium hydroxide examination of scale on the surface may more often be negative. The biopsy is also sometimes useful in confirming the presence of specific fungal structures involving hair shafts on the scalp in tinea capitis, although culture is necessary to allow species identification of the organism. Special stains highlight special structures that may otherwise be subtle in an appearance on routine staining. Whereas culture is the most specific test for fungal nail infection, special stain examination of nail clippings is the most sensitive and it obviates the need to wait weeks for a result.
Examination of involved hair-bearing areas, such as the scalp or beard, with a Wood’s lamp, may reveal fluorescence of hair infected with particular fungal organisms. Hairs that fluoresce should be selected for further examination, including culture. While ectothrix organisms fluoresce on Wood’s light examination, the endothrix organisms do not fluoresce.
Tinea Infections:
The specific types are described below:
Tinea capitis describes a fungal (dermatophyte) infection of hair and scalp, typically caused by Trichophyton and Microsporum species, with exception of Trichophyton concentricum.
Epidemiology:
Tinea capitis is most commonly observed in children between 3 and 14 years of age. The fungistatic (growth inhibition of fungi) effect of fats in sebum may help to explain the sharp decrease in incidence after puberty. The overall prevalence of the carrier state is around 4% in the United States with a peak prevalence of approximately 13% in girls of Sub-Saharan African American descent. In general, tinea capitis is more common among children of African descent for unknown reasons. Transmission is increased with decreased personal hygiene, overcrowding, and low socioeconomic status. The anthropophilic (preferring human beings) dermatophyte T. tonsurans is the most prevalent species found in the United States, while M. canis remains the most common cause of tinea capitis in Europe. Organisms responsible for tinea capitis have been cultured from fomites (inanimate objects) such as combs, caps, pillowcases, toys and theater seats. Even after shedding, hairs may harbor infectious organisms for more than 1 year. The high prevalence of asymptomatic carriers thwarts the eradication of the disease.
Pathogenesis:
Dermatophytes establish infection skin layers around the follicle (perifollicular) and spread around and into the hair shaft of actively growing (anagen) hairs before descending into the follicle to penetrate the deeper layers. With hair growth, the infected part of the hair rises above the surface of the scalp where it may break because of its increased fragility. Infection of hair by dermatophytes follows 3 main patterns:
In ectothrix infections, only a fungal spore (arthroconidia) on the surface of the hair shaft may be visualized, although hyphae (branching filaments that make up the body of a fungus) are also present within the hair shaft. The cuticle is destroyed. On lamp examination, a yellow-green fluorescence may be detected, depending on the causative organism.
In endothrix infections, fungal spore (arthroconidia) and hyphae remain within the hair shaft and leave the cortex and cuticle intact. This pattern of tinea capitis is associated with the appearance of “black dots” which represent broken hairs at the surface of the scalp. Endothrix organisms do not show fluorescence on the lamp exam.
Favus is characterized by longitudinally arranged hyphae and air spaces within the hair shaft. Arthroconidia are not usually noted in infected hairs.
Symptoms and presentation:
Also called the seborrheic form of tinea capitis since the scale is the predominant feature, noninflammatory tinea capitis is seen most commonly with anthropophilic organisms (human loving). Arthroconidia may form a sheath around affected hairs turning them gray and causing them to break off just above the level of the scalp. Alopecia (spot baldness) may be imperceptible or in more inflammatory cases there may be circumscribed erythematous (red skin due to increased blood flow) scaly patches of nonscarring alopecia with breakage of hairs. This is known as a "gray patch” type. Patches often occur on the back of the head. When involving an ectothrix pattern, infected hairs may exhibit green fluorescence during the lamp exam.
The “black dot” form of tinea capitis is typically caused by the anthropophilic (human loving) endothrix organisms. Hairs that are broken off at the level of the scalp leave behind grouped black dots within patches of alopecia with finger-like margins. Normal hairs also remain within patches of broken hairs. Diffuse scaling is also often present. While “black dot” tinea capitis tends to be minimally inflammatory, some patients may develop pustules (blister containing pus), nodules, or in rare cases kerion—a boggy, inflammatory mass studded with broken hairs and orifices oozing with pus.
The organisms that usually prefer animals other than humans (Zoophilic) or the soil (Geophilic) are more likely to cause an inflammatory type of tinea capitis. Inflammation, which is the result of a hypersensitivity reaction to the infection, in this setting ranges from pustules to furunculosis (a deep infection of the hair follicle leading to accumulation of pus) or kerion. Intense inflammation may also result in scarring alopecia. The scalp is usually itchy or tender. Inflammatory tinea capitis is often associated with lymph node enlargement which serves in differentiating tinea capitis from other inflammatory disorders involving the scalp.
Tinea favosa or favus (Latin, “honeycomb”) is a chronic dermatophyte infection of the scalp rarely involving skin free from hair, and/or nails characterized by thick yellow crusts (scutula) within the hair follicles which leads to scarring alopecia.
Epidemiology:
Favus is usually acquired before adolescence, although it may extend into adulthood. Associated with malnutrition and poor hygiene, favus has become geographically limited over the past century, and it is now seen almost exclusively in Africa, the Middle East and parts of South America. Even in these regions, its incidence has declined dramatically, and studies from South Africa, Libya, and Arabia suggest the disappearance of favus over the last few decades.
Pathogenesis:
Trichophyton schoenleinii is the most common cause of human favus, although T. violaceum and M. gypseum are also rare isolates. Although favus occurs in animals including domesticated birds and mice, there exist only a few reports of humans infected by the pathogens responsible for animal favus.
Symptoms and presentation:
Early favus (first 3 weeks of infection) is characterized by patchy erythema with slight scaling and matting of the hair. Progressive hyphal invasion distends the follicle, first producing a yellow-red swelling and then a yellow crust (scutulum) around a single dry hair that is less brittle than the hair of endothrix infections. The scutulum may reach 1 cm in diameter, engulfing surrounding hairs and coalescing with other scutula to form large adherent mats with an unpleasant cheese-like or musky odor. Over several years, the plaques advance peripherally leaving behind central, dead areas of alopecia.
Epidemiology:
Tinea barbae, as its name would imply, occurs predominantly in males. The incidence of tinea barbae has decreased as improved sanitation has reduced transmission by contaminated barbers’ razors. Direct exposure to cattle, horses, or dogs is now the more common mode of acquisition, and this accounts for a shift in prevalence toward farmers or ranchers in rural settings.
Pathogenesis:
Tinea barbae is most commonly caused by the zoophilic (animal-loving) strains of T. interdigitale, T. verrucosum, and less commonly M. canis. Among the anthropophilic (human-loving) organisms, T. schoenleinii, T. violaceum and certain strains of T. rubrum cause tinea barbae in endemic areas.
Symptoms and presentation:
Tinea barbae affects the face only on one side and involves the beard area more often than the mustache or upper lip. Two forms exist.
Caused by anthropophilic (human-loving) organisms such as T. violaceum, this form of tinea barbae is less inflammatory and resembles tinea corporis or bacterial infection. The active border shows simple and pus-filled swellings accompanied by mild erythema. Alopecia, if present, is reversible.
Usually caused by zoophilic (animal-loving) strains of T. interdigitale or T. verrucosum, inflammatory tinea barbae is the most common clinical presentation. It presents analogously to kerion formation in tinea capitis with boggy-crusted plaques and a pussy discharge. Hairs are lusterless, brittle, and easily pulled to demonstrate a pus-filled mass around the root. Pus-filled swellings may coalesce and eventuate in abscess-like collections of pus, sinuses, and scarring alopecia.
Epidemiology:
Tinea corporis may be transmitted directly from infected humans or animals, via fomites (inanimate objects), or it may occur via autoinfection from reservoirs of fungal colonization on the feet. Children are more likely to contract zoophilic pathogens, especially from dogs or cats. Occlusive clothing and a humid climate are associated with more frequent and severe eruptions. Wearing of occlusive clothing, frequent skin-to-skin contact, and minor traumas such as the mat burns competitive wrestling create an environment in which dermatophytes flourish. “Tinea corporis gladiatorum” is caused most commonly by T. tonsurans, and it occurs most frequently on the head, neck, and arms.
Pathogenesis:
Although any dermatophyte may cause tinea corporis, it is caused most commonly by T. rubrum. T. rubrum is also the most likely candidate in cases with concomitant follicular involvement. Epidermophyton floccosum, T. interdigitale, M. canis, and T. tonsurans are also common pathogens. Tinea imbricata, caused by T. concentricum, is limited geographically to areas of the Far East, South Pacific, and South and Central America.
Symptoms and presentation:
The classic presentation is that of an annular (“ring-worm”-like) or serpiginous (wavy margins) plaque with scale across the entire active erythematous border. The border is vesicular (swellings filled with clear fluid) and advances centrifugally. The center of the plaque is usually scaly but it may exhibit complete clearing. Whereas concentric vesicular rings suggest tinea incognito, often caused by T. rubrum, the erythematous concentric rings of tinea imbricata demonstrate little to no vesiculation. T. rubrum infections may also present as large plaques, especially in immunosuppressed individuals. Majocchi’s granuloma is a superficial and subcutaneous infection involving deeper portions of the hair follicles that presents as scaly follicular swellings that coalesce in an annular arrangement. It is caused most commonly by T. rubrum, T. interdigitale, and M. canis. Majocchi’s granuloma is observed on the legs in women who become inoculated after shaving or who apply topical steroids to the involved area, which facilitates infection. It is also observed increasingly among immunocompromised patients.
Tinea cruris is a fungal infection of the groin, genitalia, pubic area, and perineal and skin around the anus. The designation is a misnomer because in Latin “cruris” means "of the leg". It is the second-most common type of dermatophyte infection worldwide.
Epidemiology:
Much like tinea corporis, tinea cruris spreads via direct contact or fomites, and it is exacerbated by occlusion and humid climates. Autoinfection from distant reservoirs of T. rubrum or T. interdigitale on the feet, for example, is common. Tinea cruris is three times more common in men, and adults are affected more commonly than children.
Pathogenesis:
Most tinea cruris is caused by T. rubrum and E. floccosum, the latter being most often responsible for epidemics. T. interdigitale and T. verrucosum are implicated less commonly.
Symptoms and presentation:
Tinea cruris presents classically as a plaque with well-defined margins and a scaly raised border which extends from the upper margin of the thigh on to the inner thigh, often on both sides. Erythematous scaly patches with fluid-filled swellings involving the inner thighs are also a common but perhaps less obvious presentation. Itching is common, as is pain when plaques are secondarily infected. Plaques in tinea cruris due to E. floccosum are more likely to demonstrate central clearing, and are more often limited to the inner upper thigh. In contrast, plaques in tinea cruris due to T. rubrum coalesce with extension to the pubic, buttock, lower abdominal, and areas around the anus. Genitalia including the scrotum are infrequently affected.
Tinea pedis denotes fungal infection of the feet, whereas tinea manuum involves the palm and area between the fingers. The infection of the backsides of feet and hands is considered to be tinea corporis.
Epidemiology:
Occurring worldwide, tinea pedis and tinea manuum are the most common dermatophyte infections. High prevalence, estimated to be around 10%, is attributed primarily to modern occlusive footwear, although increased worldwide travel has also been implicated. The incidence of tinea pedis is higher among those using communal baths, showers or pools. With the ubiquitous presence of dermatophytes in the environment, however, it may be that host factors such as an individual’s immune response to dermatophytes, in addition to exposure, play a determining role in the acquisition of tinea pedis. Tinea manuum is acquired through direct contact with an infected person or animal, the soil, or via autoinoculation. Most commonly only one hand is involved, concomitant with infection of feet and toenails for which the term “two feet–one hand” syndrome has been coined. This classic presentation of tinea manus represents a secondary infection of the hand acquired from repetitive scratching and picking infected feet and toenails. Tinea manuum should be suspected in individuals who have fine dry scaling of the palm or palms, often accentuated in the creases.
Pathogenesis:
Tinea pedis and tinea manuum are caused predominantly by T. rubrum (most common), T. interdigitale, and E. floccosum.
Symptoms and presentation:
Tinea pedis may present as any of four forms, or combinations thereof.
The most common presentation of tinea pedis begins as scaling and erythema of the skin between and beneath the fingers of the feet, and in particular between the third and fourth, and fourth and fifth toes. Under appropriate conditions, the infection will spread to the adjacent sole or instep, but it rarely involves the upper side. Occlusion and bacterial coinfection soon produce the erosions between the fingers with itching and malodor that are characteristic of the dermatophyte infection complex, or “athlete’s foot.”
In chronic hyperkeratotic type tinea pedis, there is patchy or diffuse scaling on the soles and the outer and inner aspects of the feet, in a distribution similar to a moccasin shoe on a foot. The degree of erythema is variable, and there may also exist a few minute fluid-filled swellings that heal with bands of scale less than 2 mm in diameter. The most common pathogen is T. rubrum followed by E. floccosum and human-loving strains of T. interdigitale.
Vesiculobullous type of tinea pedis, typically caused by animal preferring strains of T. interdigitale, features tense vesicles larger than 3 mm in diameter, fluid and pus-filled swellings on the soles and area around the sole areas. This type of tinea pedis is uncommon in childhood but has been caused by T. rubrum.
Tinea pedis with animal preferring strains of T. interdigitale along with rampant bacterial infection produces fluid and pus-filled swellings along with pussy ulcers on the sole. Enlargement of lymph nodes and fever are frequently associated. Vesiculobullous and ulcerative types commonly produce a specific reaction, either on the outer foot or toes, or on the outer aspects of the fingers. Tinea manus, dermatophyte infection of the hand, usually has a noninflammatory presentation with diffuse dry scaling and accentuation in the creases. However, fluid and pus-filled swellings and exfoliation may be present, especially when animal-preferring dermatophytes are involved. Tinea manus commonly occurs in association with moccasin shoe type tinea pedis and fungal infection of the nails (onychomycosis), which should also be treated to minimize relapse.
Tinea nigra is a superficial dermatophyte infection caused by dematiaceous, darkly pigmented, Hortaea werneckii.
Epidemiology:
Tinea nigra occurs in tropical or subtropical areas, including Central and South America, Africa, and Asia. Its incidence is low in the United States and Europe. While the majority of the approximately 150 North American cases reported since 1950 were associated with tropical travel, endemic foci exist in the coastal southeastern United States and in Texas. Person-to-person transmission is rare. Tinea nigra has a female/male predilection of 3:1.
Pathogenesis:
Tinea nigra is almost always caused by H. werneckii, although other dematiaceous fungi such as Stenella araguata may produce the same picture. These fungi are commonly found in soil, sewage, and decaying vegetation. Tinea nigra arises after trauma to the skin, subsequent inoculation and a typical incubation period of 2–7 weeks.
Symptoms and presentation:
Tinea nigra is found on otherwise healthy people and presents typically as an asymptomatic, mottled brown to greenish-black patch with minimal to no scale on the palms or soles. The patch is often darkest at the advancing border. Because of its coloration and location on palms and soles, tinea nigra is frequently misdiagnosed as a melanoma.
Onychomycosis describes a fungal infection of the nail caused by dermatophytes or non-dermatophyte molds. Tinea unguium refers strictly to dermatophyte infection of the nail.
Epidemiology:
Onychomycosis is the most prevalent nail disease and accounts for approximately 50% of all causes of nail destruction by fungal infections. It affects up to 14% of the population with both an increasing prevalence among older individuals and an overall increasing incidence. Onychomycosis is also increasing in incidence among children and adolescents and accounts for up to 20% of dermatophyte infections diagnosed in children. Risk factors for nail infection include nail trauma, immunosuppression such as HIV infection, diabetes mellitus, and vascular disease. The increasing prevalence of this disease may be secondary to wearing of tight shoes, increasing numbers of individuals on immunosuppressive drugs, and increased use of communal locker rooms. The dermatophyte infection commonly begins as tinea pedis before extending to the nail bed, where eradication is more difficult. This site serves as a reservoir for local recurrence or for infections spreading to other areas. Up to 40% of patients with toenail onychomycosis show concomitant skin infections, most commonly tinea pedis (30%).
Pathogenesis:
In the majority of cases, onychomycosis is caused by dermatophytes, and T. rubrum and T. interdigitale are responsible for approximately 90% of all cases. T. tonsurans and E. floccosum are also well-documented causative agents. Yeast and non-dermatophyte molds are the sources of approximately 10% of toenail onychomycosis.
Symptoms and presentation:
DLSO is the most common form of onychomycosis and may be caused by any of the organisms listed above. It begins with the invasion of the nail bed, forming a whitish to brownish-yellow opacification at the edge of the nail. The infection then spreads up the nail bed.
PSO results from infection of the proximal nail fold primarily with T. rubrum and is apparent as a white to beige opacity on the nail. This opacity gradually enlarges to affect the entire nail and eventuates in the breakdown and/or destruction of the entire nail. Patients with PSO should be screened for HIV, as PSO has been considered a marker for this disease.
WSO results from direct invasion of the nail resulting in white to dull yellow sharply bordered patches anywhere on the surface of the toenail. It is usually caused by T. interdigitale.
Multiple systemic and topical antifungal agents are available to treat dermatophyte infection of skin, hair and nails.
Infections involving hair-bearing skin usually necessitate oral antifungal treatment since dermatophytes penetrating the follicle are usually out of reach for topically applied agents. Griseofulvin along with the terbinafine and oral itraconazole and fluconazole are considered safe and effective in the treatment of tinea capitis.
Griseofulvin:
Griseofulvin along with terbinafine in patients older than 4 years are oral treatments for tinea capitis approved by the US Food and Drug Administration. The previous pediatric recommendation was divided doses for 6–8 weeks taken with a fatty meal to facilitate absorption. However, high failure rates with this regimen resulted in the current dosage recommendation of griseofulvin is divided doses for 8 weeks. Although the current recommendation is not based on outcomes of controlled trials, the collective clinical experience suggests its high therapeutic efficacy. Disadvantages of griseofulvin include poor compliance related to the length of treatment and its bitter taste in liquid form. Common side effects include sensitivity to light, headache, and gastrointestinal upset.
Terbinafine:
Terbinafine can cure Trichophyton tinea capitis in 2–4 weeks; however, 4–8 weeks of treatment may be required for eradication of Microsporum. Two studies have confirmed the increased efficacy of terbinafine in the treatment of T. tonsurans infection with significantly higher cure rates compared to lower dose griseofulvin. However, even at this lower dose range, griseofulvin showed significantly higher cure rates for M. canis infections. Further, it is not clear that terbinafine has a therapeutic advantage in curing tinea capitis over the higher dose regimen of griseofulvin. Terbinafine may cause gastrointestinal upset. As with itraconazole, there are reports of liver failure in patients using terbinafine.
Itraconazole:
With daily doses over 2–4 weeks, itraconazole effectively eradicates tinea capitis caused by either Microsporum or Trichophyton. Possible adverse effects of itraconazole include gastrointestinal upset, diarrhea with the liquid formulation, and swelling of arms and feet, especially when used in conjunction with some other drugs. Itraconazole is better absorbed in the presence of food. On the contrary, antacids may decrease the absorption of itraconazole. Like with fluconazole, liver toxicity with itraconazole occurs at lower rates than with ketoconazole.
Fluconazole:
Available as both tablets and a pleasant-tasting liquid, fluconazole for 20 days is effective in curing tinea capitis. Absorption of fluconazole is not affected by food intake and antacids, and gastrointestinal side effects are less common. Hepatitis has been reported but it occurs less frequently than with ketoconazole.
Adjuvant Therapy:
Selenium sulfide, zinc pyrithione, povidone-iodine, and ketoconazole are shampoo preparations that help eradicate dermatophytes from the scalp of children. Adjunctive use of these shampoos is recommended 2–4 times weekly for 2–4 weeks. The use of ketoconazole shampoo or selenium sulfide three times weekly by all household members also reduces transmission by decreasing the shedding of spores.
Oral steroids may reduce the incidence of scarring associated with markedly inflammatory varieties of tinea capitis. Although there is no consistent evidence for improved cure rates with use of oral steroids, they appear to relieve pain and swelling associated with infections.
Like tinea capitis, an oral antifungal is usually necessary for the treatment of tinea barbae. Griseofulvin twice daily for 6 weeks, terbinafine daily for 2–4 weeks, itraconazole daily for 2–4 weeks, and fluconazole daily for 4–6 weeks are regimens that have been used effectively. Systemic steroids used for the first week of therapy are helpful in cases with severe inflammation.
For isolated plaques on the skin without hair, topical terbinafine, ketoconazole, miconazole, and clotrimazole are effective. Most are applied twice daily for 2–4 weeks. Oral antifungal agents are reserved for widespread or more inflammatory eruptions. Safe and effective regimens for children include terbinafine daily for 2 weeks, itraconazole daily for 1 week, and Griseofulvin daily for up to 2–4 weeks.
Mild tinea pedis between the fingers and toes without bacterial involvement is treated topically with terbinafine, ketoconazole, miconazole, and clotrimazole. Terbinafine cream applied twice daily for 1 week is effective in 66% of cases. The dosing schedule of oral terbinafine is one tablet daily for 2 weeks. Itraconazole in adults is given daily for 1 week, whereas itraconazole in children is administered daily for 2 weeks. Fluconazole weekly for 3–4 weeks is also effective. Topical or systemic steroids may be helpful for symptomatic relief during the initial period of antifungal treatment of vesiculobullous tinea pedis. Itching, bad smell, and softening of skin obligate a search for bacterial coinfection. Patients suspected of having bacterial coinfections should be treated with a topical or systemic antibacterial agent based on the culture and sensitivity report. Associated onychomycosis is common; if present, more durable treatment of the onychomycosis is necessary to prevent the recurrence of tinea pedis. Newer oral antifungal agents have replaced griseofulvin as the treatments of choice for severe or refractory tinea pedis when this infection is also accompanied by onychomycosis.
Tinea nigra responds readily to topical therapy with Whitfield’s ointment, salicylic acid, tincture of iodine, or topical antifungal. Treatment is continued for 2–4 weeks after clinical resolution in order to prevent relapse. Although oral ketoconazole, itraconazole, and terbinafine are also effective, systemic therapies are rarely indicated.
The management of onychomycosis depends on several factors including the severity of nail involvement, associated tinea pedis, along with efficacy and potential adverse effects of any treatment regimen. While it seems reasonable not to treat minimal nail involvement, concurrent tinea pedis should always be treated, particularly in the setting of diabetes mellitus, to prevent further bacterial infection.
Topical Therapy:
In those patients with nail involvement and/or contraindication for oral treatment, topical therapy should be considered. Ciclopirox applied daily for 48 weeks achieved cure in 29%–36% of cases and clear nails in 7% of mild to moderate cases of onychomycosis caused by dermatophytes. Despite its much lower efficacy compared with oral antifungal agents, the use of topical ciclopirox avoids the risk of drug interactions. Amorolfine applied twice weekly is another agent specifically prepared for use as a drug to applied to nails. Amorolfine has higher mycologic cure rates (38%–54% after 6 months of treatment) compared to ciclopirox.
Systematic therapy:
An oral antifungal is required for onychomycosis involving the deeper areas of the nail, or when a shorter treatment regimen or a higher chance for clearance or cure is desired. The selection of the antifungal agent is based primarily on the causative organism, the potential adverse effects, and the risk of drug interactions in any particular patient.
Terbinafine inhibits fungal growth and kills alive dermatophytes and Aspergillus. Terbinafine is not recommended for candida onychomycosis since it demonstrates variable efficacy against Candida species. A course of terbinafine daily for 6 weeks is effective for most fingernail infections, while a minimum 12-week course is required for toenail infections. Most adverse effects are gastrointestinal such as diarrhea, nausea, taste disturbance, and liver toxicity. A 3-month continuous regimen of terbinafine is the most effective oral treatment for onychomycosis of the toenails available today. Clinical cure rates among different studies are approximately 50%, although the success rate is lower in patients over 65 years.
Itraconazole inhibits growth in dermatophytes, non-dermatophyte molds, and yeasts. Safe and effective schedules include pulse dosing with itraconazole daily for 1 week per month or a continuous dose daily, both of which require 2 months or 2 pulses of treatment for fingernails and at least 3 months or 3 pulses for toenails. Liver toxicity occurs in 0.3%–5% of patients during therapy and returns to normal within 12 weeks of discontinuation. Although itraconazole has a broader spectrum of activity than terbinafine, it has a significantly lower rate of cure (about 25% vs. 50%) and a higher relapse rate (about 50% vs. 20%) compared to terbinafine.
Fluconazole is fungistatic against dermatophytes, some non-dermatophyte molds, and Candida. The usual regimen for fluconazole is once weekly for 3–12 months. Griseofulvin is no longer considered standard treatment for onychomycosis because of its prolonged treatment course, potential for adverse effects and drug interactions, and its relatively low cure rates.
Combination therapy regimens may have a higher clearance rate than either oral or topical treatments alone. Thymol 4% prepared in ethanol may be used as drops applied to the nail. The application to nails of commercially available topical preparations with thymol, such as Vicks VapoRub™, has anecdotally led to success. Final options for refractory cases include surgical avulsion or chemical removal of the nail with urea compounds in combination with topical or oral antifungals.
The most important step to prevent a tinea infection is to keep your skin dry and clean.
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