Section F: Fungal

PATIENT STORY

A 55-year-old woman presents with a red pruritic area on her face for 3 months (Figure 141-1). The annular distribution immediately is suspicious for a dermatophyte infection. Further investigation demonstrates that the patient has severe tinea pedis in a moccasin distribution. The patient is treated with an oral terbinafine 250 mg daily for 1 month and her fungal infection clears completely.

INTRODUCTION

Fungal infections of the skin and mucous membranes are ubiquitous and common. There are many types of fungus that grow on humans, but they all share a predilection for warm and moist areas. Consequently, hot and humid climates promote fungal infections, but many areas of the skin can get warm and sweaty even in cold climates, such as the feet and groin.

SYNONYMS

Pityriasis versicolor equals tinea versicolor.

PATHOPHYSIOLOGY

Mucocutaneous fungal infections are caused by:

• Dermatophytes in three genera: Microsporum, Epidermophyton, and Trichophyton. There are approximately 40 species in the three genera, and these fungi cause tinea pedis and manus, tinea capitis, tinea corporis, tinea cruris, tinea faciei, and onychomycosis (Figures 141-1, 141-2, 141-3, 141-4, 141-5, 141-6).

• Yeasts in the genera of Candida and Pityrosporum (Malassezia)—There are also multiple types of Candida species. Pityrosporum is the cause of seborrhea and tinea versicolor (Figures 141-7 and 141-8). Although tinea versicolor has the name tinea in it, it is not a true dermatophyte and may be best called pityriasis versicolor.

DIAGNOSIS

CLINICAL FEATURES OF TINEA INFECTIONS

Scaling, erythema, pruritus, central clearing, concentric rings, and maceration (Table 141-1). Changes in pigmentation are not uncommon in various types of tinea, especially tinea versicolor.

• Figure 141-1 shows tinea faciei on the face with typical scaling and ringlike pattern; hence the name ringworm. There is also erythema and central clearing. The patient was experiencing pruritus.

• Figure 141-2 shows annular pruritic lesion with concentric rings in the axilla of a young woman caused by tinea corporis. The concentric rings have a high specificity (80%) for tinea infections.

• Note that tinea infections will not show central clearing in 58% of cases, as in Figure 141-3 in which tinea cruris has no central clearing.

• Post-inflammatory hyperpigmentation is common in skin of color, as seen in Figure 141-4. Note that the hyperpigmentation is seen within the area affected by the tinea corporis.

• Hypopigmentation is frequently seen in tinea versicolor (Figure 141-8).

TYPICAL DISTRIBUTION

Literally found from head to toes:

• Figure 141-5 shows tinea capitis in a 5-year-old black girl with hair loss and an inflammatory response. Her kerion (inflammatory response to tinea) is healing with oral griseofulvin.

• The two-foot, one-hand syndrome is a curious phenomenon with tinea manus of one hand and tinea pedis of both feet (Figure 141-6). It is not clear why only one hand is involved in these cases. In this case it was the nondominant hand, but either hand can be involved.

LABORATORY STUDIES

Creating a KOH prep:

• Scrape the leading edge of the lesion on to a slide using the side of another microscope slide or a #15 scalpel (Figure 141-9). (Online video by Dr. Usatine https://www.youtube.com/watch?v=LUwNQI_0BWU&t=2s.)

• Use your coverslip to push the scale into the center of the slide.

• Add one to two drops of KOH (or fungal stain) to the slide and place coverslip on top.

• Fungal stains that come with KOH and a surfactant in the solution are very simple to use. These inexpensive stains come in small plastic squeeze bottles that have a shelf life of 1 to 3 years. Two useful stains that can that make it easier to identify fungus are chlorazol and Swartz Lamkins stains. Swartz Lamkins stain has a longer shelf life and is my preferred stain.

• Consider also gently heating with flame from a lighter. Avoid boiling. This helps to speed up the dissolution of the human cells and make the fungal elements visible more rapidly. This is not always needed and is most beneficial in KOH preparations done from nails and when the skin scrapings are thicker.

• Examine with microscope starting with 10× power to look for the cells and hyphae and then switch to 40× power to confirm your findings (Figures 141-10, 141-11, 141-12, 141-13). The fungal stain helps the hyphae stand out among the epithelial cells.

• It helps to start with 10× power to find the clumps of cells and look for groups of cells that appear to have fungal elements within them (see Figure 141-10).

• Don't be fooled by cell borders that look linear and branching. True fungal morphology at 40× power should confirm that you are looking at real fungus and not artifact. The fungal stains bring out these characteristics, including septae and nuclei (see Figures 141-11, 141-12, 141-13).

• KOH test characteristics (without fungal stains)—Sensitivity 77% to 88%, specificity 62% to 95% (Table 141-2).¹ The sensitivity and specificity should be higher with fungal stains and the experience of the person performing the test.

OTHER LABORATORY STUDIES

• Fungal culture—Send skin scrapings, hair, or nail clippings to the laboratory in a sterile urine cup. These will be plated out on fungal agar and the laboratory can report the species if positive.

• Biopsy specimens (or nail clippings) can be sent in formalin for periodic acid–Schiff (PAS) staining when KOH and fungal cultures seem to be falsely negative.

• UV light (Wood lamp), looking for fluorescence. The Microsporum species are most likely to fluoresce. However, the majority of tinea infections are caused by Trichophyton species that do not fluoresce.

MANAGEMENT

There is a wide variety of topical antifungal medications (Table 141-3). A Cochrane systematic review of 70 trials of topical antifungals for tinea pedis showed good evidence for efficacy compared to placebo² for:

• Allylamines (naftifine, terbinafine, butenafine).

• Azoles (clotrimazole, miconazole, econazole).

• Allylamines cure slightly more infections than azoles but are more expensive.²

• No differences in efficacy found between individual topical allylamines or individual azoles.² SORⒶ

There is some evidence that topical ciclopirox olamine and butenafine may help treat onychomycosis, but they both need to be applied daily for at least 1 year.³

Oral antifungals are needed for all tinea capitis infections and for more severe infections of the rest of the body.^4,5 True dermatophyte infections that do not respond to topical antifungals may need an oral agent.

• A Cochrane systematic review of 15 trials of oral antifungals for tinea pedis showed oral terbinafine more effective than oral griseofulvin.⁶ SORⒶ

• Terbinafine and itraconazole are more effective than no treatment for tinea pedis.⁶ SORⒶ

• There were no significant differences in comparisons between a number of other oral agents.⁶

Oral antifungals used for fungal infections of the skin, nails, or mucous membranes:

• Itraconazole (Sporanox).

• Fluconazole (Diflucan).

• Griseofulvin.

• Ketoconazole (Nizoral). FDA recommended limited use of oral ketoconazole in 2013 due to potentially fatal liver injury, risk of drug interactions, and adrenal gland problems. In that same year Australia and Europe removed oral ketoconazole from their markets due to concerns over increased liver toxicity, drug interactions, and endocrinologic side effects. These concerns do not apply to topical ketoconazole.^7-9

Given that there are better, safer, and less expensive alternatives to oral ketoconazole, we do not recommend its use in the treatment of fungal skin infections.

• Terbinafine (Lamisil).

A number of studies and meta-analyses suggest that terbinafine is more efficacious than griseofulvin in treating tinea capitis caused by Trichophyton species, whereas griseofulvin is more efficacious than terbinafine in treating tinea capitis caused by Microsporum species.^4,10 SORⒶ

Details of treatments for multiple types of fungal skin infections are supplied in the subsequent chapters.

REFERENCES

PATIENT STORY

A 42-year-old man (Figure 142-1) was admitted to the hospital for community-acquired pneumonia and type 2 diabetes out of control. On the second day of admission, when he was feeling a bit better, he asked about the itching he was having on his penis. Physical examination revealed an uncircumcised penis with white discharge on the glans and inside the foreskin consistent with Candida balanitis. KOH prep was positive for the pseudohyphae of Candida. The patient was treated with a topical azole and the balanitis resolved.

INTRODUCTION

Cutaneous and mucosal Candida infections are seen commonly in persons with obesity, diabetes, hyperhidrosis, and/or immunodeficiency.

SYNONYMS

Perlèche = angular cheilitis.

EPIDEMIOLOGY

Candida thrush is common in normal infants and in adults may be a sign of immunosuppression (Figure 142-2).

Candida balanitis is more common in uncircumcised men than in those who have been circumcised (Figure 142-1).

ETIOLOGY AND PATHOPHYSIOLOGY

• Infections caused by Candida species are primarily Candida albicans.¹

• C. albicans has the ability to exist in both hyphal and yeast forms (termed dimorphism). If pinched cells do not separate, a chain of cells is produced and is termed pseudohyphae.¹

RISK FACTORS

Obesity, diabetes, hyperhidrosis, immunodeficiency, HIV, heat, use of oral antibiotics, and use of inhaled or systemic steroids.¹

DIAGNOSIS

CLINICAL FEATURES

• Typical distribution—Groin, glans penis, vulva, inframammary, under abdominal pannus, between fingers, in the creases of the neck, corners of mouth, nail folds in chronic paronychia.

• Morphology—Macules, patches, plaques that are pink to bright red with small peripheral satellite lesions.

• Candidiasis of the nipple in the nursing mother is associated with infantile thrush (Figures 142-2 and 142-3). Nipple candidiasis is almost always bilateral, with the nipples appearing bright red and inflamed. In this case, the inflammation was made worse by the application of a topical antibiotic that caused a secondary contact dermatitis.

• Candida infection in the corners of the mouth is called perlèche or angular cheilitis (Figure 142-4). When accompanied by thrush it may be a sign of HIV/AIDS.

• Thrush can be caused be Candida growing on the upper plate of a denture and the roof of the mouth (Figure 142-5).

• Ask about recent antibiotic use if there is a new onset of a rash with satellite lesions. In Figure 142-6, the man with diabetes had a course of antibiotics before he developed a Candida infection in his groin.

LABORATORY STUDIES

Scrape involved area and add to a slide with KOH (DMSO optional). C. albicans exists in both hyphal and yeast forms (dimorphism). Look for pseudohyphae and/or budding yeast (Figure 142-7).

DIFFERENTIAL DIAGNOSIS

• Intertrigo is a nonspecific inflammatory condition of the skin folds. It is induced or aggravated by heat, moisture, maceration, and friction. The condition frequently is worsened by infection with Candida or dermatophytes (Figures 142-8 and 142-9). In Figure 142-8 there is significant hyperpigmentation secondary to the inflammation.

• Tinea corporis or cruris—Can be distinguished from Candida when you see an annular pattern or concentric circles in the tinea (Figure 142-9). There is no scrotal involvement in tinea cruris. Candida intertrigo may have scrotal involvement (see Chapters 144, Tinea Corporis, and 145, Tinea Cruris).

• Erythrasma—May be brown and glows a coral red with UV light (see Chapter 125, Erythrasma).

• Inverse psoriasis—Psoriasis in the intertriginous areas as seen in Figure 142-10 (see Chapter 158, Psoriasis).

• Seborrhea—Inflammation related to overgrowth of Pityrosporum, a yeast-like organism (see Chapter 157, Seborrheic Dermatitis).

MANAGEMENT

PRIMARY CANDIDAL SKIN INFECTIONS

• Topical azoles, including clotrimazole, miconazole, and nystatin (polyenes), are effective.² SORⒷ

• Keeping the infected area dry is important.³ SORⒸ

• For more details of the topical antifungals, see Table 141-3 in Chapter 141, Fungal Overview.

• In one study, miconazole ointment was well tolerated and significantly more effective than the zinc oxide/petrolatum vehicle control for treatment of diaper dermatitis complicated by candidiasis.²

• Do not use tolnaftate, which is active against dermatophytes but not Candida.

• If recurrent or recalcitrant, consider fluconazole 150 mg/wk for 2 weeks.

OROPHARYNGEAL CANDIDIASIS

• Treat initial episodes with clotrimazole troches (one 10-mg troche 5 times per day for adults) or nystatin (available as a suspension of 100,000 U/mL [dosage, 4 to 6 mL qid] or as flavored 200,000 U pastilles [dosage, 1 or 2 pastilles 4 to 5 times per day for 7 to 14 days]).³ SORⒷ

• Oral fluconazole (100–200 mg/day for 7 to 14 days) is as effective as—and, in some studies, superior to—topical therapy.³ SORⒶ

• Itraconazole solution (200 mg/day for 7 to 14 days) is as effective as fluconazole.³ SORⒶ

• Ketoconazole and itraconazole capsules are less effective than fluconazole, because of variable absorption.³ SORⒶ

• Fluconazole-refractory oropharyngeal candidiasis will respond to oral itraconazole therapy (>200 mg/day, preferably in solution form) approximately two thirds of the time.³ SORⒶ

• Children with thrush are usually treated with oral nystatin suspension.³ SORⒷ

• HIV/AIDS patients with oral candidiasis may be treated with clotrimazole troches. If unresponsive to topical therapy, fluconazole may be needed.³ SORⒶ

• Denture-related disease may require extensive and aggressive disinfection of the denture for definitive cure.³ SORⒸ

MAMMARY CANDIDIASIS IN BREASTFEEDING

• Most mammary candidiasis does not present with the red breasts seen in Figure 142-3.

• Nipple pain and discomfort along with thrush are adequate data to treat the mother and child.

• Topical nystatin and oral fluconazole are safe for infants and the mother.³

CHRONIC MUCOCUTANEOUS CANDIDIASIS

• Chronic mucocutaneous candidiasis (Figure 142-11) requires a long-term approach that is analogous to that used in patients with AIDS.³

• Systemic therapy is needed, and azole antifungal agents (fluconazole and itraconazole) have been used successfully.³

• As with HIV-infected patients, development of resistance to these agents has been described.³

PATIENT EDUCATION

Keep the infected area clean and dry. For thrush in a baby, treat sources of infection such as the mother's breasts and bottle nipples. If the baby is bottle fed, boil the nipples between uses.

REFERENCES

PATIENT STORY

An 11-year-old boy has a history of 2 months of progressive patchy hair loss (Figure 143-1). He has some itching of the scalp, but his mother is worried about his hair loss. Physical examination reveals alopecia with scaling of the scalp and broken hairs looking like black dots in the areas of hair loss. A KOH preparation is created by using a #15 scalpel to scrape some scale and small broken hairs onto a slide. With the help of a fungal stain and KOH, branching septate hyphae are seen under the microscope. The most likely cause of this tinea capitis is Trichophyton tonsurans; therefore 4 weeks of oral terbinafine is prescribed. The tinea capitis fully resolves and the hair does grow back over time.

INTRODUCTION

Tinea capitis is a fungal infection involving the scalp and hair. Common signs include hair loss, scaling, black dots, erythema, and impetigo-like plaques.

SYNONYMS

Ringworm of the scalp.

EPIDEMIOLOGY

• Tinea capitis is the most common type of dermatophytoses in children younger than 10 years (Figures 143-1, 143-2, 143-3, 143-4, 143-5). It is much less common after puberty or in adults. The infection has a worldwide distribution.

• Tinea capitis is more common in young African-American children.¹ Boys are infected more often than girls.¹

• Combs, brushes, couches, and sheets may harbor the live dermatophyte for a long period of time.

• Spread from person to person with direct contact or through fomites (especially Trichophyton tonsurans).

• Occasionally spread from cats and dogs to humans (especially Microsporum species).

ETIOLOGY AND PATHOPHYSIOLOGY

• Tinea capitis is a superficial fungal infection affecting hair shafts and follicles on the scalp.

• Caused by Trichophyton and Microsporum dermatophytes. The most common organism in the United States is Trichophyton tonsurans, which is associated with black dot alopecia.¹ Microsporum canis is less common in the United States now than decades ago. M. canis is still highly prevalent in developing countries and parts of Europe.² The natural reservoir of M. canis is dogs and cats.

RISK FACTORS

• Lack of access to clean water and soap, especially in developing countries.²

• Poverty—rural and urban.¹

• African descent, as the dermatophytes grow well in the follicles of short curly hairs.¹

• Crowded living arrangements in which infected individuals spread the tinea to others.

• Sharing combs, brushes, and hair ornaments.

• Wrestling (tinea capitis gladiatorum).

DIAGNOSIS

• The clinical appearance may be classic, but consider looking at the scalp with an ultraviolet light (Wood lamp), looking for fluorescence (see more detail under Laboratory).

• A positive KOH prep can confirm the diagnosis within a setting that has access to a microscope. A KOH preparation is created by using a #15 scalpel or the edge of another slide to scrape some scale and broken hairs onto a slide. Apply 1 to 2 drops of KOH (preferably with a fungal stain) to the slide and add a coverslip (see online video by Dr. Usatine under Provider Resources). Look for septate hyphae and arthroconidia (fungal spores) (Figure 143-6). Look for invasion of the hair shaft with fungus.

CLINICAL FEATURES

• Alopecia and scaling of the scalp (see Figures 143-1 and 143-2).

• A kerion occurs when there is an inflammatory response to the tinea. The scalp gets red, swollen, and boggy. There may be serosanguinous discharge and some crusting as this dries (see Figure 143-3).

• There may be broken hairs that look like black dots in the areas of hair loss (see Figure 143-4). This is especially common with T. tonsurans.

• Cervical lymphadenopathy occurs commonly with tinea capitis (see Figure 143-5).

• Tinea capitis can even be annular, as the name "ringworm" of the scalp implies (see Figure 143-6).

TYPICAL DISTRIBUTION

By definition it occurs on the head, but usually is found on the scalp. Rarely involves the eyebrows and eyelashes.

LABORATORY STUDIES

Whenever possible it is very important to confirm or dispel one's clinical suspicion with mycologic evidence before starting weeks of oral antifungal medicines.

• KOH preparation—Scrape the scale and infected hairs using a #15 blade. Apply KOH or a fungal stain to the slide. Use the microscope to look for septate, branching hyphae under 10× and 40× power (Figure 143-7). The hyphae or arthroconidia (fungal spores) of Microsporum may be found on the exterior of the hair (ectothrix) while the hyphae or arthroconidia of Trichophyton tonsurans and T. violaceum are found in the interior of the hair (endothrix) (Figure 143-8).

• Fungal culture—If the diagnosis is uncertain or the species is desired for therapeutic decisions, send a few loose hairs and a scraping of the scalp scale for a fungal culture. A specimen for culture may be obtained using a #15 scalpel, the edge of the slide, a cytobrush, or a sterile gauze rubbed across the infected area.² The specimen should be placed in a sterile urine cup and sent to the laboratory for culture.

• Wood lamp examination—Only the Microsporum species demonstrate bright green/blue fluorescence of infected hairs (Figure 143-9) because of their ectothrix pattern. Trichophyton tonsurans and T. violaceum are endothrix infections so do not fluoresce. However, T. schoenleinii can fluoresce dull green.² As the majority of tinea capitis in the United States and United Kingdom is caused by T. tonsurans, one should not rule out tinea capitis in these countries when fluorescence is absent.² in general, the presence of fluorescence is helpful but the absence is not.

DERMOSCOPY

Dermoscopy of the hair is called trichoscopy. Dermoscopy may help visualize black dot hair stubs, comma hairs, and corkscrew hairs in tinea capitis (Figure 143-10). One small study suggests that these features are seen more often in T. tonsurans and that "elbow" shaped hairs may be seen with Microsporum as the hairs break off at a higher level from the scalp.³

DIFFERENTIAL DIAGNOSIS

• Alopecia areata—Produces areas of hair loss with no scaling, inflammation, or scarring in the underlying scalp. It is an autoimmune process in which the immune system attacks the person's own hair follicles (see Chapter 195, Alopecia Areata).

• Seborrhea of the scalp (dandruff)—Is caused by the Pityrosporum yeast, resulting in scaling and inflammation but rarely causing hair loss. The scalp involvement tends to be more widespread than patchy and localized as seen in tinea capitis (see Chapter 157, Seborrheic Dermatitis).

• Scalp psoriasis—Rarely causes alopecia. There are mild cases with slight, fine scaling on the scalp, or severe cases with silvery, thick, crusted plaques covering the majority of the scalp. Often psoriatic plaques are seen elsewhere on the body and nail changes are visible.

• Trichotillomania—Self-inflicted alopecia caused when the patient pulls and twists her/his own hair (see Chapter 196, Traction Alopecia and Trichotillomania).

• Traction alopecia—Alopecia that occurs when the patient or parent pulls the hair to style it into braids or ponytails. There should be no scaling of the scalp (unless there is coexisting seborrhea) and the pattern of hair loss should match the hairstyle (see Chapter 196, Traction Alopecia and Trichotillomania).

MANAGEMENT

FIRST LINE

• Oral antifungal therapy is needed and topical therapy alone is insufficient.⁴ SORⒶ

• A new Cochrane meta-analysis confirms that terbinafine is more effective than griseofulvin in children with T. tonsurans infection and griseofulvin is better than terbinafine in children with Microsporum infections.^4,5 SORⒶ

• For Microsporum infections in children, a meta-analysis of two studies found that the complete cure was lower for terbinafine (6 weeks) than for griseofulvin (6–12 weeks) (34.7% vs. 50.9%).⁴ SORⒶ

• For T. tonsurans infections in children, terbinafine was better than griseofulvin (52.1% vs. 35.4%).⁴ SORⒶ

• Given the data above, all efforts should be made to distinguish between infections caused by Trichophyton or Microsporum species. First it helps to know the relative prevalence of the dermatophytes causing tinea capitis in your community or nation. Then the Wood lamp and dermatoscope may help. A KOH preparation in which an endothrix or exothrix pattern is seen may also help. This information can be used to choose the best oral antifungal agent initially. Fungal cultures are not always available and may take 1 to 2 weeks for results. However, they can confirm the diagnosis and influence the choice of ongoing oral antifungal therapy. In the United States where T. tonsurans is most common, oral terbinafine is often the best choice as the initial therapy (see cost data below).

• Other oral antifungals including itraconazole and fluconazole are at least as effective as griseofulvin in children with tinea capitis caused by Trichophyton species.⁴ SORⒶ

• Ketoconazole is less effective than griseofulvin and should be avoided because of higher risks for liver toxicity and drug interactions.^4,6

• Fluconazole daily for 3 weeks was as similarly effective as 6 weeks of fluconazole in one study of 491 patients infected with T. tonsurans and M. canis (cure rates of 30.2% vs. 34.1%).⁴ SORⒶ

• Adverse event frequency for terbinafine and griseofulvin (9.2% vs. 8.3%) was similar, and severe adverse events were rare (0.6% vs. 0.6%).⁴ SORⒶ

• Adverse events for terbinafine, griseofulvin, itraconazole, and fluconazole were all mild and reversible.⁴ SORⒶ

PRACTICAL CONSIDERATIONS

Forms available:

• Griseofulvin and fluconazole are available in liquid suspensions for children. Terbinafine is not available in a liquid form and comes as a scored 250 mg tablet. There is a terbinafine brand-name (Lamisil) granule formulation that comes in packets of 125 mg and 187.5 mg. Griseofulvin comes as microsize and ultramicrosize tablets, too. Fluconazole also comes as 50 mg, 100 mg, 150 mg, and 200 mg tablets. Itraconazole is available as a 100 mg capsule only, which limits dosing flexibility.

Recommended doses:

• Terbinafine—recommended dosage for children less than 25 kg is 125 mg daily (one half a tablet); and for children who weigh more than 35 kg, one 250 mg tablet daily. Children between 25 to 35 kg should receive 187.5 mg daily (accomplished with compounding or breaking tablets into pieces).

• Microsize griseofulvin suspension is 20–25 mg/kg per day and ultramicrosize griseofulvin tablets is 10–15 mg/kg per day. Ultramicrosize preparations are stronger per mg than the microsize, but do not come in liquid form.

• Fluconazole—recommended dosage is 5 to 6 mg/kg per day.

Length of treatment:

• Griseofulvin—8 weeks, and consider up to 12 weeks

• Terbinafine—6 weeks for Trichophyton, and 8 to 12 weeks may be needed for Microsporum.

• Fluconazole—3 to 6 weeks.

Cost:

• Oral terbinafine has become very affordable in the United States and appears on most $4 and $5 lists. Terbinafine granules (Lamisil brand name only) were expensive and were discontinued. Oral griseofulvin suspension or tablets may easily cost hundreds of dollars to the patient or healthcare system. Fluconazole and itraconazole are more expensive than terbinafine.

Other considerations:

• Oral antifungal therapy does not require laboratory monitoring at the recommended lengths of treatment for tinea capitis in an otherwise healthy child.⁷ SORⒸ

• A kerion will resolve with oral antifungal treatment alone. If it is severe and painful, some would consider a short pulse of oral steroids in addition (Figure 143-11). However, current evidence does not support the benefit of oral steroids for treatment of a kerion.² SORⒸ While a kerion appears similar to an abscess, an incision and drainage is unnecessary and harmful.

SECOND LINE

• Topical treatment can be used as adjuvant therapy: 1% to 2.5% selenium sulfide or 1% ciclopirox should be applied to the scalp and hair for 5 minutes 2 or 3 times a week for 8 weeks.⁸ SORⒷ

• Shampoos with selenium sulfide or ciclopirox have been shown to be of equal efficacy.⁸ SORⒷ

• Another use for antifungal shampoo is empirical treatment while waiting for a culture to come back in an equivocal case. Topical antifungal shampoo may decrease the spread of the tinea in crowded living environments while waiting for the oral therapy to work (Figure 143-12). SORⒸ

PREVENTION

Family members or playmates should be screened, and asymptomatic carriers should be treated. Close physical contact and sharing of toys or combs/hairbrushes should be avoided.² SORⒷ

PROGNOSIS

With some oral antifungal treatments, studies showed that complete clinical cure was greater than 90% (e.g., one study of terbinafine or griseofulvin for Trichophyton infections). In other comparison studies, the proportion cured was much lower, in the range of 50%.⁴

PATIENT EDUCATION

Patients and parents need to exercise care to avoid spreading the infection to others. Explain the importance of not sharing combs, brushes, and towels.

FOLLOW-UP

Follow-up appointments should be scheduled to make sure that the patient is taking the medication as prescribed and not suffering any adverse effects. Because the course for overall antifungal medicines is typically 4 to 8 weeks, a follow-up in 1 month provides for an opportunity to check on medication adherence and clinical response. With cure rates in many studies as low as 50%, it makes sense to follow the patient until there is full clinical and mycologic cure. Scale and inflammation should resolve initially and hair should regrow in most cases.

PATIENT RESOURCE

• MedlinePlus article for patients—http://www.nlm.nih.gov/medlineplus/ency/article/000878.htm.

REFERENCES

PATIENT STORY

A 30-year-old woman presents to a family physician with a rash on most of her forearm that is now encroaching on her hand. She states that it has been going on for 6 months and that 2 months ago she went to an urgent care where she was given two creams to apply to the rash. Fortunately, she had the creams with her, and Figure 144-1 shows the two creams adjacent to the eruption. The physician diagnosed tinea incognito. The urgent care provider recognized the original eruption as fungal but did not know that nystatin only treats Candida and not the dermatophytes that cause tinea corporis. Therefore, the nystatin was useless and the triamcinolone contributed to the rapid growth of this "fungus on steroids." The patient was given 4 weeks of oral terbinafine 250 mg daily, and the tinea incognito cleared completely.

INTRODUCTION

Tinea corporis is a common superficial fungal infection of the body, characterized by well-demarcated, annular lesions with central clearing, erythema, and scaling of the periphery.

SYNONYMS

Ringworm, dermatophytosis.

EPIDEMIOLOGY

• It is estimated that 10% to 20% of the world population is affected by fungal skin infections.¹

• Dermatophytes are the most prevalent agents causing fungal infections of the skin.²

• Trichophyton rubrum causes the majority of cases of tinea corporis.²

• The prevalence of tinea corporis gladiatorum (in wrestlers) ranges from 20% to 77%.³

• Most reported cases of tinea corporis gladiatorum have been caused by T. tonsurans.³

ETIOLOGY AND PATHOPHYSIOLOGY

• Tinea corporis is caused by fungal species from any one of the following three dermatophyte genera: Trichophyton, Microsporum, and Epidermophyton.

• Dermatophytes produce enzymes such as keratinase that penetrate keratinized tissue. Their hyphae invade the stratum corneum and spread centrifugally outward.

RISK FACTORS

• Participation in daycare centers.

• Wrestling (tinea corporis gladiatorum).³

• Living in a nursing home.

• Poor personal hygiene.

• Living conditions with poor sanitation.

• Warm, humid environments.

• Conditions that cause weakening of the immune system (e.g., AIDS, cancer, organ transplantation, diabetes).

DIAGNOSIS

The diagnosis can be made from history, clinical presentation, culture, and direct microscopic observation of hyphae and spores in infected tissue and hairs after KOH preparation. An ultraviolet light (Wood lamp) is helpful only in cases with Microsporum species. Since almost all tinea corporis is caused by Trichophyton rubrum or Trichophyton tonsurans (in wrestlers), the Wood lamp is rarely positive in current-day tinea corporis.

CLINICAL FEATURES

• Pruritus of affected area.

• Well-demarcated, annular lesions with central clearing, erythema, and scaling of the periphery. Concentric rings are highly specific for tinea infections (Figure 144-2).

• Central clearing is not always present (Figure 144-3).

• Tinea corporis is frequently pink to red in white skin but can be silver (Figure 144-3) or hyperpigmented in darker skin (Figure 144-4).

• Tinea incognito is a type of tinea infection that was previously unrecognized by the physician or patient, and topical steroids were used on the site. While the steroid is being used, the dermatophyte continues to grow and may form concentric rings (Figures 144-1, 144-5, and 144-6).

• Although scale is the most prominent morphologic characteristic, some tinea infections will actually cause pustules from the inflammatory response (Figure 144-7).

• Majochi granuloma (Figure 144-8) is a type of tinea in which the fungus has gone deep into the hair follicles and creates a granulomatous appearance. This may be caused by the application of topical steroids so that this is a deep type of tinea incognito in some cases. Shaving or occlusion of the skin may be involved in the pathophysiology as well. It is a deep and persistent suppurative folliculitis so that pustules and nodules may be present along with the superficial erythema and scale visible in typical tinea corporis.

TYPICAL DISTRIBUTION

Any part of the body including the face, known as tinea faciei (Figure 144-9).

Tinea corporis can cover large parts of the body as in Figure 144-10.

LABORATORY STUDIES

• KOH preparation of skin scraping can be very useful to confirm a clinical impression or when the diagnosis is not certain. Scrape the skin with the side of a slide or scalpel, making sure to scrape the periphery and the erythematous part. Scrape hard enough to get some stratum corneum without causing significant bleeding. False negatives can occur secondary to inadequate scraping, patient using topical antifungals, or an inexperienced microscopist.

• Use KOH (plain, with dimethyl sulfoxide [DMSO], or in a fungal stain) to break up the epithelial cells more rapidly without heating (Figure 144-11). It is easy to purchase a small bottle of Swartz Lamkins fungal stain that includes KOH, a surfactant, and blue ink. The blue ink allows the hyphae to stand out, thereby saving time and decreasing the chance of a false-negative result (Figure 144-12). If the epithelial cells are not breaking up sufficiently, use a flame under the slide for approximately 5 seconds to speed up the process.

• Skin scraping and culture—Gold standard, but more costly and may take up to 2 weeks for the culture to grow. Consider culture if the KOH is negative but tinea is still suspected, or when a microscope is not available.

• Skin biopsy sent in formalin for periodic acid–Schiff (PAS) staining when the KOH and culture remain negative but the clinical picture is consistent with a fungal infection.

DIFFERENTIAL DIAGNOSIS

• Granuloma annulare—Inflammatory, benign dermatosis of unknown cause, characterized by both dermal and annular papules (Figure 144-13) (see Chapter 182, Granuloma Annulare).

• Psoriasis—Plaque with scale on extensor surfaces and trunk. Occasionally, the plaques can have an annular appearance (Figure 144-14). Inverse psoriasis in intertriginous areas can also mimic tinea corporis (see Chapter 158, Psoriasis).

• Erythema annulare centrifugum (EAC)—Scaly red rings with normal skin in the center of the rings. The scale is trailing the erythema as the ring expands while the scale is leading in tinea corporis (Figure 144-15) (see Chapter 215, Erythema Annulare Centrifugum).

• Cutaneous larva migrans has serpiginous burrows made by the hookworm larvae, and these burrows can look annular and be confused with tinea corporis (see Chapter 150, Cutaneous Larva Migrans).

• Nummular eczema—Round coin-like red scaly plaques without central clearing (see Chapter 151, Atopic Dermatitis).

• Erythrasma—Found in the axilla and groin without an annular configuration and central clearing. Fluoresces coral red under UV lamp (see Chapter 125, Erythrasma).

MANAGEMENT

FIRST LINE

• Use topical antifungal medications for tinea corporis that involves small areas of the body such as seen in Figure 144-2.

• Across five of the best studies identified in a Cochrane review, significantly higher clinical cure rates were seen in tinea infected individuals treated with topical terbinafine compared to placebo (number needed to treat [NNT] 3).¹

• Although all the topical antifungal agents may be effective, the evidence supports the greater effectiveness of the allylamines (terbinafine) over the less-expensive azoles for tinea pedis and corporis. Allylamines cure slightly more infections than azoles and are now available over the counter.^4,5 SORⒶ

• Studies show that terbinafine 1% cream or solution applied once daily for 7 days is highly effective for tinea corporis/cruris.^6,7 The 1% cream (which is available over the counter as Lamisil AF) produced a mycologic cure of 84.2% versus 23.3% with placebo. NNT = 1.6.⁶ SORⒶ

• Oral antifungal agents should be considered for first-line therapy for tinea corporis covering large areas of the body. However, it is not wrong to attempt topical treatment if the size of the area infected is on the borderline.

• One randomized controlled trial (RCT) showed that oral itraconazole 200 mg daily for 1 week is similarly effective, equally well tolerated, and at least as safe as itraconazole 100 mg for 2 weeks in the treatment of tinea corporis or cruris.⁸ SORⒷ

• In one study, patients with mycologically diagnosed tinea corporis and tinea cruris were randomly allocated to receive either 250 mg of oral terbinafine once daily or 500 mg of griseofulvin once daily for 2 weeks. The cure rates were higher for terbinafine at 6 weeks.⁹ SORⒷ

• Majochi granuloma can be especially difficult to treat and requires oral antifungals just like tinea capitis. It might actually require months of terbinafine 250 mg daily with monthly follow-up until the infection is fully cleared.

  • Terbinafine 250 mg daily for 2 weeks.⁹ SORⒷ (Terbinafine is available as an inexpensive generic prescription on the $4 and $5 plans in the United States. It also has fewer drug interactions than itraconazole. For these reasons it is usually the preferred treatment when an oral agent is needed.)

SECOND LINE

• Itraconazole 200 mg daily for 1 week.⁸ SORⒷ (More expensive with more drug interactions than terbinafine.)

  • Itraconazole 100 mg daily for 2 weeks.⁸ SORⒷ

• Fluconazole 200 mg weekly for 4 weeks produced a 100% cure in the study of tinea corporis in wrestlers.¹⁰

PREVENTION

Tinea corporis and cruris are dermatophyte infections that are particularly common in areas of excessive heat and moisture. A dry, cool environment may play a role in reducing infection. In addition, avoiding contact with farm animals and other individuals infected with tinea corporis and cruris may help in preventing infection. Preventative measures for tinea infections include practicing good personal hygiene; keeping the skin dry and cool at all times; and avoiding sharing towels, clothing, or hair accessories with infected individuals.¹¹

In individuals involved in contact sports such as wrestling, a comprehensive skin disease prevention protocol includes some combination of the following: washing of wrestling mats before and after each practice and competition; showers before and after each practice; use of clean clothing before each practice; and exclusion of infected athletes.¹²

For wrestling teams, consider giving fluconazole 100 mg daily for 3 days twice per season to each wrestler.¹³ In the study that supports this recommendation, the incidence rate of tinea gladiatorum dropped from 67.4% to 3.5% over a 10-year study.¹³ SORⒷ

PATIENT EDUCATION

Keep the skin clean and dry. Use the topical or oral antifungal according to directions. If the rash persists after the treatment, schedule an appointment for further evaluation. Infected pets should be treated.

FOLLOW-UP

Consider follow-up appointments in 4 to 6 weeks for difficult and more widespread cases. If there are concerns about bacterial superinfection, follow-up should be sooner.

REFERENCES

PATIENT STORY

A 59-year-old man presents with itching in the groin (Figure 145-1). On examination, he was found to have scaly erythematous plaques in the inguinal area. A KOH preparation was performed with Swartz Lamkins stain, and the dermatophyte was highly visible under the microscope (Figure 145-2). He was treated with a topical antifungal medicine until his tinea cruris resolved.

INTRODUCTION

Tinea cruris is a pruritic superficial infection of the groin and adjacent skin caused by a dermatophyte fungus.

SYNONYMS

Common names: Crotch rot and jock itch.

EPIDEMIOLOGY

• It is estimated that 10% to 20% of the world population is affected by fungal skin infections.¹

• Dermatophytes are the most prevalent agents causing fungal infections of the skin.²

• Trichophyton rubrum causes the majority of cases of tinea cruris.²

• Tinea cruris is more common in men than women (threefold) and rare in children.

ETIOLOGY AND PATHOPHYSIOLOGY

• Caused by the dermatophytes Trichophyton rubrum, Epidermophyton floccosum, Trichophyton mentagrophytes, and Trichophyton verrucosum.

• Can be spread by fomites, such as contaminated towels.

• The dermatophytes release keratinases, which allow invasion of the cornified cell layer of the epidermis.

• Autoinoculation can occur from fungus on the feet or hands.

RISK FACTORS

• Wearing tight-fitting or wet clothing or underwear has traditionally been suggested; however, in a study of Italian soldiers, none of the risk factors analyzed (e.g., hyperhidrosis, swimming pool attendance) were significantly associated with any fungal infection.³

• Obesity and diabetes mellitus may be risk factors.⁴

DIAGNOSIS

CLINICAL FEATURES

The cardinal features are scale and signs of inflammation. In light-skinned persons inflammation often appears pink or red, and in dark-skinned persons the inflammation often leads to hyperpigmentation (Figures 145-3 and 145-4). Occasionally, tinea cruris may show central sparing with an annular pattern as in Figure 145-5, but most often is homogeneously distributed as in Figures 145-3 and 145-4.

TYPICAL DISTRIBUTION

By definition tinea cruris is in the inguinal area. However, the fungus can grow outside of this area to involve the abdomen and thighs (Figures 145-4 and 145-6). Tinea can be present in multiple locations, as in the patient in Figure 145-7, who had tinea in the groin, on her feet and face, and under her breasts.

LABORATORY STUDIES

Diagnosis is often made based on clinical presentation, but a skin scraping treated with KOH and a fungal stain analyzed under the microscope can be helpful (see Figure 145-2). False negatives may occur if scraping is inadequate, the patient is using topical antifungals, or the viewer is inexperienced.

Skin scraping and culture is definitive but expensive and may take up to 2 weeks for the culture to grow.

UV lamp can be used to look for the coral red fluorescence of erythrasma (see Chapter 125, Erythrasma). Since most tinea cruris is caused by T. rubrum, it will not fluoresce.

DIFFERENTIAL DIAGNOSIS

• Cutaneous Candida in the groin can become red and have scaling that extends to the thigh and scrotum. Tinea cruris does not often involve the scrotum. Candida often has satellite lesions (see Chapter 142, Candidiasis).

• Erythrasma in the groin appears similar to tinea cruris but has a less well demarcated border. It is less common than tinea cruris and may show coral red fluorescence with a UV light (Figure 145-8) (see Chapter 125, Erythrasma). If the KOH preparation is negative, consider using a UV light to examine the groin and interdigital spaces of the toes (erythrasma may be found between the toes just as in tinea pedis).

• Contact dermatitis can occur anywhere on the body. If the contact is near the groin this can be mistaken for tinea cruris (see Chapter 152, Contact Dermatitis).

• Inverse psoriasis causes inflammation in the intertriginous areas of the body. It does not have the thick plaques of plaque psoriasis. Inverse psoriasis is frequently misdiagnosed as a fungal infection until an astute clinician recognizes the pattern or does a biopsy (Figure 145-9; see Chapter 158, Psoriasis). However, even patients with psoriasis can get tinea cruris (Figure 145-10).

• Majochi granuloma (Figure 145-11) is a type of tinea in which the fungus has gone deep into the hair follicles and creates a granulomatous appearance. This may be caused by the application of topical steroids so that this is a deep type of tinea incognito in some cases. It is a deep and persistent suppurative folliculitis so that pustules and nodules may be present along with the superficial erythema and scale.

• Intertrigo is an inflammatory condition of the skin folds. It is induced or aggravated by heat, moisture, maceration, and friction. It is a nonspecific diagnosis, and the condition frequently is worsened by infection with Candida or dermatophytes.⁵ It is best to look for an etiology and reserve this diagnosis for cases where no etiology is found.

MANAGEMENT

FIRST LINE

• Tinea cruris is best treated with a topical allylamine or an azole antifungal (SORⒶ, based on multiple randomized controlled trials [RCTs]).⁶ Differences in current comparison data are insufficient to stratify the two groups of topical antifungals.⁷ In one RCT, cure rates were higher at 1 week with butenafine (once daily for 2 weeks) versus clotrimazole (twice daily for 4 weeks) (26.5% vs. 2.9%, respectively), but were not significantly different at 4 or 8 weeks.⁸

• The fungicidal allylamines (naftifine and terbinafine) and butenafine (allylamine derivative) are more convenient as they allow for a shorter duration of treatment compared with fungistatic azoles (clotrimazole, econazole, ketoconazole, oxiconazole, miconazole, and sulconazole).⁷

• Topical azoles should be continued for 4 weeks and topical allylamines for 2 weeks or until clinical cure.^6-8 SORⒶ

• Azole and steroid combination creams were slightly more effective in achieving clinical cure compared to azoles alone immediately at the end of treatment (relative risk [RR] 0.67, number needed to treat [NNT] 6), but there was no difference in mycologic cure rate (RR 0.99). The quality of evidence for these two outcomes was rated as low.¹ SORⒷ

SECOND LINE

• Systemic treatment with oral antifungals is second line when topical antifungal agents fail but are first-line therapy in widespread cases of tinea cruris in which large areas are involved (see Figures 145-4 and 145-6). Of course, it is important to make sure that the failure of topical antifungal agents is not due to a missed diagnosis of inverse psoriasis, which is a common look-alike condition with tinea cruris.

• Oral terbinafine 250 mg daily for 2 weeks is the oral treatment of choice. Patients with mycologically diagnosed tinea cruris were randomly allocated to receive either 250 mg of oral terbinafine once daily or 500 mg of griseofulvin once daily for 2 weeks. The cure rates were higher for terbinafine at 6 weeks.⁹ SORⒷ

• Fluconazole 150 mg once weekly for 2 to 4 weeks appears to be effective in the treatment of tinea cruris.¹⁰ SORⒷ

• One RCT showed that itraconazole 200 mg for 1 week is similarly effective, equally well tolerated, and at least as safe as itraconazole 100 mg for 2 weeks in the treatment of tinea corporis or cruris (clinical response: 73% and 80% at the end of follow-up, respectively).¹¹ SORⒷ

• Majochi granuloma (which involves hair follicles) can be especially difficult to treat and requires oral antifungals just like tinea capitis. It might actually require months of terbinafine 250 mg daily with monthly follow-up until the infection is fully cleared.

• If there are multiple sites infected with fungus, treat all active areas of infection simultaneously to prevent reinfection of the groin from other body sites.

FOLLOW-UP

As needed.

PATIENT EDUCATION

• Advise patients with tinea pedis to put on their socks before their undershorts to reduce the possibility of direct contamination. SORⒸ

• Dry the groin completely after bathing. SORⒸ

REFERENCES

PATIENT STORY

A 34-year-old woman presents with an itching rash on both feet for the past 6 months (Figure 146-1). She is in otherwise good health and has occasionally tried some over-the-counter (OTC) athlete's foot medicine for this rash with slight improvement. On physical exam, the patient has erythema and scale in the moccasin distribution as well as some of her interdigital spaces. A KOH preparation is positive for branching hyphae with visible nuclei enhanced by the Schwartz Lamkins stain (Figure 146-2). Patient denies a history of hepatitis or heavy alcohol use and would like to try an oral medication because she is tired of the itching. The patient is given oral terbinafine 250 mg daily for 2 weeks.

INTRODUCTION

Tinea pedis is a common cutaneous infection of the feet caused by dermatophyte fungus. The clinical manifestation presents in 1 of 3 major patterns: interdigital, moccasin, and inflammatory/vesicular. Concurrent fungal infection of the nails (onychomycosis) occurs frequently.

SYNONYMS

Athlete's foot.

EPIDEMIOLOGY

• Tinea pedis is the most common human dermatophytosis.¹

• 70% of the population will be infected with tinea pedis at some time.¹

• Prevalence increases with age and it is less common before adolescence.¹

ETIOLOGY AND PATHOPHYSIOLOGY

• A cutaneous fungal infection most commonly caused by Trichophyton rubrum.¹

• Trichophyton mentagrophytes and Epidermophyton floccosum follow in that order.

• T. rubrum causes most tinea pedis and onychomycosis.

RISK FACTORS

• Use of public showers, baths or pools—especially if protective footwear is not used.²

• Household member with tinea pedis infection.²

• Certain occupations (miners, farmers, soldiers, meat factory workers)—especially where there is use of heavy boots and the feet are warm and sweaty.²

• Persons experiencing homelessness.³

DIAGNOSIS

TYPICAL DISTRIBUTION AND MORPHOLOGY

Three types of tinea pedis:

• Interdigital type (intertriginous type)—very common (Figure 146-3).

• Moccasin type—very common (Figures 146-1 and 146-4).

• Vesiculobullous type—least common (Figures 146-5 and 146-6).

However, many persons have both the interdigital and moccasin type simultaneously, as seen in Figure 146-1. In one prospective study of 135 patients presenting consecutively with tinea pedis, lesions were suggestive of the intertriginous type in 24 patients, moccasin type in 50 patients, and both intertriginous and moccasin type in 58 patients. Among the remaining patients, 1 had the vesiculobullous type and another had both the vesiculobullous and intertriginous types.⁴

In another larger study of 1174 persons, 674 had only interdigital tinea pedis while 500 subjects had a moccasin distribution in addition to the interdigital presentation.⁵

Some authors describe an ulcerative type (Figure 146-7).

CLINICAL FEATURES

• Interdigital—white or green fungal growth between toes with erythema, maceration, cracks, and fissures—especially between fourth and fifth digits (see Figure 146-3). The dry type has more scale, and the moist type becomes macerated.

• Moccasin—scale on sides and soles of feet (see Figures 146-1 and 146-4).

• Vesiculobullous—vesicles and bullae on feet (see Figures 146-5 and 146-6).

• Ulcerative tinea pedis is characterized by rapidly spreading vesiculopustular lesions, ulcers, and erosions, typically in the web spaces (see Figure 146-7). It is accompanied by a secondary bacterial infection. This can lead to cellulitis or lymphangitis. Tinea pedis is a proven risk factor for nonpurulent leg cellulitis.⁶

• Examine nails for evidence of onychomycosis—fungal infections of nails may include subungual keratosis, yellow or white discolorations, dysmorphic nails (Chapter 201, Onychomycosis).

• Autoeczematization (dermatophytid reaction; Id reaction) is an uncommon hypersensitivity response to a fungal infection causing papules on the skin (Figure 146-8).

TYPICAL DISTRIBUTION

Between the toes, on the soles, and lateral aspects of the feet.

LABORATORY STUDIES

The most rapid method to confirm a clinical diagnosis is the KOH preparation. The involved skin is scraped with side of the microscope slide or a scalpel onto another slide. The slide is then prepared with KOH or KOH and a fungal stain. The slide is examined for hyphal elements (video https://www.youtube.com/watch?v=LUwNQI_0BWU) (see Figure 146-2). One study showed that the use of two KOH preparations from different parts of the suspected tinea pedis provided a substantial increase in diagnostic sensitivity.⁴

In a patient with tinea incognito on his foot and lower leg, the topical steroid masked the symptoms while the tinea spread up his leg (Figure 146-9). It took a KOH preparation to demonstrate that this was tinea and not lupus to get the patient the antifungal treatment he needed.

A fungal culture is sometimes needed if one does not have the microscope to do a KOH preparation or if the KOH prep is negative but fungus is still suspected. A fungal culture may take up to 2 weeks for an answer, but the lab can often provide a KOH result within 1–2 days from the same sample. Just scrape the suspected tinea into a sterile urine cup and send to the lab.

DIFFERENTIAL DIAGNOSIS

• Erythrasma is a bacterial infection found in intertriginous areas. It may appear as maceration between the toes and be mistaken for tinea pedis or coexist with tinea pedis (see Figures 125-5 and 125-6). In a study of 182 patients with interdigital lesions in a podiatry clinic, 40% were diagnosed as having erythrasma.⁷ Look for coral red fluorescence with a Wood lamp to diagnose erythrasma between the toes. A KOH preparation is helpful to confirm tinea. Fortunately, topical miconazole can treat both erythrasma and interdigital tinea pedis simultaneously⁸ (see Chapter 125, Erythrasma).

• Pitted keratolysis: well-demarcated pits or erosions in the sole of the foot caused by bacteria (Figure 146-10) (see Chapter 124, Pitted Keratolysis).

• Contact dermatitis tends to be seen on the dorsum and sides of the foot (Figure 146-11) (Chapter 152, Contact Dermatitis).

• Keratodermas: thickening of the soles of the feet that can be caused by a number of etiologies, including genetics and menopause (Figure 146-12). This condition may look like tinea pedis in the moccasin distribution.

• Dyshidrotic eczema is characterized by scale and tapioca-like vesicles on the hands and feet (Figure 146-13) (Chapter 153, Hand Eczema).

• Friction blisters: blisters on the feet of persons leading an active athletic lifestyle.

• Psoriasis can mimic tinea pedis but will usually be present in other areas as well (Figure 146-14) (Chapter 158, Psoriasis). Especially on the palms if this is palmarplantar psoriasis.

MANAGEMENT

See Table 146-1 for management of tinea pedis.

FIRST LINE

TOPICAL ANTIFUNGALS

• Systematic review of 70 trials of topical antifungals showed good evidence for efficacy compared to placebo for the following:

  • Allylamines (naftifine, terbinafine, butenafine)⁹ SORⒶ

  • Azoles (clotrimazole, miconazole, econazole)⁹ SORⒶ

  • Allylamines cure slightly more infections than azoles⁹ SORⒶ

  • No differences in efficacy found between individual allylamines or individual azoles (Table 146-2) SORⒶ

• In one meta-analysis, topical terbinafine was found to be equally effective as other topical antifungals, but the average duration of treatment was shorter (1 week instead of 2 weeks).¹⁰ SORⒶ

• Topical terbinafine is a great first-line choice for tinea pedis because of its affordable cost as an OTC cream. SORⒸ

• The moccasin distribution is more challenging to treat topically. In one large study, Naftifine gel 2% (Rx only) and vehicle treatment were applied once daily for 2 weeks.⁵ Then at week 6, the cure rates in the naftifine arm vs. the vehicle were statistically higher for mycologic cure rate (65.8% vs. 7.8%), treatment effectiveness (51.4% vs 4.4%), and complete cure rate (19.2% vs. 0.9%) for moccasin-type tinea pedis.⁵ Note that mycologic cure is defined as a negative dermatophyte culture and KOH, treatment effectiveness is defined as mycologic cure and symptom severity scores of 0 or 1, and complete cure is defined as mycologic cure and symptoms severity scores of 0. While naftifine gel was much better than vehicle, the data demonstrate that there may be significant failure to cure this type of tinea pedis and one should then consider oral antifungal treatment.

• Luliconazole cream has recently been FDA approved for interdigital tinea pedis. It requires a prescription, and one tube is over $400. There are currently no data to recommend it over the inexpensive OTC topical antifungals.

SECOND LINE

ORAL ANTIFUNGALS

• In a Cochrane systematic review of 15 trials involving 1438 participants, the evidence suggests that terbinafine is more effective than griseofulvin.¹¹ SORⒶ

• In the same review, terbinafine or itraconazole are more effective than no treatment.¹¹ SORⒶ

• No significant difference was detected between terbinafine and itraconazole, fluconazole and itraconazole, fluconazole and ketoconazole, or griseofulvin and ketoconazole, although the trials were generally small.¹¹ SORⒶ

• Terbinafine is the oral treatment of choice, as it is very affordable being on the $4 and $5 lists at many pharmacies. It is at least as effective as other oral agents and more effective than griseofulvin. It has no more side effects or precautions than other oral antifungal agents. The dosing is 250 mg PO daily for 2 weeks. Avoid use if there is hepatic impairment, absolute neutrophil count (ANC) <1000, or creatinine clearance less than 50.

Patients with onychomycosis may have recurrences of the skin infection related to the fungus that remains in the nails and, therefore, may need oral treatment for 3 months to achieve better results.

Topical ammonium lactate (6% or 12%) and urea (10% to 40%) may be useful to decrease scaling in patients with hyperkeratotic soles in addition to treating their tinea pedis.

ALTERNATIVE THERAPY

One small pilot study with 56 participants showed significant improvement or resolution of symptoms in patients treated by wearing socks containing copper-oxide fibers daily for a minimum of 8 to 10 days.¹² SORⒷ

PATIENT EDUCATION

• Do not go barefoot in public showers and locker rooms. Shower shoes may prevent tinea pedis. SORⒸ

• Keep feet dry and clean, and use clean socks and shoes that allow the feet to get fresh air. SORⒸ

• Use the topical antifungal medication again if recurrence occurs. SORⒸ

REFERENCES

PATIENT STORY

A young black man presents to the office with a 5-year history of white spots on his trunk (Figure 147-1). He denies any symptoms but worries if this could spread to his girlfriend. These spots get worse during the summer months but never go away completely. He was relieved to receive a treatment for his tinea versicolor and to find out that it is not spread to others through contact.

INTRODUCTION

Tinea versicolor is a common superficial skin infection caused by the dimorphic lipophilic yeast in the genus Malassezia, formerly known as Pityrosporum. The most typical presentation is a set of hypopigmented macules and patches with fine scale over the trunk and proximal upper extremities in a capelike distribution.¹

SYNONYMS

Pityriasis (from Pityrosporum) versicolor is actually a more accurate name, as "tinea" implies a dermatophyte infection. Tinea versicolor is caused by yeast in the genus Malassezia and not a dermatophyte.^1,2

EPIDEMIOLOGY

• Seen more commonly in men than in women.

• Seen more commonly in adolescents and young adults.

• Seen more often during the summer and is especially common in warm and humid climates.

ETIOLOGY AND PATHOPHYSIOLOGY

• Tinea versicolor is caused by yeast in the genus Malassezia which is a lipid-dependent, dimorphic fungus that is a component of normal human cutaneous flora.^2,3

• Malassezia lipophilic yeasts are causative agents in tinea versicolor, seborrheic dermatitis, and Malassezia folliculitis and can even exacerbate atopic dermatitis.² In one microbiology study using polymerase chain reaction (PCR), the authors were able to determine the prevalence of various Malassezia species on patients with Malassezia associated skin conditions.² The two most common species isolated from humans were M. globosa and M. furfur.²

• Transformation of Malassezia from yeast to the pathogenic mycelial form followed by invasion into the stratum corneum precedes the development of the classic appearance of tinea versicolor.⁴

• Versicolor refers to the variable changes in pigmentation noted in this condition.^2-4

• Hypopigmentation changes are secondary to melanocytic damage caused by azelaic acid produced by the genus Malassezia, while the hyperpigmented and erythematous lesions are a result of an inflammatory reaction to the organism.⁴

• Malassezia is lipid dependent and thrives on sebum and moisture. The lesions are more common in areas of greater sebum production, such as the upper trunk and proximal upper extremities.^2,3

DIAGNOSIS

CLINICAL FEATURES

Tinea versicolor consists of hypopigmented, hyperpigmented, or pink macules and patches on the trunk and proximal upper extremities that are finely scaled and well-demarcated. Versicolor means a variety of or variation in colors; tinea versicolor tends to come in white, pink, and brown colors (Figures 147-1, 147-2, 147-3, 147-4, 147-5).

TYPICAL DISTRIBUTION

Tinea versicolor is found on the chest, abdomen, upper arms, and back.

LABORATORY STUDIES

A scraping of the scaling portions of the skin may be placed onto a slide using the side of another slide or a scalpel. KOH (with or without a fungal stain) is placed on the slide and covered with a coverslip. Microscopic examination reveals the typical "spaghetti-and-meatballs" pattern of tinea versicolor. The "spaghetti," or more accurately "ziti," is the short mycelial form and the "meatballs" are the round yeast form (Figures 147-6 and 147-7). Fungal stains such as the Swartz Lamkins stain help make the identification of the fungal elements easier.³

DIFFERENTIAL DIAGNOSIS

• Seborrheic dermatitis on the trunk typically is more erythematous, has a thicker scale, and is located in the central chest. Patients usually have other lesions in the scalp, eyebrows, and nasolabial folds.

• Pityriasis rosea has a fine collarette scale around the border of the lesions and is frequently seen with a herald patch. Negative KOH (see Chapter 159, Pityriasis Rosea).

• Secondary syphilis is usually not scaling and tends to have macules on the palms and soles. Negative KOH (see Chapter 225, Syphilis).

• Tinea corporis is rarely as widespread as tinea versicolor, and each individual lesion usually has central clearing and a well-defined, raised, scaling border. The KOH preparation in tinea corporis shows hyphae with multiple branch points and not the "ziti-and-meatballs" pattern of tinea versicolor (see Chapter 144, Tinea Corporis).

• Vitiligo—The degree of hypopigmentation is greater and the distribution is frequently different with vitiligo involving the hands and face (see Chapter 206, Vitiligo and Hypopigmentation).

• Pityriasis alba—Lightly hypopigmented areas with slight scale that tend to be found on the face and trunk of children with atopy. These patches are frequently smaller and rounder than tinea versicolor (see Chapter 151, Atopic Dermatitis).

• Pityrosporum (Malassezia) folliculitis is caused by the same organism but presents with pink or brown papules on the back. The patient complains of itchy rough skin, and there is evidence of perifollicular inflammation (Figure 147-8).

MANAGEMENT

FIRST LINE

• Because tinea versicolor is usually asymptomatic, the treatment is mostly for cosmetic reasons.

• The mainstay of treatment has been topical therapy using antidandruff shampoos, because the same Malassezia species that cause seborrhea and dandruff also cause tinea versicolor.^1,2

• Patients may apply selenium sulfide 2.5% lotion or shampoo or zinc pyrithione shampoo to the involved areas daily for 2 weeks. Various amounts of time are suggested to allow the preparations to work, but there are no studies that compare exposure times. Although 5 minutes has been used in some studies, 2 minutes may be more realistic. A typical regimen involves applying the lotion or shampoo to the involved areas for 2–5 minutes and then washing it off in the shower.³ SORⒸ

• One study used ketoconazole 2% shampoo as a single application or daily for 3 days and found it safe and highly effective with greater than 80% cure in treating tinea versicolor.^3,5 SORⒷ

• A single-dose 400-mg oral fluconazole provides excellent clinical and mycologic cure rates, with no relapse during 12 months of follow-up.^6-8 SORⒷ

SECOND LINE

• A single dose of 300 mg of oral fluconazole repeated weekly for 2 weeks was equal to 400 mg of ketoconazole in a single dose repeated weekly for 2 weeks. No significant differences in efficacy, safety, and tolerability between the two treatment regimens were found.^7-10 SORⒷ

• However, in 2016, the FDA advised against the use of oral ketoconazole for tinea versicolor due to life-threatening hepatotoxicity, adrenal insufficiency, and multiple adverse drug-drug interactions.^11,12 SORⒷ

• Topical antifungal creams for smaller areas of involvement can include ketoconazole, clotrimazole, terbinafine, and ciclopirox.¹³ SORⒸ

• There is no evidence that establishes the need to sweat after taking oral antifungals to treat tinea versicolor.³

PREVENTION

• Prophylaxis with topical ketoconazole 2% shampoo applied to the entire body for 5 minutes once per month is an effective therapy.⁵ SORⒷ

• Oral itraconazole 200 mg given twice a day for one day a month has been shown to be safe and effective as a prophylactic treatment for tinea versicolor.^14,15 SORⒷ

PATIENT EDUCATION

Patients should be told that the change in skin color will not reverse immediately. The first sign of successful treatment is the lack of scale. The yeast acts like a sunscreen in the hypopigmented macules. Sun exposure will hasten the normalization of the skin color in patients with hypopigmentation.

FOLLOW-UP

None needed unless it is a stubborn or recurrent case. Recurrent cases can be treated with monthly topical or oral therapy.

REFERENCES