Tinea corporis classically presents as a red, annular, scaly, pruritic plaque with central clearing and an active border (Figure 1¹). Lesions may be single or multiple and range in size from 1 to 5 cm. Larger lesions and lesion confluence can also occur.^2,20 Tinea corporis may be mistaken for other skin conditions, particularly eczema, psoriasis, and seborrheic dermatitis.^9,21 In a study of 148 patients presenting to primary care with erythematosquamous skin lesions, the findings that best ruled in dermatomycosis included maceration (positive likelihood ratio [LR+] = 1.7), overall clinical diagnosis (LR+ = 1.5), concentric rings (LR+ = 1.4), and central clearing (LR+ = 1.2).²²

Tinea cruris (also called jock itch) most often affects adolescent and young adult males.⁶ It usually involves the skin on the upper thigh opposite the scrotum²⁰ (Figure 2¹). The scrotum typically is spared, and scrotal involvement may help differentiate tinea cruris from candidiasis.²

Tinea pedis (also called athlete’s foot) typically affects interdigital skin but can spread to the sole, sides, and dorsum of the foot² (Figure 3¹). Patients with acute tinea pedis typically have interdigital erythema and maceration, which may be accompanied by painful vesicles. This type of infection should be differentiated from gram-negative toe web infections, which can occur concomitantly with tinea pedis but may be associated with more pain, greater likelihood of extension to the distal sole, and in the case of the most common pathogen (Pseudomonas), a foul-smelling, greenish exudate.²³ Chronic tinea pedis, the more common form, usually involves interdigital scaling, peeling, and erythema, but other areas of the foot may be affected. The term “moccasin pattern” describes tinea pedis that involves erythema and hyperkeratosis on the plantar and lateral aspects of the foot.^2,20

Tinea corporis, tinea cruris, and tinea pedis may be strongly suspected based on patient history and visual inspection.^2,20 In-office microscopy is not commonly used for the diagnosis of tinea infections in primary care settings.²⁴ However, this testing can help differentiate tinea infection from other similar-appearing conditions. When feasible, in-office diagnostic testing (eg, potassium hydroxide [KOH] preparation with direct microscopy) can help establish a tinea infection diagnosis as demonstrated in the video at https://www.youtube.com/watch?v=LUwNQI_0BWU.¹⁸ Physicians may treat for tinea infection despite a negative result on KOH preparation if there is a strong clinical suspicion for fungal infection based on visual inspection. Figure 4 shows an example of KOH preparation.¹

If in-office microscopy is not an option, skin scrapings can be transferred to the laboratory for testing by placing them between two clean glass slides or in a sterile container. Cultures usually are not necessary for diagnosis but may be useful if there is concern for antifungal drug resistance or an unusual causative dermatophyte because isolates can be saved for testing at specialized laboratories.¹⁰ Rarely, a skin biopsy with periodic acid–Schiff stain may be used for the diagnosis of atypical or persistent lesions.²

Tinea corporis, tinea cruris, and tinea pedis usually respond to topical creams, such as butenafine, ketoconazole, or terbinafine. Oral antifungal agents may be used for patients with extensive disease, lack of response to topical treatment, immunocompromise, or hair follicle involvement.² For tinea infections that are caused by certain emerging dermatophyte species, prolonged oral antifungal therapy may be needed.^10,25,26

When the cause of a rash is uncertain, physicians may choose combination antifungal-corticosteroid products in an attempt to cover fungal and nonfungal etiologies. However, this practice is generally discouraged because the corticosteroid component is often high-potency (clotrimazole-betamethasone) or medium-potency (nystatin-triamcinolone), which can result in skin atrophy or systemic adverse effects.^27–30 The use of combination antifungal-corticosteroid creams may also contribute to the emergence and spread of antifungal-resistant dermatophyte strains.^2,27–30

When diagnostic testing or dermatology referral is impractical, a 2-week trial of topical antifungal therapy (without a corticosteroid component), with follow-up to document improvement, is a reasonable alternative.^18.27 If a nonfungal lesion is treated with an antifungal cream, the lesion likely will not improve or will worsen. Conversely, worsening of a skin condition after empiric treatment with a topical corticosteroid suggests an alternative diagnosis, including a dermatophyte infection.²

In the United States, tinea capitis is most common among Black children aged 3 to 9 years.^7,8,31 There are three main types of tinea capitis: gray patch, black dot, and favus. Black dot is most common in the United States² (Figure 5¹). The classic presentation is one or more scaly patches of alopecia with broken hairs at the skin line (black dots) and crusting; however, early disease may be limited to pruritus and scaling. Untreated tinea capitis may progress to kerion, a condition characterized by boggy, tender plaques and pustules.²

Tinea capitis is often treated empirically without diagnostic testing when the clinical presentation is typical.^31,32 Seborrheic dermatitis and alopecia areata are the most common mimics of tinea capitis. In atypical cases, a KOH preparation can be used to look for fungal spores in scrapings of the black dots (broken hairs).²⁰

Culture is generally more sensitive (51% to 97%) than KOH preparation (59% to 73%) and is performed by moistening a cotton applicator or toothbrush with tap water and rubbing it over the scalp lesion.¹ The sample can then be applied to the Sabouraud liquid medium or dermatophyte test medium. Cultures have a high false-negative rate in children with kerion.²

Systemic antifungals should be used to treat tinea capitis because topical agents do not penetrate hair follicles.^2,31,33 Concomitant treatment with selenium sulfide 1% or 2.5% shampoo, ketoconazole 2% shampoo, or ciclopirox 1.5% shampoo for the first 2 weeks may reduce transmission.^1,34,35 Although 6 to 8 weeks of griseofulvin therapy has been considered first-line treatment for tinea capitis, randomized clinical trials have shown that shorter treatment courses (4–6 weeks) of terbinafine are equally effective and safe.^2,33 Terbinafine may be superior to griseofulvin for Trichophyton species (typically associated with black dot tinea), whereas griseofulvin may be superior to terbinafine for the less common Microsporum species (typically associated with gray patch tinea).²

Cultures can take 2 to 6 weeks to yield results, but terbinafine is a reasonable first choice in patients without recent travel outside of the United States because more than 89% of US tinea capitis cases are caused by Trichophyton.^2,7 However, if cultures show that the pathogen is Microsporum, patients may require treatment with griseofulvin. Microsporum infections are more common outside of the United States, particularly in South America, Southern and Central Europe, Africa, and the Middle East.³³

Prompt treatment of kerion is critical to prevent scarring and permanent hair loss.^2,20 In patients starting terbinafine, obtaining baseline liver function tests and blood cell counts is reasonable; however, further monitoring is generally unnecessary unless the patient has an underlying liver or hematologic condition or is 65 years or older.^36,37 Terbinafine is usually well tolerated; the most common adverse effects include headache, gastrointestinal symptoms, and rash. Terbinafine-related liver damage and taste disturbances are rare.³⁸

Onychomycosis is a common cause of dystrophic toenails in adolescents and adults.⁴ The distal, subungual form of onychomycosis is characterized by thickened, brittle, discolored nails (Figure 6 ¹). Onychomycosis may also present with an uncommon proximal, subungual form, which should raise suspicion for immunocompromise, and a white superficial form, which more often occurs in children^2,4 (Figure 7¹). In a study of 169 patients with clinically suspected onychomycosis, the findings that best ruled in onychomycosis included tinea pedis in the past year (LR+ = 2.6), white crumbly areas on the nail surface (LR+ = 2.3), and dry, scaly skin on the soles or palms (LR+ = 1.7).³⁹

Onychomycosis may be confused with chronic trauma or psoriasis.⁴ Adolescents and young adults can develop dystrophic toenails from playing sports that involve repeated low-level trauma.² Exclusive involvement of the little toe suggests trauma rather than fungal infection.⁴

Diagnostic testing should be used to confirm suspected onychomycosis because the treatment course is long and nonfungal mimics are common.^4,40,41 KOH preparation with staining and direct microscopy is inexpensive and can provide rapid results, but test reliability depends on the expertise of the physician. Fungal culture has poor sensitivity (59%) and carries a risk of contamination by nondermatophyte molds. However, it can provide information on the causative organism, which can help guide treatment.^3,42

Histopathology with periodic acid–Schiff stain is performed by placing toenail clippings or curette scrapings in 10% formalin solution and transporting them to the pathology laboratory. Use of polymerase chain reaction testing is increasing in the diagnosis of onychomycosis. Although it provides rapid results, access is limited.^4,5,43

Treatment courses for onychomycosis are long (4–48 weeks), failure rates are high, and recurrence rates are 20% to 25%.^20,38 Treatment is optional depending on patient preference, but many patients request treatment for cosmetic reasons or discomfort from shoes.⁴⁴ Oral antifungal therapy is generally more effective than topical therapy^38,45,46; however, some patients prefer to avoid systemic treatment. Ciclopirox nail lacquer or tavaborole may be offered with education about their low cure rates (29%–36% and 31%–36%, respectively).^38,47–49

For most patients, oral terbinafine, 250 mg once daily for 6 to 12 weeks, is preferred over oral itraconazole, other systemic azole antifungals, and griseofulvin because it is well tolerated, inexpensive, and potentially more effective. A large meta-analysis found moderate-quality evidence that azoles were less effective than terbinafine for achieving mycological cure (risk ratio = 0.77; 95% CI, 0.68–0.88).⁵⁰ Assessment of cure takes 9 to 12 months because toenails grow slowly. Oral itraconazole is a second-line agent for onychomycosis and is typically used in patients who do not respond to terbinafine; it can be dosed daily or as pulse therapy.⁵¹ Efinaconazole (Jublia), a topical antifungal recently approved by the US Food and Drug Administration, is an effective option for distal and lateral subungual onychomycosis. It has a mycological cure rate of 61.6% but is expensive.⁵²

T indotineae (previously called Trichophyton mentagrophytes genotype VIII) is a novel pathogen that causes extensive, difficult-to-treat, often reoccurring infections in patients without immunocompromising conditions.^10,12,25 T indotineae most often spreads person-to-person by direct skin contact or fomites, and rare cases of sexual transmission have been reported.⁵⁹ It is uncommon in the United States, but cases have been documented in multiple states, most frequently in patients with travel to or contact with someone who has traveled to South Asia.¹¹

Multiple morphologies have been reported, including erythematous, scaly concentric plaques (ie, ring-on-ring appearance), papulosquamous, pustular, and corticosteroid-modified tinea.^10,25 Identifying T indotineae requires fungal culture and DNA sequencing available only at select laboratories. Based primarily on studies from India, the preferred first-line drug for T indotineae infection is itraconazole (up to 3 months) because this pathogen is frequently resistant to terbinafine.^25,58 Images of T indotineae are available at https://www.cdc.gov/mmwr/volumes/72/wr/mm7219a4.htm#F1_down.

T mentagrophytes genotype VII is an emerging dermatophyte strain with a predilection for areas of sexual contact, including anogenital skin and the face (images available at https://www.cdc.gov/mmwr/volumes/73/wr/mm7343a5.htm#F1_down).⁵⁴ These infections have been reported in men who have sex with men in France since March 2021 and in the United States since 2024.^13,14,54 Identification of T mentagrophytes genotype VII requires a fungal culture, DNA sequencing, and specialized testing that is available only at select laboratories, but clinicians can initiate empiric therapy based on epidemiologic and clinical features. Based on observational data, oral terbinafine is the recommended therapy, with treatment often required for up to 3 months.^14,53

Worldwide and in the United States, cases of terbinafine-resistant T rubrum infections are increasing, including terbinafine-resistant onychomycosis.^{15,55–57,60,61} Few US laboratories can perform antifungal susceptibility testing for dermatophytes. The American Academy of Dermatology provides a list of laboratories where testing for terbinafine-resistant T rubrum and other emerging dermatophyte species is available.⁵⁸