An estimated 20–25% of the global population are affected by dermatophytoses [1]. Trichophyton rubrum is the most common causative agent in high-income countries, and Trichophyton mentagrophytes species complex, Microsporum canis, and Epidermophyton floccosum are most prevalent globally. Trichophyton schoenleinii, Trichophyton soudanese, and Trichophyton concentricum are generally limited to parts of Europe, Asia, and Africa [5, 6]. Epidemiology varies over time due to tourism and migration [2, 5, 7]. Taxonomy changes have divided the genera Trichophyton and Microsporum and added the new genera Arthroderma, Nannizzia, Paraphyton and Lophophyton [8].

Dermatophytes infect cytokeratin comprising the stratum corneum in the hair, skin, and nails, and adhere to the host via mannan glycoproteins in the fungal cell walls [9–11]. The mold grows as linear hyphae, enabling spread to deeper layers of keratin-rich structures. To utilize keratin for growth, dermatophytes break down disulfide bridges linking epidermal keratins. Keratin is rich in cysteine. Dermatophytes secrete sulfite, a reducing agent that cleaves cystine bonds via cysteine dioxygenase, contributing to keratin degradation [9–12]. Dermatophytes produce biofilms, which have been reported in both Trichophyton and Microsporum species. It is hypothesized that biofilms contribute to dermatophyte antifungal treatment failures [13, 14].

Table 2 lists risk factors contributing to dermatophytosis susceptibility.

Dermatophyte transmission is multifactorial [15]. Dermatophytes likely persist on wet surfaces, including in bathrooms and pool facilities [15–17], and may spread via shared clothing, footwear, towels, and bedding, especially with a comprised skin barrier [15, 18, 19]. Pets and stray, farm, laboratory, and wild animals have been implicated in zoonotic spread [20–22].

There are racial disparities in the prevalence of tinea infections, particularly tinea capitis [23, 24]. In a retrospective population-based study of children < 10 years of age, incident rates per 10,000 enrolled were 252.1 claimants for Black children versus 23.1 claimants for White children (p value not reported) [25]. In a prospective, cross-sectional surveillance study of 10,514 kindergarten fifth-grade children, Black versus White and Hispanic children had higher infection rates (12.9%, 1.1%, and 1.6%, respectively; p < 0.01) [26]. A commercial database study of tinea capitis in children < 18 years of age estimated the incidence rate to be sevenfold higher in Black versus White children [27]. In a cross-sectional study of 351,629 HIV patients in a tertiary healthcare system, dermatophytoses were more common in HIV- versus non-HIV-infected individuals (p < 0.0009) [28].

In a prospective survey-based study of errors made by primary care physicians in managing skin disorders, errors related to diagnosis of dermatophytoses accounted for the largest proportion of errors (32%, 102/319) [29]. In a survey-based study of board-certified dermatologists presented with 13 clinical images of fungal infections, respondents categorized cases with > 75% accuracy in only 31% of cases [30], highlighting that visual inspection alone is unreliable for diagnosis. Dermatologists play a key role not only in accurate diagnosis of superficial fungal infections but also in educating other non-dermatologists about dermatophytoses. The American Academy of Dermatology’s guidelines for the treatment of superficial mycotic infections were last published in 1996, necessitating an updated review on diagnosis and management.

Tinea corporis is most caused by T. rubrum globally. Other causes include T. tonsurans, especially when secondary to tinea capitis infection, and M. canis, particularly with exposure to infected house pets [31, 32] (Table 3).

The most common cause of tinea cruris worldwide is T. rubrum. T. mentagrophytes and T. interdigitale are becoming more common infectious etiologies globally, particularly in India [33–35]. Tinea cruris more commonly affects male adolescents and young adult men [36] (Table 3).

Risk factors, clinical features, and differential diagnosis of tinea corporis and cruris are listed in Tables 2, 4, and 5, respectively (Figs. 1, 2).

The most rapid and cost-effective diagnostic technique for tinea corporis and cruris is direct microscopic examination with 10–15% potassium hydroxide (KOH) preparation using skin scrapings of the affected area(s) showing segmented hyphae [37]. Taking abundant scrapings from the active edge of a plaque or patch increases sensitivity. A fungal culture of skin scrapings on Mycosel agar media is considered the diagnostic gold standard since it can identify the causative organism; however, turnaround time is typically several weeks, with a significant false negative rate.

Polymerase chain reaction (PCR) may rapidly detect the presence of fungal DNA and identify the fungal species [38–43]; however, PCR for dermatophytes is not performed by all laboratories, and widespread adoption has been slow in clinical practice [44, 45].

Reflectance confocal microscopy (RCM) is a non-invasive technique that is being explored for cutaneous fungal infection diagnosis [46–48]. While results are immediate, limitations include difficulty positioning the probe in certain anatomic areas, expensive equipment, and required training.

Dermoscopy is an emerging adjunctive diagnostic technique for dermatophyte infections [49–52]. Useful dermatoscopic features distinguishing tinea corporis from other dermatologic conditions include presence of peripheral dotted vessels, white ‘moth-eaten’ scale with peripheral distribution and outward peeling direction [50].

Treatment for tinea corporis and cruris is always indicated to prevent infection spread to self and others and prevent secondary bacterial infections. In general, mild or localized infection may be treated once to twice daily with topical monotherapy antifungals, including azoles, allylamines, ciclopirox, butenafine, and tolnaftate [53–56], while more disseminated disease is treated with oral antifungals. The American Academy of Pediatrics (AAP) 2021–2024 Report of the Committee on Infectious Diseases recommended application of topical antifungals directly to lesions and 1–2 cm beyond the lesion border. Although clinical resolution may be apparent after 2 weeks of therapy, treatment is recommended for 4–6 weeks. If there is no clinical improvement after 2 weeks of topical therapy, an alternate diagnosis or systemic therapy may be considered [56].

A Cochrane Database Systematic Review of 129 studies involving 18,086 participants with tinea corporis or cruris supported the use of topical terbinafine and naftifine 1%, and clotrimazole 1%, based on clinical and/or mycological cure rates versus placebo. Azoles and benzylamines had similar mycological cures rates (risk ratio [RR] 1.01, 95% confidence interval [CI] 0.94–1.07) [57, 58]. In a mixedtreatment comparison meta-analysis of 65 articles including 14 topical antifungal treatments for tinea corporis, cruris, and pedis, mycological cure at treatment completion was not significantly different among the topical antifungals studied [59]. However, butenafine, naftifine, and terbinafine, a benzylamine and allylamines, respectively, were the most effective among 13 therapies for sustained cure, defined as maintaining cure from infection for ≥ 14 days, compared with azoles. Cost consideration is necessary in most cases since there are limited efficacy data to support one class over another. Therefore, azoles, which are cheaper on average, may be used as first-line therapy, followed by allylamines for first-line treatment failures [58]. Topical antifungals indicated for tinea corporis and cruris are listed in Table 6.

Position statements released in 2019 by the Canadian Pediatric Society recommend that adjunctive topical corticosteroid therapy be avoided due to the risk of skin atrophy [60]. Topical corticosteroid misuse is hypothesized to contribute to antifungal resistance [61, 62]. Combination topical antifungal-corticosteroid products should be avoided. Antifungal monotherapy is effective and may decrease inflammation and pruritus.

For widespread infection involving multiple areas, disease refractory to topical therapy, or tinea corporis with vellus hair involvement (Fig. 3), oral treatment with either terbinafine or itraconazole is recommended [52]. Griseofulvin and fluconazole are second-line treatments and require longer treatment courses. With partial response, therapy is continued and patient lifestyle factors, including hygiene, which may contribute to incomplete cure are assessed. With no response to treatment, a change to another oral antifungal (i.e. terbinafine to itraconazole) is indicated. Follow-up for at least 4 weeks after clinical cure is recommended to prevent recurrence.

Terbinafine is the recommended first-line therapy in treatment-naïve patients with tinea corporis or cruris [53]. In a randomized controlled trial of 50 patients with tinea corporis treated with 500 mg/day of griseofulvin versus 500 mg/day of terbinafine for 6 weeks, successful treatment rates, defined as either clinical and mycological cure or mycological cure with only slight residual clinical signs of infection, were 73% versus 87%, respectively (p value not reported) [63]. In a study of 64 patients diagnosed with tinea and/or tinea cruris receiving terbinafine 250 mg/day versus griseofulvin 500 mg/day for 2 weeks, mycological cure was 87.1% versus 54.8% at 6 weeks follow up (p < 0.05) [64]. In a prospective trial of 60 patients with tinea corporis and/or cruris randomized to terbinafine 250 mg/day versus terbinafine 500 mg/day, complete cures were similar (20% vs. 33.3%; p = 0.82) [65].

In a randomized controlled trial of 78 patients with tinea corporis or cruris treated with itraconazole 100 mg/day or griseofulvin 500 mg/day for 15 days, clinical (72% vs. 51%; p < 0.03) and mycological cure (87% vs. 57%; p < 0.03) were higher for itraconazole versus griseofulvin [66]. A double-blind, randomized controlled trial of 40 patients with clinically and mycologically confirmed tinea corporis or cruris comparing itraconazole 100 mg/day versus griseofulvin 500 mg/day for 15 days showed no difference in complete cure at treatment completion (22.2% vs. 23.8%; p = 1.000) nor at 15-day post-treatment follow-up (55.6% vs. 52.4%; p = 0.672) [67]. Physicians can consider a minimum dose of itraconazole 200 mg to treat tinea corporis and/or cruris, as underdosing may contribute to resistance development.

Recommended oral therapy dosing for tinea corporis and cruris is listed in Table 7 [64, 68, 69].

Tinea capitis primarily affects children, particularly in the prepubertal years [70, 71]. Black children are most frequently affected in the US (Fig. 4). In a prospective, cross-sectional surveillance study of 10,514 kindergarten fifth-grade children, Black children had the highest rate of T. tonsurans tinea capitis infection (12.9%) versus Hispanic (1.6%) and White children (1.1%) [p < 0.01] [25]. Although uncommon, tinea capitis may affect adults [72–74].

Common causative organisms of tinea capitis are listed in Table 3. In general, species within Trichophyton and Microsporum genera cause tinea capitis, including Microsporum audouinii, Trichopython violaceum, or Trichophyton tonsurans. In the US, T. tonsurans is the most common causative species, followed by M. canis (Fig. 5) [23].

The hair shaft infection presents in one of three distinct forms: endothrix, ectothrix, or favus (Fig. 6), which drive the clinical appearance. Endothrix and ectothrix infections are the most common presentations [8, 75]. Kerion is an inflammatory presentation of tinea capitis. Risk factors, clinical features, and differential diagnosis are described in Tables 2, 4, and 5, respectively.

Physical examination identifies signs of tinea capitis, such as black dots associated with endothrix tinea capitis. Ectothrix infections caused by Microsporum species or T. schoenleinii may fluoresce a green/yellow color or blue/white color, respectively, while endothrix infections do not exhibit fluorescence Wood’s lamp; however, Wood’s lamp examination in not reliable for definitive diagnosis [75].

Fungal culture using Mycosel agar culture remains the gold standard of diagnosis for tinea capitis for species identification. Samples are collected using a sterile toothbrush, moistened cotton swab, or by scraping with a no. 15 blade or glass slide over the affected area. Infected hairs often break off and may be sent along with scrapings [76–78]; however, the results may take 2–4 weeks, which may significantly delay therapy initiation and increase transmission risk [8, 75, 76, 79]. Intense inflammation associated with kerion may cause false negative results and, in general scrapings, should be taken prior to initiating antifungal treatment. A KOH preparation may be used to screen for tinea capitis while fungal cultures are pending. KOH is applied to a glass slide and the proximal ends of a hair shaft are examined micro-scopically. The test is positive if fungal spores are found within or outside of the hair shaft (endothrix and ectothrix, respectively).

PCR may be used for tinea capitis diagnosis, although is rarely employed in clinical practice. In a descriptive cross-sectional study of 115 scalp scrapings and hair fragments from children aged 1–16 years diagnosed with tinea capitis, PCR-ELISA had 84% sensitivity and 85% specificity compared with fungal culture used as the gold standard [80]. In a cross-sectional, descriptive study on 129 hair samples from patients clinically diagnosed with tinea capitis, real-time PCR had 89.3% sensitivity and 75.3% specificity compared with fungal culture (p < 0.05) [81]. A PCR test for M. canis identification achieved 100% sensitivity and specificity in a study of 130 clinical isolates of dermatophytes, 10 yeast/mold isolates, 12 hair and skin samples from animals with/without M. canis infection, and 35 patient specimens, 7 of which were positive for M. canis [82]. M. canis is less susceptible to terbinafine than Trichophyton species, requiring prompt therapy to avoid long-term sequelae, including permanent hair loss.

RCM has been used for tinea capitis diagnosis, whereby hyphae appear linear, with high reflectivity and conidia near the hair shaft present as round and hyperreflective [46, 83, 84]. In one case series including four patients with tinea capitis, diagnosis was achieved in approximately 5 min per patient [46].

Trichoscopy, dermoscopy of the hair and scalp, is a useful diagnostic adjunct. Trichoscopic findings include comma hairs, corkscrew hairs, broken hairs, dystrophic hairs, and/or black dots [85–88]. In a cross-sectional study comparing trichoscopic features of 15 children with tinea capitis with 10 patients with alopecia areata, yellow dots, exclamation mark hairs, and vellus hairs differentiated alopecia areata from tinea captitis [85].

Although mycological confirmation before starting treatment is considered best practice, diagnostic methods may not be readily available or may result in significant delays to therapy initiation. The 2014 British Association of Dermatologists tinea capitis guidelines indicate that it is appropriate to begin treatment when tinea capitis is strongly suspected clinically, including in the presence of scaling or kerion [89].

First-line therapy for tinea capitis is oral antifungal therapy, as topical therapy cannot effectively penetrate the hair shaft. Although many controlled trials described herein are exclusive to pediatric patients, the same medications are used in adult patients. Pediatric treatment regimens are described in Table 7, along with commonly accepted adult dosing recommendations [90].

Griseofulvin and terbinafine are US FDA-approved tinea capitis treatments and are the most commonly used therapies [56]. The AAP 2021–2024 Report of the Committee on Infectious Diseases states that higher doses of griseofulvin than are FDA-approved may be used, and high-dose griseofulvin is the standard of care for pediatric patients with M. canis tinea capitis (griseofulvin microsize 20–25 mg/kg/day, maximum 1 g/day, or ultramicrosize 10–15 mg/kg/day, maximum 750 mg/day, for ≥ 6 weeks and until clinically clear).

For tinea capitis due to Trichophyton, both griseofulvin and terbinafine are acceptable first-line therapies, but choice of agent should be tailored to speciation, if known [91]. A 2016 Cochrane review found that 4 weeks of terbinafine versus 8 weeks of griseofulvin treatment had similar efficacy in achieving complete cure across three studies including 328 participants with Trichophyton tinea capitis (84.2% vs. 79%; RR 1.06, 95% CI 0.98–1.15) [91]. In two randomized, investigator-blinded, active-controlled trials in children aged 4–12 years with clinically diagnosed and KOH-confirmed tinea capitis, terbinafine hydrochloride oral granules (n = 1040, 5–8 mg/kg/day) versus griseofulvin microsize (n = 509, 10–20 mg/kg/day) for 6 weeks had higher complete (45.1% vs. 39.2%; p = 0.024) and mycological cure rates (61.5% vs. 55.5%; p = 0.029) on pooled data at week 10. Terbinafine and griseofulvin had similar efficacy for clinical cure when compared with pooled data at week 10 (63.0% vs. 58.8%; p = 0.10). Terbinafine had greater efficacy for mycological, clinical, and complete cure in children with T. tonsurans tinea capitis specifically (complete cure 52.1% vs. 35.4%; p < 0.0001) [92]. For Microsporum tinea capitis, a meta-analysis of two studies including 334 participants found greater complete cure rates with 6–12 weeks of griseofulvin versus 6 weeks of terbinafine (50.9% vs. 34.7%; RR 0.68, 95% CI 0.53–0.86) [91]. If the exact species is unknown, griseofulvin is recommended as first-line therapy in treating tinea capitis [93].

Due to concerns about resistance of T. tonsurans to griseofulvin, fluconazole and itraconazole may be considered as non-FDA approved therapeutic alternatives [94] and for patients with contraindications to terbinafine and/or griseofulvin, or in patients who cannot tolerate high griseofulvin doses [95]. Fluconazole is FDA-approved for children <2 years of age, for indications other than tinea capitis. A randomized, multicenter, three-arm trial in children aged 3–12 years comparing fluconazole 6 mg/kg/day for 3 weeks followed by 3 weeks of placebo with fluconazole 6 mg/kg/day for 6 weeks and with griseofulvin 11 mg/kg/day for 6 weeks, showed no differences between mycological (44.5%, 49.6%, and 52.2%, respectively; p = 0.40) or clinical cure (87.8%, 89.8%, and 90.9%, respectively; p = 0.61) [95]. For griseofulvin, physicians could consider a dose of 20 mg/kg/day. A randomized controlled trial of 34 children and 1 adult comparing itraconazole 100 mg daily for 6 weeks with ultra-micronized griseofulvin 500 mg daily for 6 weeks for mostly M. canis tinea capitis showed complete cure 8 weeks after therapy completion (88% vs. 88%; p-value not reported) [96]. Another randomized, double-blind controlled trial of weight-based itraconazole and terbinafine each administered for 2 weeks for mostly T. violaceum tinea capitis showed complete cure rates of 85.7% and 77.8%, respectively at week 12 (p > 0.05) [97]. A multicenter, randomized, single-blinded trial of 200 patients treated with griseofulvin microsize 20 mg/kg/day for 6 weeks, terbinafine 62.5–250 mg (weight dependent) for 2–3 weeks, itraconazole 5 mg/kg/day for 2–3 weeks, or fluconazole 6 mg/kg/day for 2–3 weeks showed similar efficacy (measured as a combination of mycological cure and either clinical cure or only a few residual symptoms) among all arms 12 weeks after the start of therapy (griseofulvin: 92%, 95% CI 88.2–95.8%; terbinafine: 94%, 95% CI 90.6–97.4%; itraconazole: 86%, 95% CI 81.1–90.9%; fluconazole: 84%, 95% CI 78.8–89.2%) [98]. Fluconazole and itraconazole are second-line therapies. Dosing of oral antifungals is described in Table 7.

Antifungal shampoos may be used as adjunctive therapy by patients and their household members for tinea capitis in the first 1–2 weeks following diagnosis, to reduce transmission and possible re-infection [36]. In a randomized, double-blind controlled trial of 40 children aged 1–11 years diagnosed with tinea capitis and treated with an 8-week course of ultramicronized griseofulvin, selenium sulfide shampoo 1% and ciclopirox shampoo 1% showed equal efficacy in mycological cure 4 weeks after treatment completion when used as adjunctive treatment twice per week (week 12: 91.7% vs. 95.2%; p = 1) [99]. A study of ketoconazole 2% shampoo used as monotherapy for tinea capitis in 16 Black children aged 3–6 years, over an 8-week treatment period, showed 50% reduced viable arthroconidia numbers after 2 weeks of treatment, clinical cure in 93% of children at week 8, and complete cure in 33% of children 12 months post-treatment [100]. It is recommended that children and their families are instructed on disinfecting hair tools following a diagnosis of tinea capitis, to prevent re-infection or transmission to other household members [101].

It is recommended that patients are reassessed after 1 month of therapy to determine clinical response. If there is no response to therapy despite adherence to prescribed medications, an alternative antifungal is recommended [56].

Table 3 lists the most common causative species of tinea barbae and faciei, by region.

Tinea barbae may present as an inflammatory or non-inflammatory morphology, and usually involves an ectothrix infection pattern. Tinea faciei often presents similarly to tinea corporis. Risk factors, clinical features, and differential diagnosis of tinea barbae and are listed in Tables 2, 4, and 5, respectively (Figs. 7, 8).

Diagnostic methods related to tinea capitis, described in Sect. 3.3, apply to tinea barbae, whereas diagnostic methods related to tinea corporis, described in Sect. 2.3, apply to tinea faciei.

Treatment principles for tinea capitis, described in Sect. 3.4, apply to tinea barbae. Oral antifungal therapy is first-line as topical therapy cannot penetrate the hair shaft adequately. Treatment principles for tinea corporis, described in Sect. 2.4 apply to tinea faciei. Topical antifungal therapy is first-line therapy, while oral therapy is reserved for refractory or widespread involvement.

Due to dampening of the local immune response, classic clinical features of dermatophytoses may not be present in patients with tinea incognito. Steroid-modified dermatophytosis has been described as ‘tinea pseudoimbricata’ due to its similarity in appearance to tinea imbricata caused by Trichophyton concentricum, which is endemic in parts of Southeast Asia [102], presenting with concentric erythematous rings and associated with moderate to severe pruritus (Fig. 9) [103]. Risk factors and clinical features for tinea incognito are listed in Tables 2 and 4, respectively.

Because tinea incognito is a steroid-modified infection and does not present with classic features typically present with dermatophyte infections, diagnosis may be delayed. A high suspicion for tinea incognito is necessary if a patient describes a rash coupled with corticosteroid administration, resulting in a temporary improvement of the lesions, followed by worsening and spread [104].

Diagnostic methods of tinea incognito mirror those for tinea corporis and cruris, described in Sect. 2.3. It is recommended that diagnostic methods, including KOH preparation and fungal culture, are performed after steroid discontinuation. Dermoscopy may show black dots surrounded by a white-yellow halo, a sign of vellus hair involvement in dermatophytosis [105].

Once tinea incognito has been diagnosed, topical corticosteroids should be stopped and antifungal therapy initiated. If oral corticosteroids are identified as the culprit in cases of tinea incognito, an alternative treatment should be considered. The treatment thereafter follows that of tinea corporis, cruris, and/or faciei, described in Sect. 2.4.

Tinea pedis typically affects post-pubescent adolescents and adults [70] and is most often caused by T. rubrum, T. interdigitale, T. mentagrophytes, and E. floccosum [106]. Common causative species are listed in Table 3. In children, T. tonsurans is the common causative organism [69]. Tinea pedis occurs more often in older adults and may be more common in males than in females [107–111]. Tinea pedis is a common problem among developed and developing countries, with a global prevalence estimate of 3–15% [109–113]. In a study of 6932 participants with tinea pedis in the All of Us database 2017–2021, higher adjusted odds of tinea pedis were observed in Black and Hispanic participants (odds ratio [OR] 1.29, 95% CI 1.20–1.38, and OR 1.38, 95% CI 1.28–1.48, respectively), individuals ≥ 75 years of age (OR 1.45, 95% CI 1.33–1.57), individuals with income <$35,000 (OR 1.09, 95% CI 1.02–1.16), and individuals with a physical disability (OR 1.56, 95% CI 1.08–1.24) [110]. Epidemiology of tinea manuum infections is far less studied than that of tinea pedis.

There are three major clinical presentations of tinea pedis, namely interdigital (Fig. 10), hyperkeratotic (‘moccasin-type’), and vesiculobullous (inflammatory) tinea pedis, and a rare ulcerative form. T. rubrum typically causes chronic tinea pedis, whereas T. mentagrophytes is associated with inflammatory lesions [114]. Risk factors, clinical features, and differential diagnosis for tinea pedis (Fig. 11) and manuum (Fig. 12) are listed in Tables 2, 4, and 5, respectively.

Diagnosis of tinea pedis and tinea manuum is primarily based on clinical features, coupled with a positive fungal culture, KOH preparation demonstrating hyphae, or PCR.

Patient education regarding hygiene and proper foot care is an important aspect of management for tinea pedis, and consequently tinea manuum. Patients are instructed to keep feet clean and dry, including use of sweat-wicking socks to avoid sweat pooling [115, 116]. Patients are advised to wear shoes in communal areas, including in public gyms, showers, and pools. Although onychomycosis is beyond the scope of this review, proper nail care, including keeping nails short and clean, is also important for managing tinea pedis, as coexisting onychomycosis may preclude cure [38, 116, 117].

Topical antifungal therapy is the mainstay of treatment for tinea pedis. Per the AAP 2021–2024 Report of the Committee on Infectious Diseases, 2 weeks of therapy is sufficient for mild tinea pedis in children. Topical treatment in adults is recommended for at least 4 weeks. A Cochrane Library Systematic Review of 67 randomized controlled trials from 1970 to 2005 included participants using topical therapy who had mycologically diagnosed foot and toenail fungal infections. Of these, 11 trials (n = 1144) included in a meta-analysis comparing allylamines and azoles showed an RR of treatment failure of 0.63 (95% CI 0.42–0.94), favoring allylamines [118]. A 2012 systematic review on the efficacy and safety of topical antifungals for the treatment of dermatophytosis included a meta-analysis of 17 randomized controlled trials, including 1781 participants, comparing allylamines, including naftifine and terbinafine (1% or 2%) used for 1–6 weeks, with azoles or imidazoles, including econazole and miconazole (1% or 2%) used for 2–6 weeks, and found no statistically significant difference in mycological cure at the end of treatment [59]. A 2022 systematic review of randomized controlled trials examining 1042 participants with tinea pedis across seven studies found that topical terbinafine and topical butenafine, a benzylamine, were similarly efficacious (RR 1.3, 95% CI 0.4–4.4) [119]. However, limitations included lack of reporting on baseline characteristics in each treatment arm [119]. Taken together, topical treatment with azoles, allylamines, and benzylamines are all effective for tinea pedis treatment. Therefore, choice of therapy may be dictated by cost, availability of a specific class of medication, or physician preference. It has been suggested a cost-effective strategy is to utilize topical azoles as first-line therapy, followed by allylamines in cases of therapy failures [59]; however, more up-to-date studies are needed to validate this recommendation. It is important to ensure that patients complete the treatment regimen to prevent relapses [116].

Newer topical antifungals include sertaconazole 2% cream and luliconazole 1% cream. In a prospective, openlabel, randomized controlled trial of 313 total patients (232 patients with tinea pedis) using sertraconazole solution or cream twice daily for 28 days, efficacy (defined as a negative culture test and reduction of clinical severity) was achieved in 90.6% and 88.9% of patients, respectively [120]. A double-blind, randomized, vehicle-controlled, phase III study of 321 patients with tinea pedis treated with luliconazole cream 1% showed complete clearance at day 42 in 26.4% (28/106) of patients randomized to luliconazole cream 1%, versus 1.9% (2/103) vehicle (p < 0.001) [121]. In two randomized, double-blind, vehicle-controlled studies of 495 subjects with tinea pedis, patients were treated with econazole nitrate 1% foam for 4 weeks, and complete cure (negative KOH, negative fungal culture, complete clinical resolution) was achieved by 24.3% of patients at day 43 for the active drug versus 3.6% for vehicle (p < 0.001) [122].

Tinea pedis refractory to topical therapy may be treated with oral antifungals. First-line therapy for refractory tinea pedis is oral terbinafine. A 2012 Cochrane Library systematic review examining systemic treatments for fungal infections of the skin of the foot included 15 trials and 1438 participants. Of these, two trials of 71 participants compared terbinafine and griseofulvin, with a pooled RR of 2.26 (95% CI 1.49–3.44) favoring terbinafine. There was no significant difference in mycological cure between terbinafine and itraconazole (RR 1.07, 95% CI 0.92–1.25), fluconazole and itraconazole (RR 1.06, 95% CI 0.87–1.30), or fluconazole and ketoconazole (RR 1.04, 95% CI 0.92–1.17) [123]. In addition, clinical subtype of tinea pedis did not influence response to oral therapy [123, 124]. The incidence of liver injury with terbinafine is extremely low, but the drug should be avoided in patients with pre-existing liver disease, and baseline liver function testing is recommended [124–128]. Oral itraconazole may be considered as second-line due to hepatoxicity and cardiotoxicity and frequent drug–drug interactions. Oral ketoconazole should be avoided due to more severe risks of hepatotoxicity and due to more favorable safety profiles of terbinafine and itraconazole [116].

Patient preference is important when prescribing therapy for tinea pedis. In a cross-sectional study evaluating antifungal products for tinea pedis on Amazon.com in 2018, functionality was the most cited positive (14%) and negative (35%) feature for over-the-counter antifungal therapy based on consumer rating and reviews, with specific comments related to itching/burning relief and number of applications required for relief predominating [129]. Non-pharmacologic measures may be used as adjunct therapy, in addition to topical and/or oral antifungal therapy for tinea pedis and manuum. In a cross-sectional survey study of 152 patients with tinea pedis, 55.9% reported use of at least one non-pharmacological therapy for tinea pedis, including cologne, saltwater, vinegar soaks, and henna [130]. Vinegar soaks may be applied using old cotton socks, rather than tub soaks, to increase convenience and compliance [131]. Salicylic acid peels and tea tree oil may also be used to improve clinical symptoms, but are not effective for achieving mycological cure [132, 133].

The treatment algorithm for tinea manuum closely resembles that of tinea pedis, with topical antifungal agents as the preferred choice of therapy. Indications for systemic antifungals for tinea manuum include co-occurring fingernail infection and two feet-one hand syndrome [134, 135].

Risk factors for chronic or recurrent dermatophytosis are listed in Table 2.

In response to an evolving landscape of recurrent, chronic, and recalcitrant dermatophytosis affecting the Indian subcontinent in recent years, the Indian Association of Dermatologists, Venereologists and Leprologists created the Task Force Against Recalcitrant Tinea (ITART) in 2017 to develop a consensus on the management of tinea affecting the glabrous skin (tinea corporis, tinea cruris, and tinea faciei), which was updated in 2020 [53]. The task force emphasized the importance of maintaining personal hygiene as a key component of managing tinea infections, including thoroughly drying skin after bathing, thoroughly drying clothes after washing, and avoiding sharing soaps, clothes, and other linens.

The 2020 ITART guidelines recommend that patients follow-up 3 weeks after beginning oral therapy to assess clinical response, and state that with inadequate response to terbinafine 250 mg daily after 3 weeks, the dose may be increased to twice daily. However, the FDA-approved dosage is 250 mg daily. The guidelines also recommend topical and oral antifungal therapy combinations for most patients at a longer duration than would otherwise be recommended to dermatophytosis-naïve patients. The Task Force recommended prescribing dermatophytosis-naïve patients itraconazole 100 mg for 3 weeks, and patients with chronic, steroid-modified, or recalcitrant infections, 100 mg twice daily for 4 weeks [53]. Expert consensus is lacking on the most appropriate dosing regimen of itraconazole for dermatophytoses; however, because of concerns that underdosing could lead to resistance, physicians could consider dosing itraconazole 100 mg twice daily at a minimum. ITART also recommends that topical therapy be applied twice daily and for 2 weeks after clinical resolution.

In 2018, an Expert Consensus on the Management of Dermatophytosis in India, including tinea pedis, was developed [188]. Experts recommended tinea pedis of any duration and severity with combination topical and systemic antifungal therapy. Azoles were recommended as first-line topical therapy. Terbinafine 250 mg once daily was recommended for naïve tinea pedis, and itraconazole 200–400 mg/day was preferred for severe or refractory infection. Recommended treatment for naïve tinea pedis is 2–4 weeks, and > 4 weeks for chronic, severe, or recalcitrant infection [188].

Antifungal resistance may develop for a variety of reasons, including host, pathogen, environmental, and pharmacologic factors [136]. Certain dermatophyte strains, including some Trichophyton species, may acquire resistance to antifungal drugs such as terbinafine; these antifungal-resistant strains can cause infection and person-to-person transmission [193]. It is hypothesized that the increased prevalence of antifungal-resistant dermatophyte infections in India stems from overzealous use of antifungal therapies, whether through empiric treatment of suspected but unconfirmed dermatophytosis or through prescription sharing [194–197]. Steroid cream sales in India are estimated at US$329 million, with a large proportion containing an antifungal combination [192]. Corticosteroid-antifungal-antibacterial combination therapies are available over-the-counter in India and other South and Southeast Asian countries at relatively low cost. Additionally, they are overprescribed for the treatment of a variety of dermatoses, even non-fungal dermatoses. These combination topical therapies often contain high-potency steroids, such as clobetasol, and use of these therapies is likely a major driver of resistance [191, 192]. While these medications may temporarily improve clinical symptoms of dermatophyte infections, including pruritus, they are ultimately problematic in altering the classic morphology of cutaneous fungal infections, leading to delayed diagnosis [102, 191, 192, 198, 199]. These combination topical therapies reduce local cellular immunity at sites of dermatophyte infections, allowing for severe dermatophytosis to develop [191, 192].

The pathogen now widely known as Trichophyton indotineae was first identified in 2017 and was referred to as Trichophyton mentagrophytes genotype VIII. Although a member of the T. mentagrophytes species complex, T. indotineae represents a frequently terbinafine-resistant species caused by mutations in the gene encoding squalene epoxidase (SQLE), a key enzyme in the ergosterol biosynthetic pathway whose inhibition results in accumulation of squalene, depletion of ergosterol, and arrest of fungal growth [200]. Mutations in the SQLE gene lead to ineffective enzyme function and cause elevated minimum inhibitory concentrations (MICs) of terbinafine. T. indotineae is distinguished from T. mentagrophytes in part by sequence differences across the genome including the ITS region [200–203]. Therefore, T. indotineae was recognized as a separate species in 2020. This newly identified species is primarily responsible for the epidemic-level prevalence of dermatophyte infections in India [204].

While T. indotineae is believed to have been present in India, Australia, Iran, and Oman since 2004 [196], the first clinical cases of what is now known as T. indotineae dermatophytosis were described in India after 2014, where chronic and recalcitrant dermatophytosis concerned dermatologists for the past decade [53]. T. indotineae dermatophytosis was thereafter recognized in other Asian countries and across Europe [205–215]. The first cases of T. indotineae dermatophytoses in the US were reported in February 2023 in New York City, when two patients with severe tinea infections failed to clear despite treatment with oral terbinafine [197]. As such, T. indotineae dermatophytosis is now recognized as a worldwide problem [216].

Clinically, T. indotineae dermatophytoses evolve differently than classic tinea infections. T. indotineae dermatophytoses present as extensive, severe, and/or refractory tinea corporis, cruris, and/or faciei infections [33], and are characterized by intense pruritus, widespread anatomic involvement, and are highly contagious. These infections are highly inflammatory and lesions may be large and numerous [102, 199].

An added complication of identifying T. indotineae dermatophytoses is that traditional culture-based techniques utilized for dermatophytosis diagnosis fail to correctly identify T. indotineae, instead resulting in diagnoses of T. mentagrophytes or T. interdigitale dermatophytoses [53, 217, 218]. Therefore, T. indotineae dermatophytosis must be confirmed using molecular-based methods, such as PCR, to avoid misdiagnosis and delay of appropriate treatment. In the US, dermatologists are encouraged to contact their state public health department, who can assist in identifying appropriate testing protocol and laboratories that can perform genomic sequencing [197].

Optimal treatment guidelines for T. indotineae dermatophytosis are lacking and current treatment recommendations are based on individual cases or case series. Due to wide-spread resistance to otherwise first-line oral agent terbinafine, oral itraconazole is the drug of choice for treating T. indotineae dermatophytosis. In a 2020 study of 200 patients with microscopy-confirmed tinea infection in India, treatment with 8 weeks of itraconazole was superior to treatment with fluconazole, griseofulvin, and terbinafine (p < 0.001) for both clinical and mycological cure [219]. Although the patients included in this study were not confirmed T. indotineae cases, patients meeting the inclusion criteria had chronic or chronic-relapsing tinea corporis, cruris, or faciei (duration of tinea ≥ 3 months, or tinea present for ≥ 3 months that improved but relapsed within 1 month), suggesting possible T. indotineae infections. A double-blind, randomized trial of 149 adult patients with tinea corporis/cruris involving > 5% body surface area receiving different itraconazole dose regimens (100, 200, 400 mg/day) showed similar complete cure rates for the 100 mg and 200 mg doses (HR 1.44, 95% CI 0.91–2.30; p = 0.12) and treatment duration (mean ± standard deviation [SD] 7.7 ± 4.73 vs. 7.2 ± 3.81 weeks; p = 0.902), with 400 mg superior for both outcomes (100 vs. 400 mg groups; HR 2.87, 95% CI 1.78–4.62, p < 0.01; 200 vs. 400 mg groups (HR 1.99, 95% CI 1.28–3.09; p = 0.02). Although the 200 and 400 mg groups had 63% and 120% higher associated costs versus the 100 mg group in achieving cure [68], use of higher itraconazole doses to achieve complete cure may be more cost-effective overall. A dose of itraconazole 200 mg daily may be used to treat infections unresponsive to first-line oral therapies, with the caveat that treatment may be needed for > 3 months [188, 197]. Topical luliconazole cream may also be used although oral therapy is the mainstay of treatment [220].

Combination therapy with terbinafine and itraconazole has been studied for recalcitrant dermatophytoses, although larger studies are needed to validate its use. In a study of 45 patients with recalcitrant dermatophytosis treated for 4 weeks with terbinafine 250 mg and itraconazole 200 mg once daily versus monotherapy with terbinafine 250 mg twice daily or itraconazole 200 mg twice daily, at 12 weeks, 100% of the combination therapy group achieved complete cure versus 80% and 86.7% in the terbinafine-only and itraconazole-only groups, respectively (p = 0.207) [221]. In a study of 60 patients with clinical and KOH-positive tinea corporis, cruris, or faciei, at 3 weeks, 90% of patients treated with combination therapy with terbinafine 250 mg once daily and itraconazole 200 mg once daily achieved complete cure versus 35% and 50% in the terbinafine and itraconazole monotherapy groups, respectively (p = 0.002) [222].

Resistance to oral itraconazole among dermatophyte infections has been observed [205, 223–225]. In such instances, voriconazole and posaconazole, two oral azole antifungals ordinarily reserved for invasive mold infections, may be utilized. When antifungal therapies fail, physicians should investigate the cause of treatment failure, including adherence to therapy, confirmation of the diagnosis, and whether resistance is suspected. Antifungal susceptibility testing (AFST) could be pursued but is not yet well established in relation to dermatophyte infections.

It is recommended that itraconazole capsules are administered with high-fat foods and an acidic beverage, such as juice, to increase absorption and bioavailability. In contrast, the oral solution should be administered on an empty stomach, either 1 h before, or 2–3 h after, a meal [226]. Triazole antifungals are also associated with substantial drug–drug interactions and adverse effects [227]. For example, coadministering itraconazole with a proton pump inhibitor may reduce bioavailability via gastric acid suppression. Therapeutic drug monitoring may be required for triazoles to ensure adequate dosing, although target serum drug levels have not yet been established for the treatment of resistant dermatophytoses, and the correlation between serum levels and accumulation in tissue has not been established. Given the relatively infrequent use of these antifungals, dermatologists are encouraged to contact infectious disease specialists and pharmacists before prescribing. Issues with insurance coverage may arise when prescribing these less commonly used antifungal therapies, creating a barrier for patients.

T. rubrum terbinafine-resistant tinea corporis cases have been reported in the US [223]. In a retrospective study of 271 dermatophyte isolates from North American institutions from 2021 to 2022, 18.6% were resistant to terbinafine, including 21 isolates of T. rubrum [216].

Empiric treatment of suspected dermatophyte infections is discouraged. At a minimum, dermatologists can confirm mycological diagnosis using KOH with microscopy (Fig. 15), culture, or PCR before prescribing antifungal therapy [228]. If an antifungal-resistant dermatophytosis is suspected and resources are available, advanced molecular techniques (e.g., genomic sequencing of the internal transcribed spacer region) can help identify the causative organism and guide treatment [197, 229]. US dermatologists can contact their state and local health department and Centers for Disease Control and Prevention (CDC) to receive assistance with testing and report unusual cases. If advanced diagnostics are not available, empiric treatment is reasonable.

The emergence of antifungal-resistant tinea infections has several implications for clinical practice. First, prescribing combination topical antifungal-steroid medications for dermatophyte infections is strongly discouraged [53, 188, 218]. Dermatologists may educate non-dermatologists and patients on avoiding such therapies. Furthermore, dermatologists can promote the importance of not sharing prescriptions among household members, of proper adherence to recommended therapies, and of seeking examination by a dermatologist if their condition is not improving with recommended therapy [194].