Dermatophytoses

Peiying Feng¹, Macit Ilkit², Ruoyu Li³, Murat Durdu⁴, Kyung Joo Kwon-Chung⁵ and Sybren de Hoog⁶

¹Department of Dermatology, Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China; ²Division of Mycology, University of Çukurova, Adana, Türkiye; ³Department of Dermatology and Venereology, Peking University First Hospital, Beijing, China; ⁴Department of Dermatology, Dr. Turgut Noyan Application and Research Center, Başkent University, Adana, Türkiye; ⁵National Institutes of Allergy and Infectious Diseases at National Institutes of Health, Bethesda, MD, U.S.A.; ⁶Radboudumc-CWZ Centre of Expertise for Mycology, Nijmegen, The Netherlands

Latest update: 8 August 2024

Introduction

Dermatophytoses are infections of keratinized tissues affecting the epidermis, hair, and nails, caused by a group of specialized fungi, the dermatophytes. This group includes fungi belonging to the family Arthrodermataceae (order Onygenales) and they exhibit various types of association with mammals. All these genera are referred to as dermatophytes, even though some may infect warm-blooded hosts only rarely. With this definition, members of recognized dermatophytes are found in the genera Arthroderma, Epidermophyton, Lophophyton, Microsporum, Nannizzia, Paraphyton and Trichophyton (de Hoog et al., 2017). The infectious potential varies significantly among these species. The recommended collective disease name to indicate dermatophyte infections is ‘dermatophytosis’ (de Hoog et al., 2024) rather than dermatomycosis, because the latter would also cover agents of skin infection outside the Arthrodermataceae. The name ‘ringworm’ is an older designation coined to describe circular lesions produced by dermatophytes on the skin (Leung et al., 2020).
Infected hosts are mainly mammals. Among the approximately 60 species of clinically relevant dermatophytes, only Lophophyton gallinae has repeatedly been associated with infections involving the skin and wattles rather than the plumage in birds (Yamaguchi, 2019; Murata et al., 2013; Miyasato et al., 2011). In furred animals, dermatophytes are typically limited to colonization of fur and invasion of hair. The human host differs rather fundamentally because it lacks a dense fur, and fungal growth consequently often involves the glabrous skin. Human infections are mild to severe, depending on specific virulence of the fungus and on the immunological response of the host. Subcutaneous or deep infections are mostly associated with dysfunctional acquired cellular immunity.

Ecology, transmission and evolution

Dermatophytes are categorized into three main ecological groups: geophilic, zoophilic and anthropophilic, based on their natural lifestyles and their interactions with different environments. Geophilic dermatophytes thrive in soil, zoophilic dermatophytes primarily infect animals, and anthropophilic dermatophytes are adapted to humans. These three groups follow one another in the evolutionary progression, thus the genera broadly aligning with these categories. Understanding the interplay of ecology, phylogeny and medical significance has led to a more stable taxonomic system (de Hoog et al., 2017) than the previously used generic circumscriptions, which were based solely on microscopic morphology. Humans have influenced this evolutionary history significantly, since geophilic dermatophytes inhabit natural habitats, zoophilic dermatophytes are commonly found in domesticated animals, and anthropophilic dermatophytes have evolved to infect humans.

Geophilic dermatophytes

Similar to many members of the order Onygenales, geophilic dermatophytes inhabit soil. Their unique source of nutrients comprises degradation of keratinous remains of terrestrial animals. As a result, members of the family Arthrodermataceae are commonly found in mammal burrows and shelters. In these environments, they produce a sexual state in the surrounding soil. Since sexual reproduction is part of their natural life cycle, mating and ascospore production are common. Additionally, they readily produce sexual fruiting bodies in laboratories. The genus Arthroderma includes numerous geophilic species known for their sexual state. Conidia of these fungi are typically distributed asymptomatically on the fur of animals inhabiting the burrows, with the terrestrial animals themselves generally remain uninfected. Human infections are extremely rare for most geophilic species due to the lack of direct contact with contaminated soil or the mammals. While knowledge of these fungi is still limited, there is evidence of some degree of host-specificity, influenced by the animal habitat. For example, Arthroderma redellii is associated with bats (Lorch et al., 2015), and A. eboreum is found in association with badgers and rabbits (Campbell et al., 2006), both of which are burrow-building animals. However, not all dermatophytes fit neatly into these ecological categories. For example, Nannizzia gypsea is traditionally treated as a geophilic species, but is also frequently reported to cause human infections. Some case reports indicate that infections can occur directly from soil rather than from an animal carrying the fungus (Alsop & Prior 1961). Dogs with outdoor access, particularly in rural areas, can be exposed to geophilic species, like Nannizzia gypsea. These fungi can be transmitted to humans (Chermette et al., 2008; Moriello et al., 2017) through direct contact with the hair coat of the infected animals.

Diagram of hypothetical life cycles of dermatophytes. A. Geophilic dermatophyte. Clonal distribution via conidia in fur of terrestrial animals, sexual spores produced in soil. Infections in humans are very rare. B. Zoophilic dermatophyte. With respect to domesticated animals, however, the sexual cycle in soil is mostly interrupted. Host shifts to other domesticated animals occur, and human infection is common but usually does not lead to transmission. C. Anthropophilic dermatophyte. Sexual cycle is non-existent, direct transmission via contagious humans, potentially leading to epidemics.

Zoophilic dermatophytes

Animal domestication, which has created the novelty of farm and pet animals, has disrupted the alternating sexual-clonal lifecycle of the previously geophilic dermatophytes. This disruption has led to a predominance of asexual reproduction through conidia, which are spread via animal fur. Under these conditions, there is increased contact between animal species, a phenomenon less common in natural setting. When dermatophytes infect non-preferred host, they often cause inflammatory infections (Weitzman & Summerbell, 1995). However, with repeated exposure, these fungi can adapt to new hosts, process known as a host shift – often resulting in decreased virulence (Chollet et al., 2015). There has been a noted shift from preponderantly innate to more efficient acquired cellular immunity in response to these infections; for a review, see Deng et al. (2023). Host shifts from various animal hosts to humans have led to a significant number of species adapting to human hosts, resulting in what are known as the anthropophilic dermatophytes. Example of these evolutionary events include Microsporum canis (from cat) to M. ferrugineum (Zhou et al., 2023), Trichophyton benhamiae (from guinea pig) to T. concentricum (Pihet et al., 2008), and Trichophyton equinum (from horse) to T. tonsurans (Kandemir et al., 2020). New adaptations are expected with new animals being introduced in close proximity to humans.
Zoophilic dermatophytes are also known in non-terrestrial wild animals, such as Trichophyton simii in monkeys (Boehringer et al., 1999). Human infections by this species originated from infected monkeys (Krajden et al., 2022). Trichophyton mentagrophytes caused infections among American troops in Vietnam, and the source of this outbreak was traced to the rats trapped near the army living quarters (Allen & Taplin, 1973). The majority of classic zoophilic dermatophytes have been reported to infect farm animals, and human infections from these animals are frequent. Trichophyton verrucosum is prevalent in cattle (Łagowski et al., 2019), and also T. mentagrophytes is common in ruminants (Dalis et al., 2022); T. bullosum is found in horses (Lyskova et al., 2015). Farmers and members of their families who handle cattle frequently acquire Trichophyton verrucosum infection from infected animals (Papini et al., 2008) or from troughs and stalls used by infected animals. Sources of human infection due to Lophophyton gallinae (Yamaguchi, 2019) and Nannizzia nana (Bonifaz et al., 2019) have been shown to be chickens and pigs, respectively.
Under urban conditions, pet animals are a main source of human infections by dermatophytes (Paryuni et al., 2020), with Microsporum canis being the most prevalent species (Neves et al., 2018). Infections transmitted from rodents with a dense fur, such as guinea pigs, mostly belong to the Trichophyton benhamiae complex. Recently, novel popular pets such as the African pygmee hedgehog were infected by Trichophyton erinacei (Walsh et al., 2021). In animals, non-inflammatory arthroconidia often form a thick layer around infected animal hair shafts but without cutaneous involvement.

Anthropophilic dermatophytes

A small number of dermatophytes are almost exclusively found on humans. Propagules are shed in the domestic environment, but assimilative growth of the fungus occurs only after infection. Transmission proceeds from infected hosts that are contagious. Anthropophilic species which are typically not found on domesticated animals, likely have their evolutionary origin in these animals. Throughout history, humans have expanded the range of domesticated animals in their immediate environment, and as a result the human host has come to carry a notably large number of dermatophytes adapted to humans. Trichophyton concentricum possibly emerged from T. benhamiae (Čmoková et al., 2020), T. tonsurans from T. equinum (Kandemir et al., 2020), T. interdigitale from T. mentagrophytes (Tang et al., 2021), and Microsporum ferrugineum from M. canis (Zhou et al., 2023). For T. rubrum and allies and for T. schoenleinii, no ancestral species are known.
Infections are transmitted indirectly through fallen hairs and desquamated epithelium more often than through direct bodily contact. Use of contaminated barbershop instruments, combs, hairbrushes, and hats is a common way of transmission (Winge et al., 2009). Presence of infectious propagules has also been reported in clothing (Jazdarehee et al., 2022). Infections can also be transmitted by contact with contaminated bedding and seats or other furnitures (Kane et al., 1988; Ilkit et al., 2010). Evidence indicates that infections due to anthropophilic dermatophytes can also occur by shared towels or clothing even after domestic laundry (Hammer et al., 2011). Transmission within families is common (Tuknayat et al., 2020). A major source of tinea pedis is the contaminated floors of homes or public bathing facilities (Makhdoumi et al., 2021). The incidence of species such as Trichophyton rubrum and T. interdigitale dramatically increased in developed countries after public bathing facilities for sport activities became available (Lacroix et al., 2002; Shemer et al., 2016). Direct personal contact as a means of transmission also occurs; a well-known example is transmission of T. tonsurans through wrestling (Wang et al., 2023). Trichophyton concentricum is transmitted from infected mother to child soon after birth. Malnutrition (Schofield et al., 1963) and genetic predisposition influencing skin microbiota (Er et al., 2022) also play a role (Gnat et al., 2021). CARD9-related immunodeficiency frequently leads to severe dermatophytosis (Lanternier et al., 2013; Ansai et al., 2024).

Clinical manifestations

Dermatophytes not only affect the entire skin from head to toe, but also skin appendages such as nails and hair. Skin involvement may be localized to a certain anatomical area on the body or can spread throughout the body. While dermatophytes generally cause superficial infections affecting the horny layer of the skin, they can spread to the dermis and deeper tissues in immunosuppressed patients or due to external or metabolic factors. A Wood’s lamp is used for rapid detection of superficial fungal infections of the skin. Of the three dermatophyte genera (Trichophyton, Epidermophyton, and Microsporum), only Microsporum and a few Trichophyton species (e.g. T. schoenleinii) fluoresce. Therefore, when tinea capitis is suspected, a negative Wood’s lamp test does not exclude this infection; microscopic examination and fungal culture should be performed. Characteristic fluorescence is typically observed in broken hair and in the intrafollicular portion when the hair is plucked. Bright green fluorescence is observed in M. audouinii and M. canis infections. Microsporum ferrugineum emits green-yellow fluorescence due to the tryptophan metabolite it produces. A dull yellow reflex is observed in tinea capitis caused by Nannizzia gypsea, and a dull blue reflex is observed in favus lesions caused by T. schoenleinii (Sharma & Sharma, 2016). Additionally, trichoscopy (also known as hair dermoscopy) is helpful in clinical diagnosis of tinea capitis and in evaluating its response to treatment. The presence of features such as comma hairs, corkscrew hairs, zigzag hairs, Morse code-like hairs or whitish sheaths indicate tinea capitis (Güleç, 2023). Trichoscopy also reveals involvement of vellus type hairs in patients with tinea corporis.

Characteristic features of superficial dermatophyte infections according to their location.

Hair invasion

Mammal hair can be affected by dermatophyte growth in different ways (Tang et al., 2023). In humans, hair invasion frequently accompanies tinea capitis, where damage is macroscopically visible by short, broken hairs. Two basic types can be recognized, which can be visualized with potassium hydroxide (KOH) and cytologic stains:

Ectothrix. Hyphae are formed at the outside of the hairs, breaking up into small (2-3 µm) cubical to spherical arthroconidia which are clumped around the damaged region of the hair shaft. The hair cortex is mostly swollen and damaged, and broken hairs terminate with a loose, broom-like appearance. Potassium hydroxide (KOH) digestion is required to dissolve excessive keratin and cytologic staining for visualization. Breakage is a few millimeters above the hair follicle, leading to the clinical picture known as ‘gray patch‘ (Fig. 1D; Aritonang et al., 2022).
Main causative agent: Microsporum canis.

Endothrix. Fungal cells invade the hair shaft and eventually fill the inside with arthroconidia which are 5-8 μm in diam (Peixoto et al., 2019). The cuticle remains intact; the hair may burst, break, crumble and curl at the surface of the follicle opening, leaving hairless follicles, a picture which is clinically known as ‘black dot‘ (Fig. 1B).
Main causative agents: Trichophyton tonsurans, T. violaceum.

Vellus hair infection. Human thin body hair infection leading to breakage and absence of hair (Zhou et al., 2024). Accompanying cutaneous symptoms are scaling and local inflammation.
Main causative agents: Microsporum canis, Trichophyton mentagrophytes.

Superficial dermatophytoses

This category contains those disorders in which living parts of outermost skin layers, genitalia or external ears can be affected by dermatophytes. Skin lesions are often circular with slightly raised, red margins, containing numerous scales and surrounded by reddish, itching skin. This characteristic type of infection is classically known as ‘ringworm‘, a term that is often applied to the total of dermatophyte infections. The fungus remains restricted to the stratum corneum. As a result of keratinolytic activity, metabolites are produced, which provoke inflammation. The horny layer deteriorates and becomes scaly. The affected areas expand gradually, and tissue may heal at the center. The lesions are classified according to their localization on the human body: the involvement of the scalp, face, hand, groin, palm, plantar region and the remaining other skin areas are called tinea capitis, tinea faciei, tinea manuum, tinea cruris, tinea pedis and tinea corporis, respectively. Tineas of the glabrous skin are taken together as tinea glabrosa.

Tinea capitis. Tinea capitis (Fig. 1H-K) is a rather common infection occurring predominantly in children (Hay, 2017; Wang et al., 2023) and is acquired from pet animals. Manifestations are highly variable. As the term mainly refers to the location of the infection, tinea capitis encompasses several clinical types. Depending on the etiologic agent, hair invasion is prevalently of the endothrix or ectothrix type. Initial infection occurs in the perifollicular epidermis, due to hyphae affecting the hair extending downwards from the follicle, via the cuticle, and then reaching the hair cortex. ‘Gray patch‘ (tinea alba) (Pratiwi & Setyaningrum, 2020) is the most common non-inflammatory form of tinea capitis (Farooqi et al., 2014). Poorly defined, grayish, dry, finely scaling patches are visible on the scalp; lesions sometimes extend widely (Lozano-Masdemont et al., 2019). Typically, the lesions start around the hair shaft and lead the hairs to break off 2–3 mm above the scalp. Invaded hairs show an ectothrix infection and characteristically green fluorescence under Wood’s ultra-violet light. Patients may recover spontaneously without scarring during adolescence. In an endothrix infection, the cuticle remains intact; the hair may burst, break, crumble and curl at the surface of the follicle opening, leaving hairless follicles, a picture which is clinically known as a ‘black dot‘. Fungal cells invade the hair shaft and eventually fill the inside with arthroconidia, which are 5-8 μm in diameter (Peixoto et al., 2019). This subtype is more often observed in adult patients, in which hair crumbles and breaks off at the skin surface, leaving hairless follicles (Keisham et al., 2015). The lesion may leave patchy atrophic scars after recovery. In more advanced stages of infection, perifollicular inflammation leads to complete degeneration of the hairs. This provokes further intense inflammation that progresses into the subcutaneous tissue and the perivascular area (Elmas & Durdu, 2023). Suppurating reactions are common, leading to kerion or favus, described below. Fungal metabolite production during hair infection causes more severe, inflammatory reactions than on hairless skin. The inflammatory and pustular plaques provoke extensive, permanent alopecia. Epidemiology and spectrum of etiologic agents was reviewed by Chen & Yu (2024).
Main causative agents: Microsporum audouinii, M. canis (from cats / dogs), M. ferrugineum, Trichophyton verrucosum (from cattle), T. mentagrophytes (from horses / dogs), T. tonsurans, T. schoenleinii, T. violaceum, T. soudanense.

Kerion. When there is excessive inflammation against dermatophytes, pustules and draining abscess-like nodules (Kerion celsi; Fig. 1A, C, E, F) are observed. In more advanced stages of infection, perifollicular inflammation leads to complete degeneration of the hair. This provokes further intense inflammation that progresses into the subcutaneous tissue and the perivascular area (Elmas & Durdu, 2023) leading to areas of hair loss with painful, boggy, thickened scalp, which may progress to severe hair loss with scarring alopecia. Regional lymphadenopathy is common. Due to local oozing of pus, yellowish crusts are formed, and the skin feels soft to the touch. Both ecto- and endothrix hair infection is observed (Deng et al., 2024), usually leading to extensive hair loss (Fernandes et al., 2013; Tshudy & McCann, 2023). A new epidemiological study revealed that agricultural or pet animals are the most important sources of tinea capitis (Chen & Yu, 2024). Although there are multiple draining nodules in Kerion celsi, rarely, can non-draining and interconnected nodules be detected when dissecting cellulitis-like tinea capitis, which is its main cause T. tonsurans. When these nodules are very large, histopathological differentiation is required because they clinically mimic dermatophytic mycetomas. Tinea capitis is rarely observed in adults and is clinically different from juvenile t. capitis. Alopecic areas and pustules similar to folliculitis decalvans, characterized by tuft-shaped hair, may develop (Ilkit & Durdu, 2015; Chen et al., 2015). When tinea capitis affects the posterior scalp, it can cause hard papules and nodules that resemble acne keloidalis (Sterling et al., 2007).
Main causative agents: Microsporum audouinii, M. canis, Trichophyton mentagrophytes, T. soudanense.

Favus (tinea capitis favosa; Fig. 1G). Hyphae create air spaces in the hair during decomposition. This is a chronic infection (Ilkit, 2010) characterized by the presence of sulfur-yellow, circular, cup-shaped crusted lesions (scutula) emerging around hair follicles (Iwasa et al., 2019). The scutulae have a distinctive mousy odor. The hair does not break but is lost completely and permanently due to degeneration of the follicle. Subsequent loss of hair causes a sharply delimited bald spot on the haired skin. The adjacent skin is invaded, crusty and scarred.
Causative agent: Trichophyton schoenleinii.

Tinea faciei (tinea facialis; Fig. 2A-D). Circinate erythematous plaques (Meymandi et al., 2003; Khaled et al., 2007) or erythematous macules resembling impetigo (Fig. 2A; Kimura et al., 2014) on exposed parts of the face (Lin et al., 2004). Cutaneous lesions are eventually covered with golden-yellow scales or crusts which can be readily removed (Zhang et al., 2022). Acne and folliculitis-like papulopustular lesions may be present. Geophilic and zoophilic species tend to cause excessive inflammation (Hsieh et al., 2010; Tan et al., 2020), leading to impetigo-like lesions (Kang et al., 2013). Pet animals easily transfer the disorder upon cuddling (Kim & Dyer, 2024). Such infections are mainly found in children (del Boz et al., 2012); in neonates the infection is very rare (Alkeswani et al., 2018). The most common complaints of patients are pruritus and burning sensations, which increase with heat or sun exposure. Rarely, painful erythematous nodules or plaques develop (Viera et al., 2013). Infections can be promoted by maceration, e.g., by prolonged mask wear (Agarwal et al., 2021). Infections in patients with constitutional disorders are also known, such as excess of growth hormone associated with metabolic complications (Merad et al., 2021). Infections limited to the eyebrows also occur (Zhuang et al., 2007) which may extend to the skin (Ishizaki et al., 2012). Infection of the eyelashes is referred to as ‘tinea ciliaris’, or ‘tinea blepharo-ciliaris’ when associated with blepharitis (Wang & Sun, 2018; Sahin et al., 2014). Depending on the infectious agent and the immune status of the host, lesions can be recalcitrant (Fukada et al., 2024). Also, cases are known with expansion from other parts of the body (Vazheva & Zisova, 2021). Cases of tinea faciei and t. corporis with atypical presentations are often referred to as ‘tinea incognito‘. Since tinea faciei often leads to a red face syndrome, it should be distinguished from lupus erythematosus, psoriasis, rosacea, seborrheic dermatitis and polymorphic light eruption (Welsh & Vera-Cabrera, 2014). Due to this clinical confusion, if topical corticosteroid treatment is used accidentally, tinea incognito can develop (Kim et al., 2013).
Main causative agents: Microsporum canis, Trichophyton interdigitale, T. tonsurans, T. rubrum, T. erinacei.

Tinea barbae (tinea sycosis; Fig. 2E) concerns infections of the skin and hair follicles of the bearded area of the face (Bonifaz et al., 2003; Xavier et al., 2008). Two types are known. The superficial type, characterized by erythematous patches with pustular folliculitis, is mainly caused by anthropophilic dermatophytes, mainly in the Trichophyton rubrum complex. The affected hairs are sometimes easily extracted. The deeper type presents as inflammatory nodules with kerion-like swellings, pustules and draining sinuses on the surface. Hairs are loose or broken, and the follicle may be involved. Because of its deep skin involvement, this type is often indicated with the adjective ‘profunda’ (Wendrock-Shiga et al., 2017). The infection is mostly transmitted from cattle (Wollina et al., 2018) and is rather common among farmers (Sabota et al., 1996).
Main causative agent Trichophyton verrucosum.

Tinea manuum. This is the hand-affecting counterpart of, and frequently associated with, tinea pedis. Mostly the dominant hand is involved. Small lesions between the fingers with scaly rash may finally affect larger parts of the palm which becomes hyperkeratotic (Fig. 3A; Veraldi et al., 2019). The infection involves the epidermis and causes erythema, which is particularly noted in palmar wrinkles. The skin becomes scaly, and sometimes lesions are vesiculobullous or pustular (Choi et al., 2019). Symptoms may remain absent, but patients may also experience an itching, stinging, or burning sensation. Tinea manuum is often confused with eczema or psoriasis. Dermoscopy may be helpful in clinical differentiation, revealing collar-shaped white scales, scale-crusts, and orange dots/globules in eczema, while white scales localized in skin furrows are detected in tinea manuum (Jakhar et al., 2019). Outside self-inoculation from the feet, the infection often originates from pet animals, particularly the African pygmee hedgehog (Coronado-Aguilar et al., 2018; Walsh et al., 2021).
Main causative agents: Trichophyton rubrum, T. erinacei.

Tinea corporis is a superficial dermatophyte infection of the trunk and extremities (Fig. 2, excluding areas other than the palmoplantar region, groin, face and scalp (Machnikowski et al., 2017; Tanabe et al., 2023). Tinea corporis is frequently observed in children (Starace et al., 2021). Infection of the body often occurs concomitantly with and may result from lesions on nails, scalp, groin, or beard (Szepietowski et al., 2006), but the term tinea corporis is properly applied to lesions originating on the glabrous skin. Lesions initiate as erythematous, dry and scaly plaques that extend to circular, sharply circumscribed patches with slightly elevated borders of increased inflammation and scaling. Subsequent central healing leads to the characteristic annular outline known as ‘ringworm’ (Akhoundi et al., 2020). The ringworms may be single, multiple, or confluent. Central clearing usually occurs but is often incomplete and may be associated with hyperpigmentation (Diep et al., 2020). In patients with underlying immune disorders, numerous lesions join and cover large parts of the body (Gorani et al., 2002). Tinea corporis in patients with advanced HIV infection is often widespread without circular forms (Pihet et al., 2008; Costa et al., 2015; Mariyani et al., 2022). Widespread verrucous plaques localized to the feet, lower extremities and lower abdomen due to Epidermophyton floccosum were reported in a child patient with IgA deficiency (Qiangqiang et al., 2001). Such undetermined forms are sometimes difficult to recognize in clinical practice and have therefore been indicated as ‘tinea incognito‘ (Fig. 2F). The use of corticosteroids required for other pruritic diseases, such as atopic dermatitis, psoriasis or autoimmune bullous dermatosis, also causes the lesions to spread. Therefore, microscopic examination of lesions that do not respond to steroid treatment is necessary. When pustules increase, they mimic pustular psoriasis, while the presence of papulonodular lesions suggests prurigo. Lesions may also remain low inflammatory with minimal scaling and erythema, while highly inflammatory lesions, occurring particularly with geo- or zoophilic etiologic agents (Chollet et al., 2015), are composed of pustules, vesicles, and marked erythematous macules resembling impetigo (Shimoyama et al., 2016). Vesiculobullous lesions due to Trichophyton species and Microsporum canis resemble dermatitis herpetiformis, bullous pemphigoid, or linear IgA dermatosis (Aalfs & Jonkman, 2012). Both severe and low inflammatory responses to dermatophytes may delay diagnosis. The response may be low in anthropophilic species such as T. rubrum, only scaling without erythema, and can be confused with ichthyosis, or may appear like chronic hyperkeratotic tinea pedis on glabrous skin (Freitas et al., 2013). Diagnostic difficulty occurs when tinea corporis develops in patients with congenital ichthyosis (Scheers et al., 2013). Verrucous plaques located in sun-exposed areas resemble pellagra (Bishnoi et al., 2019). Bullous lesions rarely exhibit a targetoid appearance similar to erythema multiforme (Lim et al., 2021). Importantly, dermatophyte infection in any part of the body can also trigger urticarial lesions throughout the body (Mendez et al., 2002). Although it has been reported that tinea corporis is frequently observed in children, the emerging species Trichophyton indotineae spreads globally with a wider patient population (Song et al., 2024). In this newly identified antifungal-resistant dermatophyte species, tinea corporis extends despite the use of topical and systemic antifungals (Durdu et al., 2023).
Main causative agents: Microsporum canis, Trichophyton interdigitale, T. verrucosum, T. tonsurans, T. violaceum.

Tinea imbricata (tokelau) is an unusual form of tinea corporis (Leung et al., 2019). Concentric rings (Fig. 3B; Roslan & Abdul Hadi, 2022; Veraldi et al., 2014) or dense labyrinthoid (Leung et al., 2018) superficial scaling with low inflammatory response and minimal erythema, spreading out peripherally over many years, creating a distinctive appearance. The chronic disorder is generally linked to Trichophyton concentricum; if similar lesions are caused by another dermatophyte species, the terms ‘tinea indecisiva‘ (Sonthalia et al., 2015) and ‘tinea pseudoimbricata‘ (Suzuki et al., 2021) have been applied.
Causative agent: Trichophyton concentricum.

Tinea cruris (jock itch, tinea glutealis). Pruritic lesions on and around the groin affecting the warm, moist areas of the body. The infection begins as a small erythematous rash in the groin fold, usually on both sides, extending with circular lesions to the inner thighs (Fig. 3C, D; Firooz et al., 2021). The lower abdomen can be involved, and frequent extension to the perineum and perianal areas is observed. Ring-like lesions may also appear on the buttocks. The genital areas, especially the scrotum, are rarely involved. Particularly when the infection is caused by a dermatophyte with increased virulence such as Trichophyton indotineae, extension with tinea corporis is observed (Uhrlaß et al., 2022; Sardana et al., 2023). Early infections caused by this emerging dermatophyte had a sexual transmission route (Kupsch et al., 2019; Luchsinger et al., 2015; Nenoff et al., 2020). Causative agents of tinea cruris are anthropophilic dermatophytes and therefore infected patients are contagious, or the infection is transmitted by autoinoculation from a reservoir on the hands or feet. Approximately one half of patients with tinea cruris have coexisting tinea pedis. With underlying immune disorders, erythematous, oozing, crusted plaques may appear (Bhagra et al., 2013; Reddy et al., 2022). Secondary bacterial or viral involvement may occur (Mathur et al., 2023). ‘Tinea genitalis’ (Fig. 3E; white dot) is a variant of tinea cruris occurs on the scrotum of male patients. Whitish, dry, cottony superficial growth is observed with limited inflammation with or without itching. Pale yellowish crusts and scales are firmly attached to the scrotum and show erosion when removed (Lu et al., 2009; Chen et al., 2013; Yin et al., 2019), mainly caused by Nannizzia gypsea and Trichophyton rubrum.
Main causative agents: Epidermophyton floccosum, Trichophyton interdigitale, T. indotineae, T. rubrum.

Tinea pedis (athlete’s foot). Dermatophyte infection of the feet and the interdigital spaces of the toes (Fig. 3K; Ilkit & Durdu, 2015). Disorders have emerged with rural habits of wearing closed shoes (Sasagawa, 2019). The disorder is commonly observed in the elderly population, and more rarely in children (Tullio et al., 2007). It is estimated that approximately 15% of the world population carries this infection. The moist skin between toes is infected, particularly between the fourth and fifth toes; the horny layer is damaged, and painful fissures may develop. Symptoms are often slight but can also be severe and can include malodor, and pruritus. In toe webs, scaling, fissuring, maceration, and erythema (‘interdigital type‘) may be associated with an itching or burning sensation (Al Hasan et al., 2004). Adjacent infection of the sole often extends to the lower sides of the foot, known as ‘moccasin type‘ (Fig. 3L; chronic hyperkeratotic type). This type is a prolonged, chronic form of tinea infection. The sole appears hyperkeratotic and often covered with fine scales; fissuring may occur. Except for the toes, the dorsum of the foot is spared. The ‘acute ulcerative type’ has rapidly expanded, vesiculopustular lesions and ulcerations with severe inflammation. The infection is mostly located in the toe web spaces. Secondary bacterial infection is often observed and may lead to cellulitis, lymphangitis or pyrexia. This type is commonly observed in immunocompromised and diabetic patients. A ‘vesiculobullous type‘ of tinea pedis is characterized by pustules or vesicles on the plantar surface of the feet (Fig. 3M; El-Segini et al., 2002). This infection has an acute onset with intense inflammation leading to multilocular pruritic vesicles or bullae. Infection is limited to the toes, instep, and lateral aspects of the foot. The infection tends to worsen during summer, and relapses are frequent. With bacterial superinfection, erythema increases, and this may become associated with edema, cellulitis, lymphangitis, adenopathy and hyperhydrosis; this aggravation is painful. All types of tinea pedis can lead to satellite infections elsewhere on the extremities when not treated properly (Zhan et al., 2010).
Main causative agents: Trichophyton rubrum, Epidermophyton floccosum.

Tinea unguium. This condition refers to onychomycosis caused by a dermatophyte, a condition under the general term often caused by Candida albicans. Tinea unguium is an extremely common (Perea et al., 2000; Aman et al., 2001) chronic infection of the nail bed and nail (Fig. 3H-J; Asz-Sigall et al., 2017), mostly of the toenails. It is the prevalent nail disorder in adults, accounting for 15-40% of all nail diseases (Ameen et al., 2014). Dermatophytes account for about 90% cases of onychomycosis of the toenails and at least 50% of fingernail infections (Thomas et al., 2010). Predisposing factors are tinea pedis, diabetes, immunosuppression, poor peripheral circulation, trauma and advanced age. Participating in some sporting activities creates a significantly increased risk of onychomycosis (Caputo et al., 2001). The susceptibility to onychomycosis is also increased in psoriasis patients who are HLA-DR08 and HLA-DR01 positive (Carrillo-Meléndrez et al., 2016), but HLA-DR6 positivity seems to provide protection against onychomycosis in the Mexican population (Asz-Sigall et al., 2010). The infection expands from the periphery towards the centre; the nail may eventually be released due to lateral hyperkeratosis which lifts the nail distally. The distal nail bed and hyponychium gradually break and crumble, and the subungual region shows yellowish brown discoloration. Black pigmentation that mimics melanoma may develop due to the melanin pigment produced by Trichophyton rubrum. Although the most common cause of this type of onychomycosis, known as ‘distal and lateral subungual onychomycosis‘ (DLSO), is the dermatophyte T. rubrum, occasionally non-dermatophyte agents such as Candida albicans or Aspergillus, Scopulariopsis or Fusarium species are concerned (Subramanya et al., 2019). Adjacent nails usually remain unaffected. ‘Superficial white / black onychomycosis’ (SWO / SBO) is an invasion of the superficial layer of the nail plate, visible as small, white, speckled or powdery patches on its surface. The nail becomes roughened and crumbles easily. The most common etiologic agent is Trichophyton interdigitale, while T. rubrum is prevalent in the HIV-positive population. The term also covers non-dermatophytes such as species of Aspergillus, Acremonium and Fusarium for the white variant. Agents of black onychomycosis (melanonychia) mainly caused by T. rubrum or the non-dermatophyte Neoscytalidium dimidiatum (Rodríguez-Cerdeira et al., 2024). ‘Proximal subungual onychomycosis’ involves the proximal nailfold and adjacent nail plate, resulting in subungual hyperkeratosis, proximal onycholysis, leukonychia, and destruction. Trichophyton rubrum is the principal causative agent, periungual inflammation may also be caused by non-dermatophytes such as Fusarium, Aspergillus and Scopulariopsis. ‘Endonyx onychomycosis’ presents as a milky white discoloration of the nail plate (Fig. 3F), but no evidence of subungual hyperkeratosis or onycholysis is observed. Main etiologic agents are T. soudanense and T. violaceum. ‘Total dystrophic onychomycosis’ is the final stage of any of the described types of onychomycoses, with the entire nail presenting in a thickened, opaque, and yellow-brown condition.

Invasive dermatophytoses

While fungal elements are limited to the stratum corneum in superficial dermatophytic infections, they invade the dermis and subcutaneous tissues in deep dermatophytosis. For the diagnosis of deep dermatophytosis, mere isolation of the agent is not sufficient; additionally, fungal elements should be detected in the deep tissues by histopathology. For the diagnosis of a disseminated dermatophytosis, presence of the fungus in organs in addition to skin should be demonstrated (Durdu et al., 2019).

Tinea folliculorum (Majocchi’s granuloma, granuloma trichophyticum) is defined as perifollicular granulomatous inflammation (Fig. 4B, C; Sun et al., 2018; Durdu et al., 2019). Infection of hair follicles can lead to a deep dermal inflammatory reaction (Fig. 4A, E) very similar to kerion of the scalp. Fungal elements are present in the hair follicle and in the perifollicular infiltrate of the dermis, due to the rupture of the follicle wall. The lesion becomes pustular, well circumscribed, elevated and crusted. Particularly in patients with a suppressed immune system, the granuloma causes clustered nodules and abscesses that mimic bacterial infections such as furuncles and carbuncles. Incorrect diagnosis leads to prolonged, unnecessary antibiotic treatment (Drivenes et al., 2023). Infections mostly occur in the lower extremities (Coelho et al., 2009), with epilation (Mazur et al., 2018) and the use of topical steroids (Liu et al., 2015) as risk factors. Also, cosmetic product injection in the facial area presents a risk (Liu et al., 2020). In solid organ transplant patients and patients with severe immunodeficiency, lesions are not limited to a certain area and may spread to many anatomical regions (Uysal et al., 2024). Recurrent cases may be linked with chemotherapy-induced neutropenia.
Main causative agent: Trichophyton rubrum.

Mycetoma. This is a special form of deep dermatophyte infection, with three components: (i) tumoral lesions, with extensive expansion above the skin level; (ii) sinuses draining from the dermis and subcutaneous tissue into the epidermis, and (iii) densely packed hyphae, the so-called grains, which are the hallmark of mycetoma (Castro-Echeverry et al., 2017). Lesion types (i) and (ii) are referred to as ‘pseudomycetoma‘. Although most pseudomycetomas are localized to the scalp, they occasionally develop on other parts of the body and may eventually lead to dissemination (Tirado-González et al., 2012). Pseudomycetoma combined with disseminated Mycobacterium genavense infection has been reported in an HIV/AIDS patient (Benchetrit et al., 2024). Rouzaud et al. (2015) speculated that most cases of pseudomycetoma develop as a result of impaired IL-6 and IL-17 production resulting from CARD9 defects. Fatal pseudomycetoma has been reported in a patient with isolated CD4 lymphopenia without a CARD9 defect (Song et al., 2023).

Deep dermatophytosis. This is a severe and sometimes life-threatening condition, characterized by extensive dermal and subcutaneous tissue invasion (Fig. 4D), with frequent dissemination to the lymph nodes and sometimes to the central nervous system. The disorder is nearly always associated with immunosuppression because of solid organ transplantation (Wu et al., 2013; Rouzaud et al., 2018) or inherited immune disorders such as CARD9 (Boudghene Stambouli et al., 2017; Lanternier et al., 2013; Stambouli et al., 2017; Ansai et al., 2024) or other causes of lymphocytopenia (Song et al., 2023).
Main causative agents: Microsporum canis, Trichophyton mentagrophytes, T. rubrum.

Disseminated dermatophytosis. Extracutaneous spreading to other organs is rarely observed in patients with severe underlying diseases (Marconi et al., 2010). The term is somewhat misleading in that infection is mostly not disseminated beyond the skin but is widespread over large body areas, often beginning in childhood and expanding over decades. The skin becomes nodular, thickened, and scaling, without purulence or crusting.

Therapy

All dermatophyte infections should be treated comprehensively. Pharmacological treatment depends on the anatomical location of the infection and on the causative agent, either applying a topical formulation or oral therapy, or their combination. Systemic therapy is given in cases of tinea capitis and recalcitrant tinea unguium, and topical therapy is mostly sufficient for skin infections; however, systemic therapy may also be considered in cutaneous cases with extensive disease, significant hyperkeratosis, topical treatment failure or relapse. If systemic treatment is needed, the patient’s age, pregnancy status, lactation status, body weight and other medications used should be taken into consideration. The aim of treatment should be not only to decrease signs and symptoms but also to eradicate the infection, to prevent relapse and transmission. When determining the treatment method, the guidelines for this subject should be considered (Fuller et al., 2014; Nenoff et al., 2023).

Therapy of tinea capitis

In tinea capitis patients, systemic antifungal treatments are recommended. Topical antifungal creams or shampoos only prevent the transmission of spores and cannot provide sufficient penetration into the hair follicles (Fuller et al., 2014). Shampoos with 1% selenium sulfide, 1% ciclopirox and 2% ketoconazole shampoos, and application of povidone-iodine can be applied as adjunctive therapy and have shown efficacy (Fuller et al., 2014). Use of shampoos twice a week reduces the period of active shedding (Chen et al., 2010). Identification of the etiologic agens is crucial for the selection of the type of systemic treatment. A recent meta-analysis showed that griseofulvin treatment (20 mg/kg/day in patients <50 kg, 1 g/day in patients ≥50 kg) for 6-8 weeks is significantly more effective than terbinafine treatment for 4 weeks in treating tinea capitis infections due to Microsporum canis; cases did not improve despite systemic treatment with both terbinafine and itraconazole (Jung et al., 2023). Griseofulvin is however less effective against Trichophyton species, where higher doses (≥30 mg/kg/day) are required (Kassem et al., 2023). Note that griseofulvin is not available in many countries and is contraindicated during pregnancy. Approximately 20% of griseofulvin users develop side effects such as diarrhea, skin rash and headache (Gupta et al., 2003). The opposite efficacy is found with terbinafine, which shows much higher activity against Trichophyton species than against Microsporum (Kakourou & Uksal, 2010). Terbinafine granules and solutions are increasingly used in some countries. In the U.S.A., the granule formulation is approved for use in children over 4 years of age. In countries where only terbinafine tablets are available, the tablets are divided according to weight of the patient (quarter <20 kg, half 20–40 kg, one >40 kg). Terbinafine is well tolerated, and gastrointestinal disturbances and skin rashes are less common than with griseofulvin. Itraconazole (5 mg/kg/day, 4 weeks), an antifungal with activity against both Microsporum and Trichophyton species, interacts with drugs such as warfarin, antihistamines (especially terfenadine and astemizole), antipsychotics (sertindole), anxiolytics (midazolam), digoxin, cisapride, cyclosporine and simvastatin. Although ketoconazole has frequently been used in the past, it is not recommended because of its side effects (Fuller et al., 2014). If systemic ketoconazole treatment shows insufficient improvement, the dose should be increased or alternative medication should be considered (Higgins et al., 2000).

Therapy of tinea glabrosa

Tinea corporis generally responds well to topical antifungal treatments when applied for 4-6 weeks. Randomized controlled studies have not demonstrated superiority of one class of topical antifungals over another (van Zuuren et al., 2015). Antifungal creams should be applied directly to the lesion and at least 1–2 cm beyond this area (Weinstein & Berman, 2002). When there is more than one lesion, when infected vellus hairs are seen upon dermoscopy, when there is no response to topical treatment, and when the infection takes a recurrent or chronic course, in all these cases oral terbinafine or itraconazole treatment for 2–3 weeks is recommended (Gómez-Moyano & Crespo-Erchiga, 2010). Treatment of tinea corporis is recommended with terbinafine 250 mg once a day, increasing to 500 mg daily if there is no adequate response (Rengasamy et al., 2020). However, in a random comparison of 60 patients with tinea corporis and/or cruris, no statistically significant difference in effectivity was found between 250 mg terbinafine daily and 500 mg of terbinafine daily (complete recovery rates 20% vs. 33.3%; p = 0.82; Lal et al., 2023). In case of high-dose of terbinafine, 250 mg twice daily is preferred over a single dose of 500 mg (Sardana & Gupta, 2017). Since low-dose drug use contributes to the development of resistance, itraconazole should be used at a minimum dosage of 200 mg/day to treat tinea corporis and/or cruris (Hill et al., 2024). Oral griseofulvin is not effective against Trichophyton concentricum infections, and therefore either terbinafine or itraconazole should be for patients with tinea imbricata (Hay et al., 1984).
Tinea cruris is generally treated for 2-4 weeks with topical tolnaftate, terbinafine or imidazoles. If a Candida infection cannot be excluded, terbinafine and imidazoles are recommended because of their effectivity against Candida. For patients with chronic and recurrent infections, systemic treatment should be installed; follow-up for at least 4 weeks after clinical improvement is recommended to prevent recurrence (Nenoff et al., 2015).

Therapy of tinea pedis

A variety of broad-spectrum topical antimycotic agents are in use to treat tinea pedis; only nystatin is not effective against dermatophytes (Nenoff et al., 2015). Applying 50% diluted vinegar once a day for 10-15 minutes before topical antifungal application increases the success rate of treatment (Kelly et al., 2023). Antimycotic solutions, gels or sprays are recommended for macerated, erosive interdigital lesions, while creams or ointment formulations should be used for scaly and hyperkeratotic areas. For vesiculobullous or secondarily infected tinea pedis, skin-drying agents such as potassium permanganate, Castellani dye, or Burow’s solution should be applied (Ilkit & Durdu, 2015). Since hyperkeratotic squamous plaques in moccasin-type athlete’s foot prevent the penetration of topical antifungal drugs, the use of topical urea or other keratolytic drugs increases the effect of antifungal drugs (Shemer et al., 2010). Topical antifungal creams, particularly azole antifungals, may cause a burning and stinging sensation. However, these side effects develop through an irritant mechanism rather than an allergic mechanism (Liu & Warshaw, 2014).
A meta-analysis of tinea pedis involving 19 randomized controlled trials (RCT; n = 1,937) comparing azole and allylamine antifungal agents with placebo (Rotta et al., 2012) for a mycological cure and sustained therapy showed that azoles and allylamines are both effective, but a similar study (Crawford & Hollis, 2007) of 9 RCTs (n = 1003, 4-6 wk) indicated better results with allylamines (terbinafine and 1% naftifine) than with azoles cream (1-2% clotrimazole, 1% bifonazole). Another study (Rotta et al., 2012) of 6 RCTs (n = 298) showed that terbinafine was already effective with 1-2 week treatment. Imidazoles used in the topical treatment of tinea pedis are generally applied twice a day for 4 weeks, while the use of bifonazole and terbinafine once a day is sufficient. Patients should be warned to apply antifungal medication for a sufficient period of time. Butenafine and sertaconazole show anti-inflammatory activity and remain on the skin for a long time after topical application (Singal, 2008). Sertaconazole also has antipruritic activity (Liebel et al., 2006). Butenafine can be used once daily for 4 weeks or twice daily for 1 week (Gupta, 2002). Luliconazole (1%) cream provides clinical improvement even when it is used once daily for 1 week (Khanna & Bharti, 2014). In inflammatory and eczematous types of tinea pedis, combinations of an antimycotic agent and a corticosteroid may be advantageous. However, these combined preparations should not be applied for more than 2 weeks, as they may cause some side effects such as chronic and recurrent infections, skin atrophy, striae and telangiectasia. In addition, long-term application of corticosteroids may stimulate emergence of resistant genotypes (Benedict et al., 2024) and is therefore not recommended in view of public health (Singh et al., 2019). Oral antifungal therapy is recommended for widespread chronic hyperkeratotic, inflammatory and vesicular forms of tinea pedis. In systemic treatment, terbinafine (250 mg/day, 2-4 weeks) is more effective than griseofulvin (1,000 mg/day, 4 weeks) or itraconazole (200 mg/day, 4 weeks; Bell-Syer et al., 2012).

Therapy of tinea unguium

In onychomycosis, topical antifungal agents such as 28% thioconazole, 8% ciclopyroxolamine, efinaconazole, 5% taneborole solution, and amorolfine nail polish can be used to treat superficial cases involving less than 50% of the nail and limited to the distal nail plate. Topical therapy is also necessary when systemic antifungals are contraindicated, but these are absolutely required for proximal subungual onychomycosis and distal subungual onychomycosis affecting the lunula region. Topical treatment increases the effectiveness of systemic antifungal therapy (Gupta et al., 2024). 5% Amorolfine or 8% ciclopiroxolamine nail lacquer is commonly used and has been proven to be beneficial; the latter is the only nail lacquer approved in the U.S.A. and Canada for the treatment of onychomycosis. Ciclopirox is a hydroxypyridone derivative with broad-spectrum antifungal activity against Trichophyton rubrum and non-dermatophytes. 8% Ciclopirox nail lacquer can be used once daily for 48 weeks in cases of mild to moderate onychomycosis.
Fingernail onychomycosis usually responds to oral terbinafine (250 mg/day for 6 weeks), itraconazole (400 mg/day for 1 week per month for 2-3 months), or fluconazole (150–300 mg once a week). Toenail infections require long-term treatment; for example, terbinafine or itraconazole therapy may require 3-4 months. As terbinafine is generally more effective than itraconazole and fluconazole, it is used as a first-line drug for treatment of onychomycosis. Itraconazole is considered a second-line drug because of its side effects and drug interactions, but on the other hand its relapse rate is more than twice that of terbinafine (Hay et al., 1984). The therapeutic effect of griseofulvin on onychomycosis lesions is quite low, and recurrence is frequently observed. The unresponsiveness to antifungal drugs increases (40–70%) in several clinical conditions: (i) in the presence of concomitant diseases (diabetes mellitus, arterial or venous insufficiency, Down syndrome, Raynaud syndrome, primary or secondary immunodeficiency), (ii) if nail involvement is >50%, when the lateral part of the nail plate is affected, (iii) in the presence of subungual hyperkeratosis thicker than 2 mm, (iv) if the nail is white/yellow or orange/brown lines (dermatophytoma), (v) if the matrix is involved, and (vi) if there is periodic trauma to the nail (Ameen et al., 2014). Risk factors should be controlled or if available treated. If the response to systemic treatment is not sufficient, a closed dressing with cream containing 40% urea may be necessary.
Photodynamic therapy (Sotiriou et al., 2010) using methylene blue as a photosensitizer has recently been reported to be effective for treating Trichophyton rubrum onychomycosis but affected toenails must be filled or treated with urea before application of 5% δ-aminolevulinic acid (ALA; Dong et al., 2023). Efficacy of iontophoresis (Amichai et al., 2010) has as yet insufficiently been proven. Laser devices, including Nd-YAG lasers and diode lasers, have also been used in the treatment of onychomycosis (Kozarev & Vižintin, 2010; Landsman & Robbins, 2012). Penetration of the nail plate and targeting of fungi occurs at wavelengths of 750–1300 nm. Several laser systems have been FDA-cleared for onychomycosis. However, these techniques are still in their infancy, and clinical trials are required prior to wider application. Additionally, laser therapy is contraindicated in onychomycosis patients with lower extremity neuropathy (Kiran et al., 2024).

Therapy of resistant dermatophytes

Infection by Trichophyton indotineae, an emerging dermatophyte that rapidly expands at a global scale, should be considered in patients with widespread tinea corporis that persists for ≥ 3 months despite systemic antifungal treatment, and in patients with facial involvement or who improve with systemic antifungal drugs but relapse within 1 month (Singh et al., 2020). The treatment approach for this species varies. Recalcitrant strains have a mutation in the gene encoding squalene epoxidase (SQLE), a key enzyme in the ergosterol biosynthetic pathway for terbinafine resistance; the resistance should be first confirmed by a molecular method such as PCR. The first-line systemic treatment of the infection is itraconazole (200 mg/day, >3 months; Rengasamy et al., 2020). Luliconazole, sertaconazole or topical ketoconazole combined with systemic treatment have synergistic effects (Nenoff et al., 2019). In a prospective study conducted with a small number of patients (n = 45), the combination of terbinafine (250 mg/day) plus itraconazole (200 mg/day) resulted in higher treatment success rates than did terbinafine (250 mg/day) or itraconazole (200 mg/day) alone. However, these differences were not found to be statistically significant (Hassaan et al., 2023). In another study involving 60 patients, a 50% response was obtained with 3-weeks of itraconazole (200 mg/day) treatment alone, a 35% response was obtained with terbinafine (250 mg/day) treatment alone, and a 90% response was obtained with combined treatment. In this study, mild headache was detected as a side effect in patients receiving combined treatment compared to those receiving treatment alone (Sharma et al., 2020). The increase in the number of T. indotineae cases continues to provide us with new data. Brasch et al. (2021) determined that the species can be resistant to itraconazole as well as to terbinafine. In such double drug-resistant cases, fluconazole (150–200 mg/day, 4–8 weeks), voriconazole (200 mg/day, 2–4 weeks) or posaconazole (800 mg/day) treatment can be applied (Sonego et al., 2024; Caplan et al., 2024).

Prevention and control

Personal hygiene is very important for adequate treatment of dermatophyte infections and prevention of recurrence. People living in hot and humid conditions have a higher risk of developing infection. After each bath, the entire body surface, especially the body folds and between the toes, has to be dried thoroughly. Sweat-absorbing socks should be used to prevent feet from remaining damp, and socks should be changed frequently. The use of interdigital-type hygiene socks both accelerates the treatment and prevents recurrence. Washing clothing and bed linen in hot water at 60°C and drying in sunlight may help prevent continued infection. Additionally, clothes of infected patients should be stored and washed separately to prevent the spread of infection. Sharing soap, clothing, towels and bed linen with others should be prevented; synthetic and tight clothing should be avoided. Regular cleaning of the house will also reduce environmental contamination of dermatophytes. Ensuring weight loss in obese patients will prevent recurrence of infection, especially in the intertriginous region. Other infected household members should be treated simultaneously (Rengasamy et al., 2020; Gupta et al., 2004).