Dermatophytosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Dermatophytosis is a fungal infection of the skin. It gets worse during summer and the symptoms are alleviated during winter. Dermatophytes of the genera Trichophyton and Microsporum are the most common causative agents. Mode of transmission of Dermatophytes is via direct or indirect contact with skin (or) scalp lesions of infected people,animals (or) fomites. Following transmission, the dermatophytes use proteases to adhere to the stratum corneum of the skin. Penetration by dermatophytes is achieved by secreting multiple serine–subtilisins and metallo-endoproteases (fungalysins) formerly called keratinases that are found only in the dermatophytes. Acutely, the host responds to fungal invasion by Type IV delayed type hypersensitivity reaction (also known as “Trichophytin reaction”) leading to a cell mediated response. Dermatophytosis should be differentiated from other superficial skin infections which may all present as a red, pruritic, annular and scaly rash on different parts of the body such as tinea versicolor, tinea nigra, white piedra, black piedra, superficial candidiasis. Tinea corporis should also be differentiated from other annular skin eruptions, especially subacute cutaneous lupus erythematosus (SCLE), granuloma annulare, and erythema annulare centrifugum. Worldwide, the prevalence of dermatophytosis is 20000-25000 per 100,000 persons. The common risk factors for dermatophytosis are xerosis (dry skin), skin-skin contact with an infected person, contact with infected pets, topical immunosupressive drugs, low socioeconomic status, occlusive footwear, high humidity, rural settlement, poor hygiene, excessive sweating, public showers, obesity, diabetes mellitus. The skin is characterized by erythematous, papulosquamous, annular, well-ircumscribed, superficial rash with central clearing which may be located on the scalp, neck, trunk, extremities and groin. Laboratory findings consistent with the diagnosis of dermatophytosis include KOH preparation showing refractile, long, smooth, undulating, branching, and septate hyphal filaments with or without arthroconidiospores; culture and sensitivity may yield the diagnosis but it takes 7-14 days for colony growth; hemotoxylin and eosin stain may be used in diagnosis of Majocchi’s granuloma in which KOH examination of scales may be false negative. Polymerase chain reaction (PCR) testing may be used to identify various dermatophytic infections and even help in evaluating drug resistances of different species of dermatophytes. The mainstay of therapy for dermatophytosis is topical antifungals. Topical Antifungalrug|antifungals]] include imidazoles, allylnines and other agents including ciclopirox olamine, benzoic acid preparations (Whitfield’s ointment), tolnaftate, haloprogin, drying agents and salicylic acid. In some situations, systemic antifungal therapy may be used for dermatophytosis which includes griseofulvin, ketoconazole, terbinafine, itraconazole and fluconazole. Effective measures for the primary prevention of dermatophytosis include avoiding sharing clothing, sports equipment, towels or sheets of infected individuals. Washing clothes worn by infected individuals with fungicidal soap and avoiding infected pets.

Dermatophytosis was first described by David Gruby, a Hungarian physician, in 1841. Before Gruby, various scientists described lesions which were ring-like, and were thought to be infective. The description of lesions dates back to the Roman era. Around 1890, Raimond Sabouraud advanced knowledge of dermatomycology by studying extensively into the taxonomy, morphology, and treatment of dermatophytes, even classifying these fungal agents into four genera (three of which are still current to mycologists). Dermatophytosis has been prevalent as early as the year 1906 and before. At that time ringworm was treated with compounds of mercury or sometimes sulfur or iodine. Hairy areas of skin were considered too difficult to treat, so the scalp was treated with x-rays and followed up with antiparasitic medication.

A number of different species of fungi are involved. Dermatophytes of the genera Trichophyton and Microsporum are the most common causative agents.

Dermatophytes are usually transmitted via contact to human host. Following transmission, the dermatophytes use proteases to adhere to the stratum corneum of the skin. Penetration by dermatophytes is achieved by secreting multiple serine–subtilisins and metallo-endoproteases (fungalysins) formerly called keratinases that are found only in the dermatophytes. Acutely, the host responds to fungal invasion by Type IV delayed type hypersensitivity reaction (also known as “Trichophytin reaction”) leading to a cell mediated response. Fungus secreted proteases are one of the most important virulence factors of dermatophytes and are thought to be responsible for evasion from host defense mechanisms. Secreted subtilisin proteases expressed in the dermatophytes could play a role in keratin degradation. Dermatophyte infections of the skin surface (tinea corporis and tinea faciei) mostly present as erythematous, scaly papules that gradually progress to annular or circular red patches or plaques, with central clearing and scaling at the periphery. On microscopic examination of the skin, there may be neutrophils retained in the stratum corneum, parakeratosis, spongiosis and dermal edema.

Dermatophytes cause non-lethal infection of the superficial skin, therefore, the agents causing dermatophytosis are not life-threatening. Common genera of dermatophytes causing infections include the Epidermophyton, Microsporum and Trichophyton. Causes of dermatophytosis according to the organ system involvement include, tinea corporis which is infection of body surfaces other than the feet, groin, face, scalp hair, or beard hair; Tinea pedis which is infection of the foot; tinea cruris which is infection of the groin; tinea capitis which is infection of scalp hair; tinea unguium (dermatophyte onychomycosis) which signifies infection of the nail; tinea faecei which is infection of the face; tinea barbae which is infection of the facial hair; tinea mannum which includes infection of the hands.

Dermatophytosis should be differentiated from other superficial skin infections which may all present as a red, pruritic, annular and scaly rash on different parts of the body such as tinea versicolor, tinea nigra, white piedra, black piedra, superficial candidiasis. Tinea corporis should also be differentiated from other annular skin eruptions, especially subacute cutaneous lupus erythematosus (SCLE), granuloma annulare, and erythema annulare centrifugum.

Worldwide, the prevalence of dermatophytposis is 20000-25000 per 100,000 persons. Dermatophytosis commonly affects school-aged (5-15 years of age) children. Overall, dermatophytosis is more prevalent in women than in men. Scalp infections are more common in blacks as compared to Caucasians. There is a large variation in the type on dermatophytosis affecting individuals, depending upon the geographic location.

The common risk factors for dermatophytosis are xerosis (dry skin), skin-skin contact with an infected person, contact with infected pets, topical immunosupressive drugs, low socioeconomic status, occlusive footwear, high humidity, rural settlement, poor hygiene, excessive sweating, public showers, obesity, diabetes mellitus. Less common risk factors for dermatophytosis are occupational (farmer, worker and retired), presence of fungal infection in family, cancer and psoriasis.

According to the the U.S. Preventive Service Task Force (USPSTF), there is insufficient evidence to recommend routine screening for dermatophytosis but the wood lamp examination may be used as a screening tool for tinea capitis in suspected cases.

Dermatophytosis tends to get worse during summer, with the symptoms alleviating during winter. Skin medicine usually treats ringworm within 4 weeks. If the ringworm infection is severe or it does not respond well to self-care, it will usually respond quickly to antifungal pills.

The hallmark of dermatophytosis is an enlarged, raised red ring with central clearing. Infection on the skin of the feet may cause athlete’s foot and infection of the groin area may result in jock itch. Involvement of the nails is termed onychomycosis, and they may thicken, discolor, and finally crumble or fall off.

Patients are usually well-appearing in dermatophytosis. The skin is characterized by erythematous, papulosquamous, annular, well-circumscribed, superficial rash with central clearing which may be located on the scalp, neck, trunk, extremities and groin. Abnormalities of the head/hair may include, dry scaling, which may be similar to seborrheic dermatitis; black dots, which are areas of broken hair on a scaly surface; smooth areas of hair loss. Neck in tinea corporis may show, red, itchy, scaly, circular skin rash and cervical lymphadenopathy. Genitals may be involved in tinea cruris and examination may show pustules and vesicles at the active edge of the infected area along with maceration. Hands in tinea mannum may show dry and hyperkeratotic palmar surface. Feet in tinea pedis may show fissuring, maceration, and scaling in the interdigital spaces of the fourth and fifth toes.

Laboratory findings consistent with the diagnosis of dermatophytosis include KOH preparation showing refractile, long, smooth, undulating, branching, and septate hyphalfilaments with or without arthroconidiospores; culture and sensitivity may yield the diagnosis but it takes 7-14 days for colony growth; hemotoxylin and eosin stain may be used in diagnosis of Majocchi’s granuloma in which KOH examination of scale may be false negative. Polymerase chain reaction (PCR) testing may be used to identify various dermatophytic infections and even help in evaluating drug resistances of different species of dermatophytes.

There are no X-ray findings associated with dermatophytosis.

There are no CT scan findings associated with dermatophytosis.

There are no MRI findings associated with dermatophytosis.

There are no other imaging studies associated with dermatophytosis.

Most of the time, ringworm can be diagnosed by looking at the skin. Other diagnostic studies that can be used to diagnose dermatophytosis are matrix-assisted laser desorption ionization test and reflectance confocal microscopy.

The mainstay of therapy for dermatophytosis is topical antifungals. Topical antifungals include imidazoles, allylnines and other agents including ciclopirox olamine, benzoic acid preparations (Whitfield’s ointment), tolnaftate, haloprogin, drying agents and salicylic acid. In some situations, systemic antifungal therapy may be used for dermatophytosis which includes griseofulvin, ketoconazole, terbinafine, itraconazole and fluconazole.

Surgery is not the first-line treatment option for patients with dermatophytosis. Surgical drainage of superficial vesicles, bullae, and pustules may be done.

Effective measures for the primary prevention of dermatophytosis include avoiding sharing clothing, sports equipment, towels or sheets of infected individuals. Washing clothes worn by infected individuals with fungicidal soap and avoiding infected pets.

Secondary prevention of dermatophytosis is similar to primary prevention.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Dermatophytosis was first described by David Gruby, a Hungarian physician, in 1841. Before Gruby, various scientists described lesions which were ring-like, and were thought to be infective. The description of lesions dates back to the Roman era. Around 1890, Raimond Sabouraud advanced knowledge of dermatomycology by studying extensively into the taxonomy, morphology, and treatment of dermatophytes, even classifying these fungal agents into four genera (three of which are still current to mycologists). Dermatophytosis has been prevalent since early 1900’s, at which time ringworm was treated with compounds of mercury or sometimes sulfur or iodine. Hairy areas of skin were considered too difficult to treat, so the scalp was treated with x-rays and followed up with antiparasitic medication.

• In 30 A.D. Aulus Cornelius Celsus, the Roman encyclopedist, who in his book called ‘De Re Medicina’ described a suppurative infection of the scalp that later was called kerion of Celsus.^[1]
• The term tinea was first used for a moth of the clothes because the holes made by moths in woolen garments are circular and dermatophyte lesions are ring-like on smooth skin.
• In the 16th century, the term ‘ringworm’ for these infections was used. This term described the form of the lesion and relates it to the Roman tinea.
• In the 19th century, the fungal etiology of ringworm was deciphered and described by various scientists like Robert Remak, Johann L. Schönlein, and David Gruby.
• In 1835, Remak observed microscopic structures from crusts of favic lesions (favus is ringworm of the scalp).
• Schönlein identified the specimen having fungal origin.
• Remak ultimately described the fungi as Achorion schöenleinii.
• In 1841, David Gruby confirmed the work of Remark and described various types of fungal infections, for example, tinea favosa, ectothrix and endothrix trichophytosis and microsporiosis.^[2]
• Independently of Remak and Schönlein, Gruby published papers from 1841 to 1844 about the about the cause and nature of Favus, significantly expanding the understanding of dermatophytosis.
• Around 1890, Raimond Sabouraud advanced knowledge of dermatomycology by studying extensively into the taxonomy, morphology, and treatment of dermatophytes, even classifying these fungal agents into four genera (three of which are still current to mycologists).^[3]
• Sabouraud developed a medium for culturing dermatophytes that, after a few modifications, is even still used today and is named, Sabouraud glucose agar.
• In the year 1886 cultures of the dermatophytes were independently achieved for the first time.
• By the year 1935 more than 118 species of dermatophytes had been described and classified into nine genera.

• In 1906, dermatophytes was treated with compounds of mercury or sometimes sulfur or iodine. Hairy areas of skin were considered too difficult to treat, so the scalp was treated with x-rays and followed up with antiparasitic medication.
• A variety of fungicides including griseofulvin, tolnaftate, haloprogin, and allylamines have been used to fight dermatophytes in the last 100 years.
• Although some species have almost eradicated from humankind, for example, T. schoenleinii, M. audouinii, and M. ferrugineum, other species have begun to show resistance to drug therapy in the last 30 years.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Dermatophytes may be classified according to genera, mode of transmission and disease patterns. Dermatophytes of the genera Trichophyton and Microsporum are the most common causative agents.

Dermatophytes may be classified according to various schemes.^[1][2]

Based upon their genera, dermatophytes can be classified into three groups: 

• Trichophyton (which causes infections of the skin, hair, and nails)
• Epidermophyton (which causes infections of the skin and nails)
• Microsporum (which causes infections of the skin and hair)

Based upon mode of transmission, these have been classified as:

• Anthrophillic
• Zoophilic
• Geophilic

Dermatophytosis may be classified into the following types based on disease patterns:

• Tinea pedis (athlete’s foot) affects the feet
• Tinea unguium affects the fingernails and toenails
• Tinea corporis affects the arms, legs, and trunk
• Tinea cruris (jock itch) affects the groin area
• Tinea manuum affects the hands and palm area
• Tinea capitis affects the scalp
• Tinea barbae affects facial hair
• Tinea faciei (face fungus) affects the face

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Dermatophytes mode of transmission is direct (or)indirect contact with skin (or) scalp lesions of infected people,animals (or) fomites. Following transmission, the dermatophytes use proteases to adhere to the stratum corneum of the skin. Penetration by dermatophytes is achieved by secreting multiple serine–subtilisins and metallo-endoproteases (fungalysins) formerly called keratinases that are found only in the dermatophytes. Acutely, the host responds to fungal invasion by Type IV delayed type hypersensitivity reaction (also known as “Trichophytin reaction”) leading to a cell mediated response. Fungus secreted proteases are one of the most important virulence factors of dermatophytes and are thought to be responsible for evasion from host defense mechanisms. Secreted subtilisin proteases expressed in the dermatophytes could play a role in keratin degradation. Dermatophyte infections of the skin surface (tinea corporis and tinea faciei) mostly present as erythematous, scaly papules that gradually progress to annular or circular red patches or plaques, with central clearing and scaling at the periphery. On microscopic examination of the skin, there may be neutrophils retained in the stratum corneum, parakeratosis, spongiosis and dermal edema.

• Dermatophytes survive on the outer layer of skin called stratum corneum.
• Stratum corneum has been known to be not only source of nutrition for the dermatophytes, but also the growing fungal mycelia.^[1]

After the inoculation in the host skin, suitable conditions favor the infection to progress through the following stages:

• Dermatophyte-secreted proteases not only mediate adherence to the host skin but also help in germination of arthroconidia and hyphal growth leading to growth of the fungi in multiple directions.^[2][3]
• Fungal arthroconidia attach to keratinocytes via long and sparse microprojections (fibrils).^[3]

• Penetration by dermatophytes is achieved by secreting multiple serine–subtilisins and metallo-endoproteases (fungalysins) formerly called keratinases that are found only in the dermatophytes.^[4]
• Fungal mannans in the dermatophyte cell wall have immunosupressive ability and inhibit the action of T cells. T. rubrum cell wall mannans (TRM) may lead to inhibition of lymphoproliferative response of mononuclear leukocytes. This leads to fungal growth and proliferation on the host skin.

• Fungal metabolic products diffuse through the stratum basale and stratum spinosum to cause erythema, vesicle or even pustule formation and pruritus.
• Acutely, the host responds to fungal invasion by Type IV delayed type hypersensitivity reaction (also known as “Trichophytin” reaction) leading to a cell mediated response.^[5]
• Interferon-α secretion from type 1 T-helper lymphocytes, cytokines like interferon-γ (IFN-γ), IL-8 and macrophages are the effector mechanisms involved in defense against dermatophytes acutely.^[6]
• Dermatophyte species have cell wall carbohydrate molecules (β-glucan) that are recognized by the innate immune mechanisms, such as Dectin-1 and Dectin-2, which consequently stimulate toll-like receptor 2 and 4 (TLR-2 and TLR-4). Dectin-1 augments the production of tumor necrosis factor-α and IL-17, IL-6, and IL-10, all of which activate the adaptive immunity.
• IL-8 mediated chemotaxis allows polymorphonuclear leukocytes adhere to opsonized and unopsonized hyphae to inhibit growth of the dermatophyte.^[4]
• The dermatophyte antigen is thought to be processed by epidermal Langerhans cells and presented in local lymph nodes to T lymphocytes which proliferate, migrate to the infected site, and produce inflammation.^[7]
• The immune response, and especially the level of inflammation, is different for various dermatophyte species, the host species and the pathophysiological status of the host. In general, the zoophilic species cause more inflammatory infections, which may heal spontaneously and result in relative resistance to re-infection. The anthropophilic species usually cause more chronic, less circumscribed infections, which consequently lead to a poor resistance to re-infection.
• Cell-associated as well as secreted factors contribute to the dermatophyte’s ability to exaggerate or suppress an inflammatory response.
• Many host factors for example, number and activity of sebaceous glands (due to inhibitory effect of sebum on dermatophytes) in a particular body region, breaks in the integrity of skin barrier, moisturized and macerated skin can promote invasion of dermatophytes.
• Fungus secreted proteases are one of the most important virulence factors of dermatophytes and are thought to be responsible for evasion from host defense mechanisms.^[7]

• The genomes of the dermatophytes are similar in size, ranging from 22.5 Mb for T. rubrum to 24.1 Mb for T. equinum.
• The LysM domains are implicated in evasion of the host innate immune response (14) by securing fragments of chitin, so that the chitin cannot stimulate the immune response.^[8]
• Secreted subtilisin proteases expressed in the dermatophytes could play a role in keratin degradation.^[9]
• Dermatophytes have a large number of genes connected to secondary-metabolite production.
• Genes for protein kinases activate mitogen-activated protein kinase (MAPK) pathways and produce cytokines.
• T. equinum infection of epidermal tissue increase the expression of other human genes associated with inflammation, including the tissue remodeling matrix metalloprotease, its regulatory gene Timp1, and the proinflammatory mediator gene COX2.^[10]

• Dermatophyte infections of the skin surface (tinea corporis and tinea faciei) mostly present as erythematous, scaly papules that gradually progress to annular or circular red patches or plaques, with central clearing and scaling at the periphery.^[11]
• Pustules, vesicles, or large blisters may be infrequently seen grossly.

The following features may be seen on microscopic examination of the skin in dermatophytosis:^[12]

• Parakeratosis
• Spongiosis
• Neutrophils in the stratum corneum
• Compact orthokeratosis
• Papillary dermal edema
• Fungal hyphae between 2 zones of cornified cells (called the ‘sandwich’ sign)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Dermatophytes cause non-lethal infection of the superficial skin, therefore, the agents causing dermatophytosis are not life-threatening. Common genera of dermatophytes causing infections include the Epidermophyton, Microsporum and Trichophyton. The causes of dermatophytosis according to the organ system involvement include, tinea corporis which is infection of body surfaces other than the feet, groin, face, scalp hair, or beard hair; Tinea pedis which is infection of the foot; tinea cruris which is infection of the groin; tinea capitis which is infection of scalp hair; tinea unguium (dermatophyte onychomycosis) which signifies infection of the nail; tinea faecei which is infection of the face; tinea barbae which is infection of the facial hair; tinea mannum which includes infection of the hands.

• Dermatophytes cause non-lethal infection of the superficial skin, therefore, the agents causing dermatophytosis are not life-threatening.

The common etiologic agents of the dermatophytosis can be categorized into one of three genera:^[1][2]

• Epidermophyton
• Microsporum
• Trichophyton

The following are the causes of dermatophytosis by organ system involvement:^[3][4][5][6]

• Tinea corporis: Infection of body surfaces other than the feet, groin, face, scalp hair, or beard hair
• Tinea pedis: Infection of the foot
• Tinea cruris: Infection of the groin
• Tinea capitis: Infection of scalp hair
• Tinea unguium (dermatophyte onychomycosis): Infection of the nail
• Tinea faecei: Infection of the face
• Tinea barbae: Infection of the facial hair
• Tinea mannum: Infection of the hands

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Dermatophytosis should be differentiated from other superficial skin infections which may all present as a red, pruritic, annular and scaly rash on different parts of the body such as tinea versicolor, tinea nigra, white piedra, black piedra, superficial candidiasis. Tinea corporis should also be differentiated from other annular skin eruptions, especially subacute cutaneous lupus erythematosus (SCLE), granuloma annulare, and erythema annulare centrifugum.

Dermatophytosis should be differentiated from other superficial skin infections which may all present as a red, pruritic, annular and scaly rash on different parts of the body such as tinea versicolor, tinea nigra, white piedra, black piedra, superficial candidiasis. Tinea corporis should also be differentiated from other annular skin eruptions, especially subacute cutaneous lupus erythematosus (SCLE), granuloma annulare, and erythema annulare centrifugum.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Worldwide, the prevalence of dermatophytposis is 20000-25000 per 100,000 persons. Dermatophytosis commonly affects school-aged (5-15 years of age) children. Overall, dermatophytosis is more prevalent in women than in men. Scalp infections are more common in blacks as compared to Caucasians. There is a large variation in the type of dermatophytosis affecting individuals, depending upon the geographic location.

• Worldwide, the prevalence of dermatophytosis is 20000-25000 per 100,000 persons.^[1]

• Worldwide, the incidence of dermatophytosis ranges from a low of 10000 per 100,000 persons to a high of 15000 per 100,000 persons.

• Dermatophytosis is a non-fatal, superficial infection of the skin.

• Dermatophytosis commonly affects school-aged (5-15 years of age) children.^[2][3]

• Overall, dermatophytosis is more prevalent in women than in men.^[4]
• Groin infections occur with a higher frequency in males than in females.^[5]
• Nail infections occur more commonly in females than in males.^[6]

• In a study comparing the prevalence of dermatophytosis in black and Caucasians showed that, scalp infections occur predominantly in blacks; fingernail infections occur more often in Caucasians than blacks; toenails are more frequently infected in Caucasians than in blacks.^[7]

• In Europe, the countries reporting the highest incidence of M. canis infections (Tinea capitis) are mainly in the Mediterranean but also bordering countries like Austria, Hungary, Germany and Poland.^[8]
• The largest overall increase with anthropophilic dermatophytes has been noted with Trichophyton tonsurans mainly in the UK and with Trichophyton soudanense and Microsporum audouinii in France.^[9]
• Large-scale studies on onychomycosis conducted in the US and Canada in the late 1990s showed a prevalence rate of 14000 per 100,000 persons and 8000 per 100,000, respectively. In Europe, the prevalence rate is even more variable, with 2700 per 100,000 in the UK and Spain, 8400 per 100,000 in Finland, 12400 per 100,000 in Germany and 16800 per 100,000 in France in a more recent study.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

The common risk factors for dermatophytosis are xerosis (dry skin), skin-skin contact with an infected person, contact with infected pets, topical immunosupressive drugs, low socioeconomic status, occlusive footwear, high humidity, rural settlement, poor hygiene, excessive sweating, public showers, obesity, diabetes mellitus. Less common risk factors for dermatophytosis are occupational (farmer, worker and retired), presence of fungal infection in the family, cancer and psoriasis.

The common risk factors for dermatophytosis are:^{[1][2][3][4][5][6][7]}

• Xerosis (dry skin)
• Skin-skin contact with an infected person
• Contact with infected pets
• Topical immunosupressive drugs
• Low socioeconomic status
• Occlusive footwear
• High humidity
• Rural settlement
• Poor hygiene
• Excessive sweating
• Public showers
• Obesity
• Diabetes mellitus

Less common risk factors for dermatophytosis are:^[8]

• Occupational (farmer, manual laborer and retired)
• Presence of fungal infection in the family
• Extremes of age
• Cancer
• Psoriasis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Dermatophytosis tends to get worse during summer, with symptoms alleviating during the winter. Skin medicines usually treat ringworm within 4 weeks. If the ringworm infection is severe or it does not respond well to self-care, it will usually respond quickly to antifungal pills.

The symptoms of dermatophytosis usually develop in people living in low socio-economic, tropical and sub-tropical areas; where high humidity, excessive sweating, poor sanitation predispose individuals to superficial fungal infections. Patients may also present with a history of recent intake of immunosuppressive drugs, exposure to infected pets, diabetes mellitus or long-term use of occlusive footwear (for example athletes). If left untreated, dermatophytosis may lead to significant distress for the patient due to chronic pruritis and development of complications such as cellulitis, alopecia, bullous eruption on the area involved or disseminated infection.^{[1]1][2][3][4][5][6][7]}

Complications that can develop as a result of dermatophytosis are:^{[2][3][4][5][6][7][8][9][10][11][12]}

• Alopecia
• Superimposed bacterial infections leading to cellulitis
• Lymphangitis
• Kerion
• Bullae formation
• Erythema nodosum
• Baboon syndrome secondary to ketoconazole use (contact allergen-related maculopapular eruption that typically involves the flexural and gluteal areas)
• Urticaria
• Erythema multiforme
• Disseminated infection leading to fungemia

Dermatophytosis is associated with an excellent prognosis and early therapy leads to successful resolution of symptoms.^[13][14][15]

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