Superficial Fungal Infections - Diagnosis, Treatment & Types PDF

Here is the transcription of the presentation on superficial fungal infections into a structured markdown format: # Superficial fungal infections Presented by DR.Biniam M, Dermato-venereologist, Feb, 2025 ## Outline * INTODUCTION * EPIDEMOLOGY * PATHOGENESIS * CLINICAL FEATURES * DIFFE...

Here is the transcription of the presentation on superficial fungal infections into a structured markdown format: # Superficial fungal infections Presented by DR.Biniam M, Dermato-venereologist, Feb, 2025 ## Outline * INTODUCTION * EPIDEMOLOGY * PATHOGENESIS * CLINICAL FEATURES * DIFFERENTIAL DIAGNOSIS * DIAGNOSIS * TREATMENT ## INTODUCTION * Common fungal infections are subdivided into three major groups: 1. superficial 2. deep 3. systemic * Superficial fungal infection are defined as infection of fully keratinized tissues including skin, hair, and nails. * Caused by dermatophytes, non-dermatophytec fungal and Candida species. ## Dermatophytes * The most common causes superficial fungal species contains 3 generas: Trichophyton, Epidermophyton & Microsporum. * Based on thiere natural habitats dermatophytes divided into 3: * Anthropophilic: caused by direct Person-to-person or by fomites. * Zoophilic: Animal-to-human by direct contact. * Geophilic: Environmental ### TYPES OF DERMATOPHYTES BASED ON MODE OF TRANSMISSION | Category | Mode of transmission | Typical clinical features | | :-------------- | :------------------- | :-------------------------------- | | Anthropophilic | Human to human | Mild to non-inflammatory, chronic | | Zoophilic | Animal to human | Intense inflammation (pustules and vesicles possible), acute | | Geophilic | Soil to human or animal | Moderate inflammation | | | Most Common | Less Common | | :---------------------------------------------------- | :------------------------- | | Trichophyton:-mentagrophytes var. mentagrophytes interdigitale rubrum ton­surans verrucosum violaceum | Trichophyton ajelloi concentricum equinum gourvilii megninii schoenleinii soudanense terrestre yaoundei | | Microsporum canis ferrugineum gypseum | Micro. amazonicum audouinii persicolor cookei praecox equinum fulvum racemosum gallinae nanum vanbreuseghemi | | Epidermophyton floccosum | | ## PATHOGENESIS * Dermatophyte infections involve three main steps: * Adherece to keratinized tissue need to overcome the effects of ultraviolet light, variation in temperature and moisture. * Penetration by secreting proteinases, lipases, & other enzymes to facilitate penetration. * Host response is influenced both by the patients immune status & by the organism involved. ## CLINICAL FEATURES * Classifications * Tinea capitis * Tinea barbae * Tinea corporis * Tinea faciei * Tinea cruris * Tinea pedis * Tinea manuum * Tinea unguium * Tinea incognito ## Tinea Capitis * Tinea capitis is a dermatophyte infection of the scalp and associated hair. * Epidemiology * Most commonly affects 3-14 years. * Most common pediatric dermatophytosis. * Transmission is through direct contact & fomites. * Infected hair can shed organisms for up to 1 year. * Etiology: * Virtually any species of Microsporum or Trichophyton can cause Tinea capitis. * The most common causes are M. canis in worldwide and T. tonsurans- in US. ### Clinical presentation * Different clinical features are based on the causative species and the degree of inflammatory host response. * Itching is variable. * May result in hair loss, scaling, varying degree of an inflammatory response. * Tinea capities can be: * Non-inflammatory * Seborrheic type * Gray patch type * Black dot type * Inflammatory * Kerion * Favus * Agminate folliculitis ### A. Non-inflammatory * Commonly anthropophilic * Minimal inflammation * Ectothrix organisms eg. M. audouinii * Endothrix organisms eg. T. tonsurans & T. Violaceum #### Seborrheic type * Prominent scaling, minimal inflammation. * Resembles that of dandruff. * Usually no halopcia. * Image: A close-up of a scalp with seborrheic type tinea capitis. There is scaling and minimal inflammation visible. #### Gray patch type * Well-defined patches of hair loss with breaking-off of hairs and dusty scaling. * Image: Top-down view of a head suffering hair loss in a circular area. #### Black Dot type * Hair breaks at the level of the scalp and leave grouped black dots behind. * Diffuse scaling with minimal inflammation and hair loss. * Image: Close up of scalp with hair loss and black dots visible. ### B. Inflammatory * Usually with zoophilic or geophilic. * Commonly M. canis & M. gypseum. * Due to hypersensitivity reaction to the infection. * Inflammation varies from minimal to pustular folliculitis or fruncle like lesions to kerion. * Commonly associated pain & tenderness with or without alopecia. ### Kerion * The most severe pattearn of reaction. * Characterized by erythematose boggy, sterile, Painless swelling. * Painful with purulent discharge (if super infected). * May have sinus formation. * lymphadenopathy is frequent. * Scarring alopecia is a sequele. * Image: A scalp with a severe kerion. A dome-shaped, boggy lesion with drainage is visible. ### Favus * Typically a chronic associated with severe inflammation. * Characterized by thick yellow crusts called Scutula. * Over several years, the lesions advance peripherally, leaving central, atrophic clearings of scarring alopecia. * Image: Scalp exhibiting favus, with thick yellow crusts (scutula) and scarred areas. ### Differential Diagnosis of Tinea Capitis | | | | :------------------- | :------------------------------------------------------------------------------------------------------------------------------------------------- | | **Most Likely** | Seborrheic dermatitis, contact dermatitis, pustular or plaque psoriasis, atopic dermatitis, bacterial pyodermas, folliculitis decalvans, lichen planopilaris, and dissecting cellulitis of the scalp | | **Consider** | Alopecia areata, trichotillomania, pseudopelade, psoriasiform reaction to tumor necrosis factor-a inhibitor | | **Rule Out** | Discoid lupus erythematosus, syphilis | ### Diagnosis 1. Microscopic -КОН 2. culture 3. histology 4. Wood's light examination ### Treatment * Since, the infections are involving hair-bearing skin oral antifungals are the treatment choice. * Griseofulvin is still the first line oral treatment for Tinea capitis 20-25mg/kg/day for 6-8 weeks given with fatty meal. * Terbinafine * <20kg--62.5mg/day * 20kg - 40kg--125mg/day * \>40kg--250mg/day for 4-6 weeks * The oral terbinafine, itraconazole and fluconazole also appear to be safe, effective, & have the advantage of shorter treatment durations than Griseofulvin. ### Adjuvant treatment * Adjunctive use of shampoos is recommended 2 to 4 times weekly for 2 to 4 weeks. * Selenium sulfide (1% and 2.5%) * zinc pyrithione (1% and 2%) * povidone-iodine (2.5%), and * ketoconazole (2%) are shampoo preparations that help eradicate dermatophytes from the scalp. * Household transmission may be prevented through the treatment of infected family members or animals. * Combs, brushes and head wear used by the patient should be disinfected or preferably discarded. ## Tinea barbae * Dermatophyte infection occurs predominantly in the beard and moustache areas of males face. * It could be transmited by contaminated barbers' razor. * Direct exposure to cattle, horses, or dogs is now the more common mode of acquisition. * Most commonly seen in rural settings among farmers. * Present as mild diffuse erythema and perifollicular papules and pustules, or annular lesions with central clearing. * Kerion type Sharply demarcated red edematous nodule studded with multiple yellowish weeping pustules may also be seen. ### DDx * Bacterial folliculitis(sycosis vulgaris) * Pseudofolliculitis barbae * acne vulgaris * Rosacea * contact dermatitis * perioral dermatitis * candidal folliculitis * Herpes simplex or zoster * cervicofacial actinomycosis * dental sinus tract ### Treatment * Oral antifungals are essential: * Fluconazole 200mg daily for 4 to 6 weeks * Itraconazole 200mg daily for 2 to 4 weeks * Terbinafine 250 mg daily for 2 to 4 weeks * Griseofluvine 500mg daily 6-8 weeks * Systemic glucocorticoids can be used for the first week for severe inflammation. ## Tinea Corporis * Refers to any dermatophytosis of glabrous skin except palms, soles, and the groin. * Any dermatophyte can potentially cause tinea corporis, but T. rubrum is the most common. * Transmission by direct contact with other infected individuals, fomites or by infected animals. * The classical presentation is the typical annular lesion with an active erythematous border composed of papules, vesicles, scaling or crusts with central clearing. * Image: A ring-worm rash on a persons back. * Image: A close up of ring-worm on the neck. ### Clinical variants of t. corporis * Majocchi granuloma * Tinea profunda * Tinea imbricata * Images: Showing the different variants listed above. ### Differential Diagnosis of Tinea Corporis | | | | :------------------- | :--------------------------------------------------------------------------------------------------------------------------------- | | **Most Likely** | Erythema annulare centrifugum, nummular eczema, psoriasis, tinea versicolor, subacute cutaneous lupus erythematosus, cutaneous candidiasis | | **Consider** | alopecia areata, trichotillomania, pseudopelade, psoriasiform reaction to tumor necrosis factor-a inhibitor | | **Rule Out** | Discoid lupus erythematosus, secondary syphilis | ### DIAGNOSIS * Microscopic * KOH:- septated branching hyphae * Culture:-Sabouraud's dextrose agar(SDA) * Image of hyphae under microscope ### Treatment * Topical is recommended for a localized infection. * Topical therapy once or twice a day for at least 2-4 weeks. * Clotrimazole 1% cream * Ketoconazole 2% cream * Miconazole 2% cream or lotion * Naftifine 1% cream or gel * Terbinafine 1% cream * Systemic therapy may be indicated for Immunocompromised patient, extensive, refractory to topical therapy or involvement of hair follicle. * Fluconazole 150mg for 2-4wks * Itraconazole 200mg/d for 1-2 wks * Terbinafine 250mg/d for 1-2 wks * Griseofulvin 500mg d for 2-6wks ## Tinea faciei * Infection of the glabrous skin of the face with a dermatophytes. * Usually the infection is caused by T. rubrum, T. mentagrophytes, M. Canis. * c/p:-Annular erythematous plaques, with an active border composed of papules, vesicles, scaling /or crusts * Image: face with ringworm. ### DDX * Impetigo * Rosacea * POD * SD * Contact dermatitis * Psoriasis * Acne * DLE ### Treatment * Minimal lesions respond well to topical imidazoles. * Oral antifungal therapy for extensive or refractory to topical lesions. ## Tinea cruris * Clinical Features * A dermatophyt infection of the groin, genitalia, perianal skin & pubic area. * Predisposing factors: warm, humid env't, tight clothing, and obesity. * C/p :-Well demarcated, slightly elevated red or scaly plaque on both sides of the groin. * Pruritus is common(jock itch). * The scortum is typically unaffected. * Image: infected area on groin. ### Lab Findings * KOH * Culture: Sabaroud's * Histopathology ### Treatment * Topical antifungals are the mainstay of therapy. * Oral antifungals are reserved for widespread or more inflammatory lesions. | | | | :------------------- | :------------------------------------------------------------------------------------------------------------------------------------------------- | | **Most Likely** | Erythrasma, cutaneous candidiasis, intertrigo, contact dermatitis, inverse psoriasis, seborrheic dermatitis, lichen simplex chronicus, folliculitis | | **Consider** | Familial benign pemphigus, Darier-White disease, histiocytosis | ## Tinea Pedis * Dermatophytlc Infection of the feet. * Epidemiology * Tinea pedis is thought to be the world's most common dermatophytosis. * Approximately 10 % of the total population can be expected to have foot infection at any given time. * More commonly affects males than females. * Prevalence increases with age commonly occurring after puberty. * Predisposing factors * Occlusive footwear * Hot and humid weather * Excessive sweating * Using common shower, bath or pool * Etiology: * T. rubrum, T. interdigitale, T. mentagrophytes, & E.floccosum are common causes of tinea pedis. * T. rubrum is the most common cause worldwide. ### Clinical Features * Clinical classifications of Tinea pedis: 1. Interdigital type * Most common clinical type of T. pedis. * Presenting with erythema, maceration, fissuring, & scaling in the interdigital area. * Most often between the 4th &5th toes are involved. * Fungal infection followed by bacterial invasion “dermatophytosis complex” can develop. * Pruritus is common. 2. Chronic Hyperkeratotic / Moccasin / type * Diffuse hyperkeratosis, erythema scaling & fissures on one or both plantar surface. * Can be asymptomatic & pruritic. * Often bilateral, patchy or diffuse scaling limited to the thick skin, soles, the lateral & medial aspects of the feet. * In addition to the feet, the hands may be involved:- “one hand, two feet syndrome” 3. Inflammatory / Vesiculobullous type * Characterized by painful, pruritic vesicles or bullae, most often on the anterior plantar surface. * Lesions can contain either clear or purulent fluid; after they rupture, scaling with erythema persists. * May be Complicated as cellulitis, lymphangitis, & adenopathy. 4. Ulcerative type * Characterized by rapid acutely spreading vesiculopustular lesions, ulcers, & erosions, typically in the web spaces and is accompanied by a secondary bacterial infection. * Cellulitis, lymphangitis, pyrexia, & malaise can accompany this infection. * Commonly seen in immunocompromised patients. | | | | :------------------- | :------------------------------------------------------------------------------------------------------------------------------------------------- | | **Most Likely** | Interdigital: erosio interdigitalis blastomycetica, erythrasma, bacterial coinfection<p></p>Hyperkeratotic: dyshidrosis, psoriasis, contact dermatitis, atopic dermatitis, hereditary or acquired keratodermas Vesiculobullous: dyshidrosis, contact dermatitis, pustular psoriasis, bacteridor other autoeczematization, palmoplantar pustulosis, bacterial pyodermas, scabies | | **Consider** | Pityriasis rubra pilaris | | **Rule Out** | Reactive arthritis | ### Treatment * Patients should try to minimize risk factors by:- * limiting the use of occlusive footwear. * Use of antifungal powder. * Use of antiperisperant. * First line therapy is with topical agents * Clotrimazole 1%,, Ketoconazole 2%, Terbinafine 1%. * keratolytics for hyperkeratotic type. * Systemic antifungals specially for those recalcitrant or extensive, inflammatory variants, onychomycosis, diabetes, peripheral vascular disease, or Immunocompromised patients. ## Tinea manuum * Tinea manuum affects the palm and interdigital areas of the hand. * Acquired by direct contact with an infected person or animal, the soil. * Often associated with Tinea pedis. * Diffusely hyperkeratosis of the palms & fingers is the most common variety. * unilateral in about half of cases. * Treatment:- * topical antifungal * Systemic antifungal for extensive or refractory to topical 2-4wks. ## Onychomycosis * Defined as infection of the nail caused by dermatophyte and non-dermatophyte fungus. * Onychomycosis the most prevalent nail disease & accounts for approximately 50% of nail diseases. * The common causatives are T.unguium, T. rubrum, T. tonsurans and T. interdigitale. T. rubrum is the most common. * Risk factors for include: * Tight shoes * Communal bathing * Poor peripheral circulation * Immunosuppression * Diabetes * Repeated nail trauma ### Clinical Variants * Distal/lateral subungual onychomycosis (DLSO) * Proximal subungual onychomycosis (PSO) * White superficial onychomycosis (WSO) * Endonyx onychomycosis(EO) * Mixed pattern onychomycosis(MPO) * Totally dystrophic onychomycosis(TDO) * Candidal onychomycosis * Secondary onychomycosis ### Distal/lateral subungual onychomycosis * Begins with invasion of the stratum corneum of the hyponychium and distal nail bed forming a yellowish opacification\_at the distal edge of the nail. * The infection then spreads proximally up the nail bed to the proximal nail plate. * Hyperproliferation of the nail bed subungual hyperkeratosis & progressive invasion of the nail plate. ### Proximal subungual onychomycosis * Involves the nail plate mainly from the proximal nailfold. * It is evident as a white opacity on the proximal nail plate. * Is an indication of HIV infection. ### White superficial onychomycosis * It is a direct invasion of the dorsal nail plate which begins with scaling. * Resulting in white to dull yellow sharply bordered patches any where on the surface of the nail. * It is usually caused by T. mentagrophytes * Non-dermatophyte molds such as Aspergillus, Fusarium & Acremonium, are also known etiologies. ### Candidal onychomycosis * Candida species invade the entire thickness of the nail plate. * Produces destruction of the nail and massive nail bed hyperkeratosis, ridging, yellow discoloration & total nail dystrophy. * Periungal areas are red & edematous & fingertips are often bulbous. * Common in immunosuppressive individuals and children. ### Treatment * Depends both on the severity of nail involvement and on the causative fungus. * Can be divided into cases with and without matrix area involvement. * In cases without nail matrix involvement,topical treatment alone can be sufficient. * Ciclopirox (8% lacquer) is applied daily for 48wks * Amorolfine - morpholine derivative nail lacquer applied once weekly * Combination treatments are recommended for matrix involvement. * Fluconazole 400mg po weekly for 6-9 month finger nail &12-18 month for toe nail. * Itraconazole-200mg daily for 2 month finger nail & 3 month toe nail. * Terbinafine- 250mg daily for 6wks/finger nail & for 12 weeks toe nail. * Final options for refractory cases include: * Surgical nail avulsion and * Chemical removal with 40% urea compounds in combination with topical or oral antifungals ~ reserved for patients with very thick nails & who do not tolerate mechanical avulsion. I hope this is helpful!