Tinea & Scabies Flashcards
Etiology of Tinea Capitis
Refers to head
Caused by a variety of fungal species
Trichophyton species (T. tonsurans) Microsporum species (M. canis)
Epidemiology of Tinea Capitis
Age: Children
Ethnicity: African Americans
Decreased personal hygiene, low socioeconomic status, overcrowding
Asymptomatic carriers
Clinical Presentation of Tinea Capitis
- Scaly patches with alopecia (hair loss)
- Patches of alopecia with black dots
- Widespread scaling with subtle hair loss
- Kerion (a boggy edematous painful plaque)
- Favus (multiple cup-shaped yellow crusts / scutula)
Associated Signs of Tinea Capitis
Cervical adenopathy
Dermatophytid reaction (similar to eczema)
Erythema Nodosum (rare): reddish, painful, tender lumps or nodules most commonly located in the front of the legs below the knees
Diagnosis of Tinea Capitis
Physical exam
KOH prep
Wood’s Lamp
Culture
Dermascope
Treatment of Tinea Capitis
Treated with systemic antifungal therapy (oral meds)
Griseofulvin x 6-12 weeks
- Tx of choice for Microsporum or empiric tx
Terbinafine x 2-4 weeks
- Tx of choice if suspect Trichophyton
Itraconazole (4-6 weeks) and fluconazole (3-6 weeks) or pulse therapy (8-12 weeks)
Etiology of Tinea Corporis
Refers to body
Caused by different species of fungus
T. rubrum E. floccosum T. interdigitale M. canis T. tonsurans
Epidemiology of Tinea Corporis
Occurs more frequently in:
Caregivers with children with tinea capitis
Athletes with skin to skin contact (tinea corporis gladiatorum)
Immunocompromised
Presentation of Tinea Corporis
Pruritic (itchy), Annular (round), Erythematous (skin redness) plaque
Central clearing
Raised, advancing border
Diagnosis of Tinea Corporis
History and physical exam
KOH prep to confirm
Culture
Treatment of Tinea Corporis
Usually treated with topical medications
Topical antifungals:
- Clotrimazole, ketoconazole, etc.
- at least two weeks duration
Consider systemic tx in special circumstances (itraconazole, terbinafine, fluconazole):
- Immunocompromised
- Failed topical tx
- Tinea corporis gladiatorum (no participation for 10-15 days)
- Duration varies with drug choice (1-4 weeks)
Improper Treatment of Tinea Corporis
Tinea Incognito
Mojocchi’s Granuloma
Etiology of Tinea Cruris
Refers to the crotch/genitals
Fungal infection that begins in the inguinal fold
T. rubrum
E. floccosum
T. interdigitale
T. verrucosum
Epidemiology of Tinea Cruris
Male gender
Sweaty/humid
Occlusive clothing
Obesity/skin folds
Athlete’s foot
Clinical Presentation of Tinea Cruris
Well-marginated, scaly, annular plaque with raised border
Extends from the inguinal fold to inner thigh
Scrotum typically spared
Pruritus and pain
Can be chronic and progressive
Diagnosis of Tinea Cruris
History and physical exam
KOH prep to confirm
Culture
Treatment of Tinea Cruris
Topical antifungals (clotrimazole)
Resistant cases: oral itraconazole
Treatment accompanying or associated with tinea pedis and/or onychomycosis
Daily drying powder
Lifestyle considerations: avoid tight clothing, weight loss
Etiology of Tinea Pedis
Athlete’s foot
Typically caused by the same species as tinea cruris
T. rubrum
T. interdigitale
E. floccosum
Chronic vs. Acute
Epidemiology of Tinea Pedis
Most common dermatophytosis in the world
Risk factors:
- occlusive footwear
- communal baths/showers/pools
Clinical Presentation of Tinea Pedis
Acute:
- presents as a self-limited, intermittent, and recurrent infection
- itchy/painful vesicles or bulla following sweating
- secondary staph infections are common
Chronic:
- presents as a slowly progressive infection that persists indefinitely
- erosions/scales between toes (esp. 3rd and 4th)
- interdigital fissures
- “moccasin ringworm”: sharp demarcation with accumulated scale in the skin creases
- may present with tinea manuum (two feet, one hand)
Diagnosis of Tinea Pedis
History and physical exam
KOH prep to confirm
Culture
Gram stain if bacterial infection suspected
Treatment of Tinea Pedis
Treated similarly to corporis/cruris but typically requires longer treatment
Topical antifungal cream (clotrimazole) x 4 weeks
Oral meds for chronic/extensive disease (itraconazole, terbinafine, fluconazole)
Burow’s wet dressings for vesiculation or maceration, 20 minutes BID-TID
Treat secondary infections
Lifestyle considerations: foot powder, treatment of shoes, proper footwear
Etiology of Onychomycosis
Infection of the nail by fungus, yeast, or non-dermatophyte molds
T. rubrum
T. mentagrophytes
Candida Albicans (yeast)
Nondermatophyte molds
Risk Factors for Onychomycosis
Advanced age
Tinea pedis
Genetics
Immunodeficiency
Household infection
Distal Subungual Onychomycosis
- Most common subtype by far
- Typically starts with great toe, but all can be affected
- White/brown/yellow discoloration starts at distal corner and spreads towards the cuticle
- Distal end of the nail breaks, exposing the nail bed
Proximal Subungual Onychomycosis
- Starts near the cuticle and progresses distally
- Relatively uncommon presentation
- Usually seen in severely immunocompromised population (AIDS)
White Superficial Onychomycosis
- Starts with dull white spots on the surface of the nail plate
- Spreads centrifugally until entire nail is involved
- Lesions can be scraped for lab sample
Fingernail Onychomycosis
Commonly caused by yeast (Candida Albicans)
Thickening of nail with yellow/brown discoloration
May cause chronic paronychia (An infection of the tissue folds around the nails)
Diagnosis of Onychomycosis
KOH prep of nail scrapings
Culture
Histopathology (biopsy)
Treatment of Onychomycosis
No obligatory, but should be considered if the patient:
- Has a history of cellulitis
- Diabetic
- Desires cosmetic improvement
- Complains of discomfort/pain
Dermatophyte onychomycosis:
- Oral terbinafine (6 weeks for fingernails, 12 weeks for toenails)
- Alternative options: fluconazole, intraconazole
Nondermatophyte onychomycosis:
- Oral intraconazole (6 weeks for fingernails, 12 weeks for toenails)
Etiology of Candida Intertrigo
Any infectious or noninfectious inflammatory condition of two closely opposed (intertriginous) skin surfaces
Often due to Candida species
Risk Factors of Candida Intertrigo
Moisture (humidity, incontinence)
Skin friction (obesity, sumo wrestling)
Immunocompromised
Clinical Presentation of Candida Intertrigo
Typically affects the groin, mammary/abd folds, web spaces, and axilla
Erythematous, macerated (soggy or softened) plaques and erosions
Satellite papules/pustules
Fine peripheral scaling
Diagnosis of Candida Intertrigo
History and physical exam
KOH prep
Culture
Treatment of Candida Intertrigo
Preventative measures:
- drying agents
- weight loss
- address underlying medical conditions
Topical medications x 2-4 weeks
- Nystatin
- Azoles
Systemic medications in resistant/severe cases
- Fluconazole x 2-6 weeks
Etiology of Tinea Versicolor
Fungal infection of the skin
Caused by Malassezia sp.
Normal fungal skin flora that becomes pathologic when it transforms into the mycelial form
Epidemiology of Tinea Versicolor
Tropical climate
Adolescents/young adults
Risk Factors:
- Hyperhidrosis, Genetics, immunosuppression, not contagious
Clinical Presentation of Tinea Versicolor
Varies with skin tone/location (can be hypo/hyper pigmented, erythematous)
- Macules (flat lesions), patches, plaques on trunk/UE
- Can coalesce
- Often have fine scale
Typically asymptomatic but can be mildly pruritic
Diagnosis of Tinea Versicolor
History and physical exam
KOH prep
Wood’s Lamp: yellow to yellow-green fluorescence in 1/3
Treatment of Tinea Versicolor
Usually treated with topical antifungal medications
Topical treatments:
- Azole antifungals (clotrimazole) x 2 weeks
- Selenium sulfide (lotion, shampoo, foam) x 1 weeks
- Zinc Pyrithione shampoos x 2 weeks
Systemic:
- reserved for extensive disease or failed topical therapy
- Not used in children
- Oral azole antifungals (itraconazole x 5-7 days)
pigment changes can persist for months after successful tx
recurrence common, consider prophylaxis
Scabies Etiology
A parasitic infection
Caused by Sarcoptes scabiei mite:
- host harbors 3-50 female mites
- female mite excavates a burrow in the stratum corneum in which she lays 2-3 eggs/ days for her 30-day lifespan
- eggs hatch in 10 days
- can live for 3 days away from host
Clinical Presentation of Scabies
Initial lesion
Burrow is pathognomonic (indicative of a particular disease or condition)
Severe pruritus, worse at night
Scabies in the Immunocompromised
Crusted Scabies (Norwegian scabies)
- Fissures provide avenue for bacteria which can lead to sepsis
- Requires oral medications
Diagnosis of Scabies
Visualization of the burrow
Microscopic identification of the mite, eggs, or fecal pellets (Scybala)
Dermatoscope
Treatment of Scabies
Permethrin 5% cream - initial tx + 2nd application 10-14 days later
Oral Ivermectin - single dose repeated two weeks later
Patient education
- treat household and close contacts simultaneously
- Post scabetic itch can persist up to 2 weeks
- oral anihistamines and emollients can provide symptomatic relief
- wash linens in hot water and dry under high heat
Pubic Lice
Parasites, larger than scabies
Caused by the crab louse, Phthirus pubis
Most commonly affects teens and young adults
Transmitted primarily via sexual contact
Presents with itching in groin/axilla
Diagnosed by visualizing the lice or egg (nit)
Using a microscope helps
Treatment is permethrin 1% cream, repeat/recheck in 10 days
Treat sexual partners
Have another STI about 30% of the time
