Scabies is an infestation of the skin by the Sarcoptes scabiei mite which presents most commonly with intense pruritus, characteristic linear burrows, and erythematous papules. Direct, human-to-human contact is the largest risk factor for transmission. Diagnosis is most often clinical but can be confirmed by dermatoscopy. Treatment includes permethrin cream for both the patient and close personal contacts (cohabitants and sexual partners) as well as thorough cleaning of bedding and clothing.
Table of Contents
- > 300 million cases reported worldwide
- Relatively common infestation that can affect individuals of any age or socioeconomic status
- Most vulnerable groups include young children and the elderly
- Highest incidence occurs in countries with significant poverty
- More common during instances of overcrowding, including
- Natural disasters
- In children, scabies can be transmitted from institutional settings.
- Psychiatric wards
- Nursing homes
- Day-care facilities
Onychomycosis (Nail fungus) and Scabies (Sarcoptic Mange) by Carlo Raj, MD
Scabies, Head Lice (Pediculosis Capitis) and Tinea Corporis (Ringworm) in Children by Brian Alverson, MD
Life Cycle and Transmission
- S. scabiei: an eight-legged, whitish-brown mite
- Life cycle
- After mating, the female mites burrow into the stratum corneum.
- Lays 2–3 eggs per day before dying (lifespan is ~4–6 weeks)
- Larvae hatch in 3–4 days and reach adulthood in the burrow
- Mite burden
- Low in Classic Scabies (10–15 mites)
- High in Crusted Scabies (up to 2 million mites)
- Mites can survive without a host for ~24 to 36 hours; thus, fomite transmission may occur
- Direct: Person-to-person transmission upon prolonged skin-to-skin contact; usually between family members or sexual partners
- Environmental: Crusted scabies can be transmitted via fomites (scarves, hats, bedding,etc.)
- Rare transmission between animal and human
- The infection takes the form of
- Initial infection:
- Sensitization occurs over 4 to 6 weeks
- This delay in symptom onset occurs due to a delayed-type hypersensitivity reaction.
- Patient is already sensitized, and pruritus occurs within 1-3 days.
- Initial infection:
- In immunocompromised patients, there is an imminent risk of developing hyperkeratotic/crusted scabies.
Key characteristic features include severe nocturnal itching and a characteristic rash distribution.
- Commonly involved areas:
- Interdigital folds
- Mammilla region
- Axillary folds
- Flexor aspects of the wrists
- Note: Back and head are usually spared in classic scabies.
- Scratching may result in
- Bacterial superinfections of the skin can occur as a complication.
- Pruritus, usually worse at night
- Delayed-type hypersensitivity reaction to the mite, mite feces, and mite eggs
- For primary infestation, symptoms begin in 3 to 6 weeks.
- For previously infected individuals, symptoms begin within 1 to 3 days.
- Cutaneous Findings:
- Multiple small, erythematous papules that are often excoriated
- Distribution is rarely localized to a single area
- Burrows (2–15mm, thin, gray or brown lines) are often not visible due to excoriation or secondary infection
- Miniature wheals, vesicles, pustules, and, rarely, bullae also may be present
- Nodular scabies is a less common manifestation of classic scabies.
- Involves persistent, firm, erythematous, pruritic, dome-shaped papules 5–6mm in diameter
- Also called scabies crustosa or Norwegian scabies
- Massive mite infestation most commonly in immune-suppressed patients (AIDS, long-term glucocorticoid/cytostatic therapy, leukemia)
- Cutaneous Findings:
- Poorly defined, erythematous patches that quickly develop prominent scaling
- Scales may become warty, crusts and fissures may also appear
- Occurs most prominently on the scalp, hands, and feet
- Nails are often thickened, discolored, and dystrophic
- Pruritus may be minimal or absent
Diagnosis is confirmed through the detection of scabies mites, eggs, or fecal pellets (“scybala”) through microscopic examination. However, diagnosis can be clinically based on history and physical exam findings.
- History and physical exam
- Widespread itching that is worse at night and spares the head and back
- Characteristic pruritic lesions and distribution
- Other household members or sexual contacts with similar symptoms
- Scabies prep
- Remember that classic scabies has a low mite count, so a negative scabies preparation does not rule out infection.
- Scraping or strong tape: add mineral oil and potassium hydroxide (KOH), view under microscope
- Dermoscopic examination
- Delta wing sign: a dark triangular shape that represents the head of the mite within a burrow
- Labs: Blood tests are not indicated. However, eosinophilia has been reported.
- Occasionally, scabies may be misdiagnosed as atopic dermatitis. This often occurs due to the appearance of the erythematous papules. Patients that are misdiagnosed will have initial symptom alleviation with topical glucocorticoids; however, this will not treat the underlying cause – mite infestation.
- Two pillars of successful therapy in scabies:
- Hygienic measures
- Medication therapy and compliance
- First-line treatment of adults:
- Classic scabies: topical permethrin 5%
- Crusted scabies: topical permethrin 5% and oral ivermectin
- First-line treatment in children:
- Administration of topical permethrin and antibiotic therapy (if secondary scabies lesions become infected)
- Second application of permethrin one to two weeks later may be necessary to eliminate mites
- Nodules that persist after eradication of mites can be treated with potent topical corticosteroids or intralesional corticosteroid injections.
- Pruritus might increase after the introduction of a scabicidal agent.
- Oral antihistamines such as hydroxyzine hydrochloride or diphenhydramine hydrochloride help with the severe pruritus.
- Changing and washing clothes, bedding, and towels on a daily basis
- Topical permethrin for family and close personal contacts
- Including cohabitants or those with prolonged skin-to-skin contact in the preceding six weeks
- Secondary bacterial skin infections including impetigo, ecthyma, and furunculosis.
- Psychological issues including embarrassment and delusion of parasitosis.
- Atopic dermatitis: Sometimes called allergic eczema; chronic pruritic inflammatory skin disease that occurs most frequently in children, but also in adults. Often associated with elevated IgE and a personal or family history of atopy.
- Insect bites: Be sure to rule out insect bites as an underlying etiology. Take into consideration the patient’s history and physical exam, symptom onset, and affected close contacts.
- Dermatitis herpetiformis: Autoimmune cutaneous eruption associated with gluten sensitivity. Affected patients typically develop intensely pruritic inflammatory papules and vesicles on the forearms, knees, scalp, or buttocks. Skin biopsy shows granular deposits of IgA in the dermal papillae.
- Bullous pemphigoid: Autoimmune blistering disorder usually in older adults. Associated with a prodrome of pruritic, urticaria-like skin lesions followed by tense bullae on an erythematous urticarial base. Skin biopsy shows linear deposition of IgG and/or C3 along the basement membrane.