Scabies

Epidemiology

• > 300 million cases reported worldwide
• A relatively common infestation that can affect individuals of any age or socioeconomic status
• Most vulnerable groups are young children, the elderly, and the immunocompromised.
• The highest incidence occurs in countries with significant poverty.
• More common during instances of overcrowding, including:
  • Natural disasters
  • War
• In children, scabies can be easily transmitted in institutional settings, such as:
  • Psychiatric wards
  • Nursing homes
  • Day-care facilities

Life Cycle and Transmission

• Sarcoptes scabiei: 8-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 approximately 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 approximately 24–36 hours; thus, fomite transmission may occur.

• Transmission
  • Direct: person-to-person transmission upon prolonged skin-to-skin contact, usually between family members or sexual partners; casual skin contact is unlikely to result in infection
  • 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.
  • Reinfestation: occurs if the patient is already sensitized, so pruritus occurs within 1–3 days.
• In patients with compromised cellular immunity, there is a high risk of developing hyperkeratotic/crusted scabies.

Clinical Presentation

Key characteristic features

• Severe nocturnal itching 
• Characteristic rash distribution
• Commonly involved areas:
  • Interdigital folds
  • Flexor aspects of the wrists
  • Axillary folds
  • Extensor aspects of the elbows and knees
  • Male genitalia
  • Periareolar skin (especially in women) 
  • Periumbilical skin
  • Waist
  • Inferior portions of buttocks and adjacent thighs
  • Lateral and posterior aspects of the feet
• Areas usually spared in classic scabies: head (except in young children) and back
• Scratching may result in:
  • Excoriations
  • Crusts
  • Eczema
  • Bacterial superinfections of the skin can occur as a complication.

Classic scabies

• Pruritus, usually worse at night
  • Delayed-type hypersensitivity reaction to the mite, mite feces, and mite eggs
  • For primary infestation, symptoms begin in 3–6 weeks.
  • For previously infected individuals, symptoms begin within 1–3 days.
• Cutaneous findings:
  • Multiple small, erythematous papules that are often excoriated 
  • Distribution is rarely localized to a single area.
  • Burrows (2–15 mm; 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:
  • A less common manifestation of classic scabies
  • Present as pruritic, firm, and erythematous papules measuring 5–6 mm in diameter
  • Usual sites involved: axillary folds, groin, genitalia, buttocks
  • May represent a focally heightened hypersensitivity reaction
• Crusted scabies (also called scabies crustosa or Norwegian scabies)
  • Occurs in conditions that compromise cellular immunity (AIDS, cytostatic therapy, leukemia), and with long-term topical glucocorticoids; also seen in older adults and in patients with Down syndrome
  • Massive mite infestation
  • 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

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 examination 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 preparation
  • Scraping: Apply mineral oil to the skin and vigorously scrape the surface with a number-15 scalpel blade. Add potassium hydroxide (KOH) if crusted scabies present, then view under the microscope.
  • Adhesive tape test: Use strong transparent (packing-type tape), remove rapidly, then apply to a microscope slide and view under the microscope.
  • Classic scabies has a low mite count, so a negative scabies preparation does not rule out infection. Sensitivity of scabies preparations: 40%–90%; specificity: 100%
• Dermoscopic examination:
  • Delta wing sign: a dark triangular shape that represents the head of the mite within a burrow
  • It is less specific than scabies preparations.
• 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 who are misdiagnosed will have initial symptom alleviation with topical glucocorticoids; however, this will not treat the underlying cause (i.e., mite infestation).

Treatment

Treatment

• 2 pillars of successful therapy in scabies:
  1. Hygienic measures
  2. Medication therapy and compliance
• First-line treatment in 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 1–2 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 
  • May increase after the introduction of a scabicidal agent.
  • Oral antihistamines such as hydroxyzine hydrochloride or diphenhydramine hydrochloride help with severe pruritus.

Prevention

• 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 6 weeks

Complications

• Secondary bacterial skin infections including impetigo, ecthyma, and furunculosis
• Psychological issues including embarrassment and delusion of parasitosis

Differential Diagnosis

• 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: It is important 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 seen 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.