Scabies Scabies is an infestation by the mite Sarcoptes scabiei, usually spread by skin-to-skin contact, characterized by generalized intractable pruritus

often with minimal cutaneous findings. Epidemiology and Etiology Age of Onset Young adults (usually acquired by body contact); elderly and bedridden patients in the hospital (contact with mite-infested sheets); children (often 5 years). Etiology S. scabiei var. hominis. Thrive and multiply only on human skin. Mites of all developmental stages burrow/tunnel into epidermis shortly after contact, no deeper than stratum granulosum; deposit feces in tunnels. Females lay eggs in tunnels. Burrow 2 to 3 mm daily. Usually burrow at night and lay eggs during the day. Female lives 4 to 6 weeks, laying 40 to 50 eggs. Eggs hatch after 72 to 96 h. In classic scabies, about a dozen females per patient are present. In hyperkeratotic or crusted scabies, >1 million mites may be present, or up to 4700 mites/g skin. Incidence Estimated at 300 million cases/year worldwide. In the past, epidemics occurred in cycles every 15 years; the latest epidemic began in the late 1960s but has continued to the present. Demography Major public health problem in many less-developed countries. In some areas of South and Central America, prevalence is about 100%. In Bangladesh, the number of children with scabies exceeds that of children with diarrheal and upper-respiratory disease. Transmission Mites transmitted by skin-to-skin contact as with sex partner, children playing, or health care workers providing care. Mites can remain alive for >2 days on clothing or in bedding; hence, scabies can be acquired without skin-to-skin contact. Patients with crusted scabies shed many mites into their environment daily and pose a high risk of infecting those around them, including health care professionals. Risk Factors In nursing homes, risk factors include age of institution (>30 years), size of institution (>120 beds), ratio of beds to health care workers (>10:1). Pathogenesis Hypersensitivity of both immediate and delayed types occurs in the development of lesions other than burrows. For pruritus to occur, sensitization to S. scabiei must take place. Among persons with their first infection, sensitization takes several weeks to develop; after reinfestation, pruritus may occur within 24 h. Various immunocompromised states or individuals with neurologic disease predisposed to crusted Norwegian scabies. Infestation is usually by only approximately 10 mites. In contrast, the number of infesting mites in crusted scabies may exceed a million. History Patients are often aware of similar symptoms in family members or sexual partners. Patients with crusted scabies are usually immunocompromised (HIV disease, organ transplant recipient) or have neurologic disorders (Down's syndrome, dementia, strokes, spinal cord injury, neuropathy, leprosy). Incubation Period Onset of pruritus varies with immunity to the mite: first infestation, about 21 days; reinfestation, immediate, i.e., 1 to 3 days. Duration of Lesions Weeks to months unless treated. Crusted scabies may be present for years. Skin Symptoms Pruritus Intense, widespread, usually sparing head and neck. Itching often interferes with or prevents sleep. Often present in family members. One-half of patients with crusted scabies do not itch. Rash Ranges from no rash to generalized erythroderma. Patients with atopic diathesis scratch, producing eczematous dermatitis. Other individuals experience pruritus for many months with no rash. Tenderness of lesions suggests secondary bacterial infection.

Physical Examination

Skin Findings Common cutaneous findings can be classified: lesions occurring at the sites of mite infestation, cutaneous manifestations of hypersensitivity to mite, lesions secondary to chronic rubbing and scratching, secondary infection. Variants of scabies in special hosts including those with an atopic diathesis, nodular scabies, scabies in infants/small children, scabies in the elderly, crusted (Norwegian) scabies, scabies in HIV disease, animal-transmitted scabies (zoonosis), scabies of the scalp, dyshidrosiform scabies, urticarial/vasculitis scabies, and bullous scabies. Lesions at Site of Infestation Intraepidermal Burrows Gray or skin-colored ridges, 0.5 to 1 cm in length, either linear or wavy (serpiginous), with minute vesicle or papule at end of tunnel. Each infesting female mite produces one burrow. Mites are about 0.5 mm in length. Burrows average 5 mm in length but may be up to 10 cm. In light-skinned individuals, burrows have a whitish color with occasional dark specks (due to fecal scybala). Fountain-pen ink applied to infested skin concentrates in tunnels, highlighting and marking the burrow. Blind end of burrow where mite resides appears as a minute elevation with tiny halo of erythema or as a vesicle. Distribution

Areas with few or no hair follicles, usually where stratum corneum is thin and soft, i.e., interdigital webs of hands > wrists > shaft of penis > elbows > feet > genitalia > buttocks > axillae > elsewhere. In infants, infestation may occur on head and neck. Scabietic (Scabious) Nodule Inflammatory papule or nodule; burrow sometimes seen on the surface of a very early lesion. Hyperkeratosis/Crusting Psoriasiform In areas of heavily infested crusted scabies, well-demarcated plaques covered by a very thick crust or scale. Warty dermatosis of hands/feet with nail bed hyperkeratosis. Erythematous scaling eruption on face, neck, scalp, trunk. Cutaneous Manifestations of Hypersensitivity to Mite

Pruritus

Some individuals experience only pruritus without any cutaneous findings. "Id" or Autosensitization-Type Reactions

Characterized by widespread small urticarial edematous papules mainly on anterior trunk, thighs, buttocks, and forearms. Urticaria

Usually generalized. Eczematous Dermatitis

At sites of heaviest infestation: hands, axillae. Lesions Secondary to Chronic Rubbing and Scratching Excoriation, lichen simplex chronicus, prurigo nodules. Generalized eczematous dermatitis. Psoriasiform lesions. Erythroderma. Atopy Postinflammatory Hyper- and Hypopigmentation

Secondary Infection S. aureus or Group A Streptococcus Infection Impetiginized excoriations (crusted, tender, surrounding erythema), ecthyma, folliculitis, abscess formation; lymphangitis, lymphadenitis; cellulitis; bacteremia, septicemia. Acute poststreptococcal glomerulonephritis reported associated with streptococcal impetiginization. Nodular Scabies Nodular lesions develop in 7 to 10% of patients with scabies. Nodules are 5 to 20 mm in diameter, red, pink, tan, or brown in color, smooth. A burrow may be seen on the surface of early nodule. Distribution Penis, scrotum, axillae, waist, buttocks, areolae. Resolve with postinflammatory hyperpigmentation. May be more apparent after treatment, as eczematous eruption resolves. Upper back, lateral edge of foot (infants). Nodules are usually countable. Crusted or Norwegian Scabies Predisposing factors: glucocorticoid therapy, Down's syndrome, HIV disease, HTLV-I infection, organ transplant recipients, elderly. May begin as ordinary scabies. In others, clinical appearance is of chronic eczema, psoriasiform dermatitis, seborrheic dermatitis, or erythroderma. Lesions often markedly hyperkeratotic and/or crusted. Distribution Generalized (even involving head and neck in adults) or localized. Scale/crusts found on dorsal surface of hands, wrists, fingers, metacarpophalangeal joints, palms, extensor aspect of elbows, scalp, ears, soles, and toes. In patients with neurologic deficit, crusted scabies may occur only in affected limb. May be localized only to scalp, face, finger, toenail bed, or sole. General Findings Lymphadenopathy in some cases.