eMedicine Specialties > Emergency Medicine > Infectious Diseases

Scabies

Amy L McCroskey, MD, Resident Physician, Department of Emergency Medicine, Wayne State University Detroit Medical Center, Detroit Receiving Hospital
Adam J Rosh, MD, MS, Assistant Professor, Department of Emergency Medicine, Wayne State University/Detroit Receiving Hospital

Updated: Jul 17, 2009

Introduction

Background

Scabies is a common parasitic infection of global proportion. Worldwide, an estimated 300 million cases occur annually.¹ The arthropod Sarcoptes scabiei var hominis causes an intensely pruritic and highly contagious skin infestation,² which affects males and females of all socioeconomic status and ethnic groups. Scabies infestation has been reported for more than 2500 years. Aristotle discussed "lice in the flesh," which resulted in vesicles, and Celsus recommended sulfur mixed with liquid pitch as a remedy for the disease.³ However, the disease was first ascribed to the mite by Giovan Cosimo Bonomo in 1687. It was the first human disease recognized to be caused by a specific pathogen.

Pathophysiology

Mode of transmission

Transmission of scabies is predominantly through direct skin-to-skin contact, and for this reason, scabies has been considered a sexually transmitted disease. Those at high risk include men who have sex with men and men with sexual contacts.⁴ A person infested with mites can spread scabies even if he or she is asymptomatic.¹  It is less frequently transmitted by indirect contact through fomites such as infested bedding or clothing. However, the greater the number of parasites on a person, as in crusted scabies, the more likely that indirect contact will transmit the disease.

The S scabiei var hominis mite that infects humans is female and can be seen with the naked eye (0.3-0.4 mm long). The male is about half this size. The mite has 4 pairs of legs. It does not penetrate deeper than the outer layer of the epidermis. Mites are unable to fly or jump. They crawl at a rate of 2.5 cm/min.⁴ While the mite's life cycle occurs completely on its host, they are able to live on bedding, clothes, or other surfaces at room temperature for 2-3 days, while remaining capable of infestation and burrowing. At temperatures below 20°C, S scabiei are immobile, although they can survive such temperatures for extended periods.

Life cycle

The scabies mite is an obligate parasite and completes its entire life cycle on humans. Other variants of the scabies mite can cause infestation in other mammals such as dogs, cats, pigs, ferrets, and horses, and these variants can irritant human skin as well. However, they are unable to reproduce in humans and only cause a transient dermatitis.

Life cycle stages¹

1. Eggs incubate and hatch in 3-4 days (90% of the hatched mites die).
2. Larvae (3 pairs of legs) migrate to the skin surface and burrow into the intact stratum corneum to make short burrows, called molting pouches (3-4 d).
3. Larvae molt into larger nymphs and then into adults.
4. Mating takes place once, and the female is fertile for the rest of her life (1-2 mo), and the male dies soon after mating.
5. She makes a serpentine burrow using proteolytic enzymes to dissolve the stratum corneum of the epidermis, laying eggs in the process, and she continues to lengthen her burrow and lay eggs for the rest of her life (1-2 mo).
6. Transmission of impregnated females from person-to-person through direct or indirect skin contact.

Classic and Norwegian scabies

In classic scabies infection, anywhere from 5-15 mites (range, 3-50) live on the host.⁴ Little evidence of infection exists during the first month (range, 2-6 wk), but after 4 weeks and with subsequent infections, a delayed-type IV hypersensitivity reaction to the mites, eggs, and scybala (packet of feces) occurs. The time required to induce immunity in primary infestations probably accounts for the latent period of 4 weeks of asymptomatic infection. In reinfestation, the sensitized individual may develop a rapid reaction (within hours). The resultant skin eruption, and its associated intense pruritus, is the hallmark of classic scabies.

Scabies on the hand. Courtesy of William D. James, MD.

Crusted, or Norwegian scabies (so named because the first description was from Norway in the mid 1800s), is a distinctive and highly contagious form of scabies. In this variant, hundreds to millions of mites infest the host individual, who is usually immunocompromised, elderly, or physically or mentally disabled and impaired. Extensive, widespread, crusted lesions appear with thick, hyperkeratotic scales over the elbows, knees, palms, and soles. Serum immunoglobulin E (IgE) and immunoglobulin G (IgG) levels are extremely high in these patients, yet the immune reaction does not seem to be protective. Cell-mediated immunity in classic scabies demonstrates a predominantly CD4 T-cell infiltrate in the skin, while one study suggests a CD8 predominance in crusted scabies.

Atypical infestations may also befall the very young (neonates).

Norwegian scabies. Courtesy of William D. James, MD.

Frequency

International

While many accounts of the epidemiology of scabies suggest that epidemics or pandemics occur in 30-year cycles, this may be an oversimplification of its incidence. These accounts coincided with the major wars of the 20th century. Because it is not a reportable disease, and data are based on variable notification, the incidence of scabies is difficult to ascertain.

Although epidemics have been reported (1919-1925, 1936-1949, 1964-1979), it is clearly an endemic disease in many tropical and subtropical regions. Scabies is one of the six major epidermal parasitic skin diseases (EPSD) that is prevalent in resource-poor populations, as reported in the Bulletin of the World Health Organization in February 2009.⁵ Prevalence rates are extremely high in aboriginal tribes in Australia, Africa, South America,⁶ and other developing regions of the world. Incidence in parts of Central America and South America and in one Indian village approach 100%. In parts of Bangladesh, the number of children with "the itch" exceeds the number with diarrheal and respiratory diseases combined.⁵ In 2009 retrospective study of 30,078 children in India, scabies was found to be the second most common skin disease in all age groups of children, and the third most common skin disease in infants.⁷

Worldwide, the prevalence of scabies has been estimated at 300 million cases annually.¹ In the United States and in other developed regions around the world, scabies occurs in epidemics in nursing homes, hospitals, long-term care facilities, and other institutions. It is seen frequently in the homeless populations but occurs episodically in other populations as well. No recent published data are available on its incidence in the United States. A study published in 2009 conducted in Brazil identified major risk factors for scabies in an impoverished rural community. The risk factors were young age, presence of many children in the household, illiteracy, low family income, poor housing, sharing clothes, and towels, and irregular use of showers.⁸

Mortality/Morbidity

Classic scabies is primarily a nuisance. However, it can indirectly lead to long-term morbidity. Scabies and other parasitic skin diseases can lead to long-term colonization of skin lesions by group A streptococci. Several studies have demonstrated a correlation between poststreptococcal glomerulonephritis (PSGN) and scabies. Conversely, in one World Health Organization sponsored study in the Solomon Islands, an intervention of mass treatment with ivermectin or permethrin led to a decrease in prevalence of scabies from 25% to less than 1% (p< 0.001) and a 40% to 20% decrease in pyoderma (secondary infection). There was also a decline in hematuria, which was a sign of renal damage by the group A Streptococcus secondary infection in children.⁹ It also decreased occurrence of streptococcal skin disease.

In remote Aboriginal communities in Australia where scabies is endemic, the repeated infestations and secondary streptococcal infections appear to be related to the extremely high levels of renal failure and rheumatic heart disease observed in the communities.

While the microbiology of secondary bacterial infection in scabies lesions probably changes based on geographic location, one study demonstrated that the predominant aerobic and facultative bacteria recovered from lesions were Staphylococcus aureus, group A streptococci, and Pseudomonas aeruginosa. Multiple anaerobes were recovered as well, suggesting polymicrobial colonization of lesions.¹⁰

Other complications of scabies include impetigo, furunculosis, and cellulitis. The staphylococci or streptococci in the lesions can lead to pyelonephritis, poststreptococcal glomerulonephritis, abscesses, pyogenic pneumonia, sepsis, and death.

Clinical

History

• Suspect scabies in any patient, regardless of age or socioeconomic status, who presents with severe persistent pruritus. The patient with scabies has generally been itching for a short time. On the other hand, the infestation can persist indefinitely, thus the appellation "the seven year itch."
• Signs and symptoms tend to crescendo progressively over 2-3 weeks before compelling the patient to seek medical attention.
• In developed nations, scabies occurs more commonly in fall and winter months.
• Scabies appears to occur in clusters. If there is an outbreak in the community, consider scabies in an individual presenting with itching and a rash.
• Consider a diagnosis of scabies if multiple family members are involved.
• Nocturnal pruritus is a highly characteristic complaint associated with scabies infestation.
• Although unusual in the neonate, scabies has been reported in this age group.
• Debilitated or immunocompromised patients may not have the urge to scratch.¹¹

Physical

• Primary lesions of scabies
  • Burrows, papules, pustules, nodules, occasionally urticarial papules and plaques¹¹ located between web space of fingers, flexor aspects of the wrists, axilla, antecubital area, abdomen, umbilicus, genital and gluteal areas, and feet¹²

Scabies on the buttocks. Courtesy of William D. James, MD.

• Burrows
  • A short elevated pink or gray, straight or tortuous line, serpiginous (S-shaped) track in the superficial epidermis, with a small vesicle at the tip is known as a burrow; this is pathognomonic of scabies infestation.¹¹
  • A burrow appears as a thin (approximately the width of a human hair), short (perhaps 2-3 mm in length), gray brown, wavy channel on the skin.

• In women, the nipples and areola of the breasts often are affected.
• In men, red papules or nodules on the penile glans, shaft, and scrotum are typical of scabies.

Scabies on the penis. Courtesy of William D. James, MD.

• Compared with adults, scabies in infants and young children tend to be more disseminated and, while the head and face usually are spared in adults, they may be affected in the very young.
• Geriatric scabies demonstrates a propensity for the back, often appearing as excoriations.
• Occasionally, the mite is visible to the naked eye as a small white dot.
• A small vesicle or papule may appear at the end of the burrow, where the mite enters the skin.
• Nodular scabies may erupt on covered parts of the body as either few or many lesions. They are characterized by firm, red nodules approximately 0.5 cm or larger.
• Norwegian scabies presents with extensive crusting of the skin with thick, hyperkeratotic scales overlying the elbows, knees, palms, and soles.
• Bullous lesions may be observed in immunocompromised patients.
• Canine scabies does not exhibit the classic burrow. Instead, papules and vesicles are the most prominent lesions surfacing on the arms, chest, abdomen, and thighs.
• Secondary lesions that may occur include urticaria, impetigo, and eczematous plaques.¹³
  • Pyoderma: One study found aerobic and anaerobic bacteria were grown from specimens obtained from children with secondary infections. Aerobes were present in 47% of children: Staphylococcus aureus, group A streptococci, and Pseudomonas aeruginosa. Anaerobes were found to be present in 20% of children: Peptostreptococcus, Prevotella, and Porphyromonas species. Mixed anaerobic-aerobic flora were present in 33% of patients.¹⁰

Causes

• Scabies is caused by the mite S scabiei var hominis, an arthropod of the order Acarina.
• Patients who are immunocompromised (eg, HIV, systemic corticosteroid therapy) may develop a severe form called Norwegian scabies.⁵
• Animal forms of scabies exist and are generally referred to as mange. S scabiei causes mange in many companion and livestock animals and is responsible for epizootic diseases in wild populations of cats, ungulates, boars, wombats, ferrets, koalas, and great apes. It is considered to be a major cause of mortality among red foxes, coyotes, and wombat.
• Animal scabies causes a transient pruritic papular or vesicular erythremic lesion that occurs 24 hours after an exposure to an infested animal. This differs from the rapid sensitivity that occurs with primary infections in humans. This may be due to previous sensitization in the human host. The immediate itching may lead to a protective mechanism in the human host—scratching—which can prevent the mite from burrowing.
• Animal mites do not multiply on the human host.¹

Differential Diagnoses

Bites, Insects
Categories
Dermatitis, Atopic
Dermatitis, Contact
Psoriasis
Urticaria

Other Problems to Be Considered

Classic scabies

Insect bites
Atopic dermatitis
Contact dermatitis
Psoriasis
Fiberglass exposure
Lichen planus
Dermatitis herpetiformis
Bullous pemphigoid
Urticaria
Chronic lymphocytic leukemia
Necrotizing vasculitis
B-cell lymphoma with monoclonal infiltrate
Eczema

Crusted scabies

Eczema
Psoriasis
Ichthyosis
Adverse drug reactions
Seborrheic dermatitis
Erythroderma
Langerhans cell histiocytosis

Scabies: Classical or Norwegian

Workup

Laboratory Studies

• Diagnostic testing: Definitive testing relies on the identification of mites, eggs, eggshell fragments, or mite pellets (scybala).³ This is best undertaken by placing a drop of mineral oil directly over the burrow and then scraping longitudinally and laterally across the skin with a scalpel blade. (Avoid causing bleeding.) The sample is placed on a microscope slide and examined under both low and high power. Potassium hydroxide should not be used since it can dissolve mite pellets. Failure to find mites is common and does not rule out the diagnosis of scabies.

Scabies mite. Courtesy of William D. James, MD.

Scabies mite scraped from a burrow (original magnification, 400X). Courtesy of Audra Malerba, DO.

• Tips on localizing the burrow
  • Applying topical tetracycline to the skin and washing off the excess may reveal burrows. The burrows retain the tetracycline, which fluoresces under a Wood lamp, allowing easy identification.
  • Rubbing a washable felt-tip marker across the suspected site and removing the ink with an alcohol wipe may also localize a burrow more precisely. When a burrow is present, the ink penetrates the stratum corneum and delineates the site.
• Final diagnosis is based on history, physical examination (burrows), and microscopic examination of mites, eggs, and scybala on mineral oil preparation.

Other Tests

• Videodermatoscopy or epiluminescence microscopy: Hand-held device magnifies 20-60 times.¹⁴
• DNA amplification by polymerase chain reaction (PCR) followed by enzyme-linked immunosorbent assay (ELISA) are tools also used by some dermatologists in tertiary centers.⁴ These methods are not readily available in the emergency department or in many dermatology departments.
• Elevated immunoglobulin E (IgE) titers and eosinophilia may be demonstrated in some patients with scabies.⁴
• Skin biopsy
• Most commonly, scabies is diagnosed clinically based on the appearance and distribution of the rash and the presence of burrows.¹

Treatment

Emergency Department Care

• Prescribe an appropriate scabicide (eg, permethrin, lindane).
• Provide relief of symptoms.
  • Itching may persist for 1-2 weeks, even following successful treatment. Pruritus may be alleviated partially with an oral antihistamine, such as hydroxyzine hydrochloride (Atarax), diphenhydramine hydrochloride (Benadryl), or cyproheptadine hydrochloride (Periactin), or with a short course of topical or oral steroids. 
  • The rash is often misdiagnosed and treated with only steroids, and long-term use with steroids can causes crusting and diffuse erythema.¹²
• Treat secondary infections with the appropriate antibiotics.
• Treat household members and close personal contacts.
• Notify infection control personnel and a dermatologist when an epidemic in a nursing home or a hospital is suspected.
• Provide reassurance that scabies is not a reflection of poor personal hygiene. 

Consultations

Consultation with a dermatologist or an infectious disease specialist may be required for severe, refractory scabies or for disseminated scabies in patients who are immunocompromised. Caution must be exercised when treating pregnant patients and children.

Medication

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Scabicides

Treatment options include either topical or oral medication. Topical options include permethrin cream (drug of choice), lindane, benzyl benzoate, crotamiton lotion and cream, sulfur, Tea tree oil, or oil of the leaves of Lippia multiflora Moldenke, a shrub found growing in West Africa Savannah. Oral options include ivermectin (not approved by FDA for treatment of scabies). A second course of treatment is often recommended 7-10 days later because of some developing larvae that may survive the initial treatment.¹²

Special population recommendations are as follows:³

• Infants - Permethrin 5% cream (>2 months age) (Ivermectin and lindane contraindicated)
• Children - Permethrin 5% cream, benzyl benzoate 12.5%
• Pregnant and breastfeeding women - 6% sulfur (Ivermectin, permethrin, and lindane contraindicated)
• Crusted or Norwegian scabies - Oral ivermectin (may require multiple doses, or in combination with a topical scabicide); hyperkeratosis treated with a keratolytic agent (5-10% salicylic acid in petrolatum)

The Centers for Disease Control and Prevention recommends treatment with either permethrin lindane or ivermectin. Permethrin is the drug of choice in the United States and the United Kingdom, but it is not available in France. In some studies, it has been shown to be more effective than a single dose of oral ivermectin, although it has equivalent efficacy when 2 doses of ivermectin are used at time zero and 2 weeks later. In severe cases, a topical medication may be used with oral medication (ivermectin).

A 2002 Cochrane Review that focused on interventions for treating scabies recommended the following:

• Topical permethrin appeared to be the most effective treatment for scabies.
• Topical permethrin appeared more effective than oral ivermectin, topical lindane, and topical crotamiton.

Permethrin cream 5% (Elimite)

CDC recommends as first-line treatment.
Drug of choice particularly for infants >2 months old and small children.
Highly effective, minimally absorbed and minimally toxic.¹²
Even after successful treatment, post scabietic nodules and pruritus may persist for months. In vitro resistance and treatment failures have been documented. Most expensive of all topical scabicides.³

Dosing

Adult

Apply 30 g to entire body from chin to toes; shower off the medication 8-14 h after initial application; repeat in 7 d if necessary

Pediatric

Apply as in adults; can apply to head and neck in children <5 y; not recommended for children <2 mo

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Avoid contact with the mouth, eye, and nose; may transiently exacerbate redness, swelling, and itching

Lindane 1% (Kwell, gamma benzene hexachloride)

Stimulates nervous system of parasite, causing seizures and death. Considered second-line treatment if other agents fail or are not tolerated. Not very safe in children due to transcutaneous absorption leading to neurotoxicity. The systemic absorption rate of lindane is 10 times greater than permethrin, and its serum levels are more than 40 times higher.¹¹ Overall, permethrin is a safer choice.

Dosing

Adult

Apply a thin layer on cool dry skin from chin to toes (estimated dermal absorption factor 10-20%), and shower off 6-10 h later; do not leave on skin for more than 12 h; repeat in 1 wk

Pediatric

Not recommended

Interactions

Oil-based hairdressings may increase toxicity

Contraindications

Documented hypersensitivity; neonates; acutely swollen skin or damaged skin; Norwegian scabies

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution if history of seizures; do not apply to eyes, face, or mucous membranes; caution if history of keratinization/ichthyosis disorders, or any condition that has altered skin integrity due to the increased systemic absorption

Sulfur in petrolatum (2 -10%, with 6% preferred, cream or ointment)

Not FDA approved for treatment of scabies. The oldest antiscabietic. One of a few scabicidal treatments that may be used safely in very small children (<2 mo) and in pregnant women.^11,15 Sulfur is messy, malodorous, stains clothes, and requires repeat applications, thus reducing compliance.¹⁵ . Sulfur should only be used when a patient cannot tolerate permethrin, lindane, or ivermectin.¹⁵ It is inexpensive and can be used for mass therapy in resource-poor economies.¹⁵

Dosing

Adult

Apply to entire body below the head on 3 successive nights and bathe 24 h after each application

Pediatric

Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Crotamiton 10% cream or lotion (Eurax)

For the treatment of scabies. Mechanism of action is unknown. Weak antipruritic agent. Success rates vary 50-70%.³

Dosing

Adult

Apply thin layer on to skin of entire body from neck to toes; repeat in 24 h; take a cleansing bath 48 h after last application; may need to apply twice daily for 5 consecutive days after bathing and changing clothes³

Pediatric

Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; can cause seizures

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not apply to face, urethral meatus, eyes, mucous membranes, or swollen skin; can cause seizures

Benzyl benzoate

Ester of benzoic acid and benzyl alcohol. Neurotoxic to mites. Not available in the United States⁴ and not FDA approved as a scabicide, but used in Europe. Cheaper alternative to other treatments.³

Dosing

Adult

Use 25% emulsion; apply below neck 3 times within 24 h without an intervening bath

Pediatric

May reduce adult dose to 12.5% or less due to stinging

Interactions

None reported

Contraindications

Documented hypersensitivity; pregnancy, breastfeeding women; infants and children <2 y

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

May cause stinging

Ivermectin (Mectizan, Stromectol)

Binds selectively with glutamate-gated chloride ion channels in invertebrate nerve and muscle cells, resulting in paralysis and cell death. Half-life is 16 h; metabolized in liver. Single oral dose has similar efficacy to permethrin and may be most successful in patients with immunodeficiency or crusted scabies,¹³ and in patients with skin conditions that should not use topical medications. Not FDA approved for the treatment of scabies.

Dosing

Adult

150-200 mcg/kg/d (0.2 mg/kg) PO once; may repeat in 10-14 d; commercially available as 3 mg tab

Pediatric

<5 years: Not recommended
>5 years: Administer as in adults

Interactions

May interact with other ligand-gated chloride channels, such as those gated by GABA

Contraindications

Documented hypersensitivity; CNS disorder³

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Treat mothers who intend to breastfeed only when risk of delayed treatment outweighs possible risks to the newborn caused by ivermectin excretion in milk
Repeat courses of therapy may be required in immunocompromised patients
May cause nausea, vomiting, and mild CNS depression; may cause drowsiness

Follow-up

Deterrence/Prevention

• All household members and close personal contacts (eg, sexual partners) should be treated,¹⁶ whether or not they are symptomatic.
• Clean clothing should be applied after disinfection.¹
• Bedding, towels, and clothing (used within 3 days prior to treatment¹ should be washed in water 60°C or higher and then machine dried.
• If items cannot be washed, they should be isolated (eg, in a plastic bag) for at least 72 hours.¹
• Patients should be in contact isolation at a hospital or other institution for 24 hours after the start of therapy.¹⁷
• Healthcare providers should use standard and contact precautions in all patients with pruritic eruptions.²
• Patients should be reexamined 2 weeks after treatment to evaluate effectiveness of therapy.
• Use of insecticide sprays and fumigants is not recommended but rooms used by patients should be thoroughly cleaned and vacuumed.

Complications

• Persistent symptoms may last up to 2-4 weeks after treatment. Anxiety or a hypersensitivity state may prolong symptoms even after the mites have been destroyed.¹⁶ Residual pruritus may require antihistamines or a short course of topical or oral steroids. If symptoms last greater than 2-4 weeks, treat with another dose of scabicides.¹
• Reasons for persistent symptoms
  • Treatment failure
  • Allergic dermatitis due to the topical medicine used
  • Ordinary household mites can cause a cross reactivity and can drive persistent symptoms.
  • Acarophobia - Delusional parasitosis; requires psychiatric intervention
  • Secondary infection requiring antibiotics
• Treatment failures are uncommon but do occur. The most common causes of treatment failure include the following:³
  • Improper application
  • Inadequate application
  • Reinfestation: Recurrence of the eruption usually means reinfection has occurred.
  • Resistance: Resistance to lindane has been widely reported. Less frequently, cases of resistance to permethrin have been noted. Resistance to ivermectin is still rare but has been reported in patients who have received multiple doses of the drug over several years.³
  • Norwegian scabies may require several treatments with scabicides and sometimes several different medications¹⁶
• Scabetic nodules may require intranodular steroid injection.
• Secondary infections
  • Since the epidermis is damaged by scratching; the excoriations allow for the entry of pathogenic bacteria.¹⁸
  • Staphylococci and streptococci are the most common microorganisms present and often cause pyoderma.
  • Group A Streptococcus is the most common streptococcal serogroup, and there is an increased risk for the development of poststreptococcal glomerulonephritis (PSGN).¹⁸

Patient Education

• For excellent patient education resources, visit eMedicine's Infections Center. Also, see eMedicine's patient education article Scabies.
• Additional information can be gleaned through the Centers for Disease Control and Prevention, Scabies.

Miscellaneous

Medicolegal Pitfalls

• Failure to consider scabies because of minimal skin findings is a pitfall. Always consider scabies infestation in patients with intense pruritus, especially when a sexual partner or other family members are similarly affected.

Special Concerns

• Norwegian scabies demonstrates a predilection for immunocompromised, elderly, debilitated, and institutionalized patients.
• In infants, eczematous eruptions may appear on the face. In contrast, the head and neck are almost never involved in older children, adolescents, or adults.

Multimedia

Media file 1: Scabies mite. Courtesy of William D. James, MD.

Media file 2: Scabies mite scraped from a burrow (original magnification, 400X). Courtesy of Audra Malerba, DO.

Media file 3: Scabies. Courtesy of William D. James, MD.

Media file 4: In crusted scabies, sections show multiple mites (arrows) within the hyperkeratotic stratum corneum (H&E, original magnification 100X). The epidermis is spongiotic. Courtesy of Audra Malerba, DO.

Media file 5: In routine scabies, a single mite is seen. Eosinophilic spongiosis may be present (H&E, original magnification 400X). Courtesy of Audra Malerba, DO.

Media file 6: Norwegian scabies. Courtesy of William D. James, MD.

Media file 7: Scabies on the leg. Courtesy of William D. James, MD.

Media file 8: Erythematous vesicles and papules are present on torso extremities, some with adjacent linear excoriations. Courtesy of Audra Malerba, DO.

Media file 9: Scabies on the buttocks. Courtesy of William D. James, MD.

Media file 10: Scabies on the hand. Courtesy of William D. James, MD.

Media file 11: Scabies on the penis. Courtesy of William D. James, MD.

Media file 12: Scabies on the penis. Courtesy of Hon Pak, MD.

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Keywords

scabies, scabies treatment, scabies symptoms, Sarcoptes scabiei var hominis, Norwegian scabies, canine scabies, mange, intense pruritus, nocturnal pruritus, itch mite, 7-year itch, 7 year itch, seven year itch, seven-year itch, mite infestation, skin infestation, scabies causes

Contributor Information and Disclosures

Author

Amy L McCroskey, MD, Resident Physician, Department of Emergency Medicine, Wayne State University Detroit Medical Center, Detroit Receiving Hospital
Amy L McCroskey, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Student Association/Foundation, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Adam J Rosh, MD, MS, Assistant Professor, Department of Emergency Medicine, Wayne State University/Detroit Receiving Hospital
Adam J Rosh, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
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Medical Editor

Joseph A Salomone III, MD, EMS Medical Director, Kansas City, Missouri; Associate Professor and Staff Physician, Truman Medical Centers/UMKC School of Medicine
Joseph A Salomone III, MD is a member of the following medical societies: American Academy of Emergency Medicine, National Association of EMS Physicians, and Society for Academic Emergency Medicine
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Jeter (Jay) Pritchard Taylor III, MD, Compliance Officer, Attending Physician, Emergency Medicine Residency, Department of Emergency Medicine, Palmetto Health Richland, University of South Carolina; Medical Director, Department of Emergency Medicine, Palmetto Health Baptist
Jeter (Jay) Pritchard Taylor III, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine
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CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
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Chief Editor

Robert E O'Connor, MD, MPH, Professor and Chair, Department of Emergency Medicine, University of Virginia Health System
Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society
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The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, William D Binder, MD, and Joseph Sciammarella, MD, to the development and writing of this article.

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