AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Human scabies is an intensely pruritic skin infestation caused by the host-specific mite, Sarcoptes scabiei var hominis. Scabies has been a source of human infestation for more than 2500 years, dating back to Roman times. Originally, the Romans used the term scabies to denote any pruritic skin disease. In the 17th century, Giovanni Cosimo Bonomo identified the mite as one cause of scabies. The name Sarcoptes scabiei is derived from the Greek words sarx (the flesh) and koptein (to smite or cut) and the Latin word scabere (to scratch).¹

Today, the term scabies refers to the skin lesions produced by this mite. A readily treatable infestation, scabies remains common primarily because of diagnostic difficulty, inadequate treatment of patients and their contacts, and improper environmental control measures. Scabies is a great clinical imitator. Its spectrum of cutaneous manifestations and associated symptoms often results in delayed diagnosis. In fact, the phrase "7-year itch" was first used with reference to persistent, undiagnosed infestations with scabies.

Scabies is a worldwide public health problem, affecting persons of all ages, races, and socioeconomic groups. Overcrowding, delayed diagnosis and treatment, and poor public education contribute to the prevalence of scabies in both industrial and nonindustrial nations. Prevalence rates are higher in children and sexually active individuals than in other persons. Patients with poor sensory perception due to entities such as leprosy and persons with immunocompromise due to conditions such as status posttransplantation, HIV disease, and old age are at particular risk for the crusted variant. These populations present with clinically atypical lesions and often are misdiagnosed, thus delaying treatment and elevating the risk of local epidemics.

Pathophysiology

Human scabies is caused by the S scabiei mite, var hominis, an obligate human parasite (see Media File 1). Animal scabies mites may result in transient symptoms in humans, but they are not a cause of persistent infestations. The most efficient means of transmission is via direct and prolonged contact with an infected individual. Mites can survive up to 3 days away from human skin, so fomites such as infested bedding or clothing are an alternate but infrequent source of transmission.

The entire life cycle of the mite lasts 30 days and is spent within the human epidermis. After copulation, the male mite dies and the female mite burrows into the superficial skin layers and lays a total of 60-90 eggs. The ova require 10 days to progress through larval and nymph stages to become mature adult mites. Less than 10% of the eggs laid result in mature mites.

Mites move through the top layers of skin by secreting proteases that degrade the stratum corneum. They feed on dissolved tissue but do not ingest blood. Scybala (feces) are left behind as they travel through the epidermis, creating linear lesions clinically recognized as burrows.

An affected individual harbors a variable number of living mites, typically less than 100 and usually no more than 10-15. In immunocompromised hosts, the weak immune response fails to control the disease and results in a fulminant hyperinfestation termed crusted scabies. The number of mites in a patient with crusted scabies can exceed 1 million. In these cases, the mite can survive off the host for up to 7 days, feeding on the sloughed skin in the local environment such as bedsheets, clothing, and chair covers. Failure to implement environmental control measures in this situation may result in relapse and reinfestation after successful treatment of the host.

Certain patient populations are susceptible to crusted scabies. These include patients with primary immunodeficiency disorders or a compromised ability to mount an immune response secondary to drug therapy. A modified host response may be a key factor in patients with malnutrition. Motor nerve impairments result in the inability to scratch in response to the pruritus, thus disabling the utility of scratching to remove mites and destroy burrows. Rare cases immunocompetent patients developing the crusted variant without clear explanation have been described.

The incubation period prior to onset of symptoms depends on whether the infestation is an initial exposure or a relapse/reinfestation. Upon initial infestation, a delayed type IV hypersensitivity reaction to the mites, eggs, or scybala develops over the ensuing 4-6 weeks. Previously sensitized individuals can develop symptoms within hours of reexposure. The hypersensitivity reaction is responsible for the intense pruritus that is the clinical hallmark of the disease.

Frequency

International

Approximately 300 million cases of scabies are reported worldwide each year. In developed countries, scabies epidemics occur primarily in institutional settings such as prisons and long-term care facilities such as nursing homes and hospitals. Prevalence rates in developing countries are higher than those in developed nations. Natural disasters, war, and poverty lead to overcrowding and increased rates of transmission.

Mortality/Morbidity

Complications of scabies are rare and generally result from vigorous rubbing and scratching. Disruption of the skin barrier puts the patient at risk for secondary bacterial invasion, primarily by Streptococcus pyogenes and Staphylococcus aureus. Superinfection with S pyogenes can precipitate acute poststreptococcal glomerulonephritis and even rheumatic fever. More common pyodermas include impetigo and cellulitis, which may rarely result in sepsis. Scabies infestations can exacerbate underlying eczema, psoriasis, Grover disease, and other preexisting dermatoses. Even with appropriate treatment, scabies can leave in its wake residual eczematous dermatitis and/or postscabietic pruritus, which can be debilitating and recalcitrant.

Crusted scabies carries an increased mortality rate because of the frequency of secondary bacterial infections resulting in sepsis.

Race

No racial predilection has been proven.

Sex

No predilection is recognized.

Age

Classic scabies is more common in children and in people who are sexually active. Crusted scabies occurs predominantly in patients who are immunocompromised, elderly, institutionalized, or bedridden.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

The historical aspects of scabies infestations are quite reliable in suggesting the diagnosis. Lesion distribution, intractable pruritus that is worse at night, and similar symptoms in close contacts should immediately rank scabies at the top of the clinical differential diagnosis.

Lesion distribution differs in adults and children. Adults manifest lesions primarily on the flexor aspects of the wrists, the interdigital web spaces of the hands, the dorsal feet, axillae, elbows, waist, buttocks, and genitalia. Pruritic papules and vesicles on the scrotum and penis in men and areolae in women are highly characteristic.

Infants and small children develop lesions predominantly on the face, scalp, neck, palms, and soles, although any site may be involved. All cutaneous sites are susceptible in immunocompromised and elderly patients, who often have a history of a widespread, pruritic eczematous eruption.

Consider the diagnosis of scabies in any patient presenting with a recent onset of intense itching that is accentuated at night.

Physical

Clinical findings include both primary and secondary lesions. Primary lesions are the first manifestation of the infestation, and these typically include small papules, vesicles, and burrows. Secondary lesions are the result of rubbing and scratching, and they may be the only clinical manifestation of the disease. If so, the diagnosis must be inferred by the history, lesion distribution, and accompanying symptoms.

• Primary lesions
• • The distribution is highly characteristic in typical cases.
  • Burrows are a pathognomonic sign and represent the intraepidermal tunnel created by the moving female mite. They appear as serpiginous, grayish, threadlike elevations ranging from 2-10 millimeters long (see Media File 2). They are not readily apparent and must be actively sought. A black dot may be seen at one end of the burrow, indicating the presence of a mite. High-yield locations for burrows include the webbed spaces of the fingers, flexor surfaces of the wrists, elbows, axillae, belt line, feet, scrotum in men, and areolae in women. In infants, burrows are commonly located on the palms and soles (see Media File 3). The actual mites are microscopic and cannot be visualized with the unaided human eye.
  • One- to 3-mm erythematous papules and vesicles are seen in typical distributions in adults. The vesicles are discrete lesions filled with clear fluid, although the fluid may appear cloudy if the vesicle is more than a few days old (see Media File 4). Papules rarely contain mites and most likely represent a hypersensitivity reaction. Papules are common on the shaft of the penis in men and on the areolae in women (see Media Files 5-6). Unlike adults, who rarely present with facial and neck involvement, this presentation is fairly typical in children.
  • In very young children and infants, a widespread eczematous eruption primarily on the trunk is common (see Media File 7). In neonates unable to scratch, pinkish-brown nodules may develop and range in size from 2-20 mm. Mites are rarely found within the nodules (see Media Files 8-9).
  • Crusted scabies, previously referred to as Norwegian scabies, manifests with marked thickening and crusting of the skin. Lesions are often hyperkeratotic, crusted, and cover large areas. Marked scaling is common, and pruritus may be minimal or absent. Nail dystrophy and scalp lesions may be prominent. The hands and arms are usual locations, but all sites are vulnerable (see Media File 10). Mites can number in the thousands to millions in this form. Predominantly affected are those with immunosuppression, neurological disorders, or institutionalization. Possible risk factors for profound infestation in these specific populations include an inability to mount an immune response, perceive pruritus, and/or physically scratch the skin (a mechanism to rid the body of mites).
  • Nodular scabies occurs in 7-10% of patients with scabies, particularly young children as noted above. Pink, tan, brown, or red nodules may be present, ranging from 2-20 millimeters in diameter.
• Secondary lesions
• • These are the result of scratching, secondary infection, and/or the host immune response against the mites and their products.
  • Characteristic findings include excoriations, widespread eczema, honey-colored crusting, postinflammatory hyperpigmentation, erythroderma, prurigo nodules, and frank pyoderma.

Causes

• Human scabies is caused by the host-specific mite, S scabiei var hominis, an obligate human parasite. It is a member of the class Arachnida, subclass Acari, order Astigmata, and family Sarcoptidae.
• Human infestation with S scabiei varieties of animal origin can occur. Both domestic and wild animals worldwide are susceptible to infestation with S scabiei, and the resultant disease is referred to as sarcoptic mange. Mange due to S scabiei varieties other than hominis has been reported in dogs, pigs, horses, camels, black bears, monkeys, dingoes, and wild fox, among others. Although reports have described transfer to humans from animals, experimental studies have demonstrated limited cross-infectivity between different host species. Further, genotyping studies have revealed that the Sarcoptes mites segregate into separate host-associated populations, thus limiting the transmission across host species.
• In the rare instance of transmission of nonhuman scabies from animals to humans, the clinical manifestations differ in many respects. The incubation period is shorter, the symptoms are transient, the infestation is self-limiting, no burrows are formed, and the distribution is atypical compared with infestation caused by S scabiei var hominis. Contacts of patients with scabies contracted from an animal source require no treatment.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Pruritus with or without rash
Adverse cutaneous drug reaction
Fiberglass dermatitis
Dermatographism
Dermatitis herpetiformis
Animal scabies
Delusions of parasitosis
Metabolic pruritus
Paraneoplastic Pruritus

Nodular scabies
Urticaria pigmentosa (in young child)
Lymphoma

Crusted scabies
Psoriasis
Seborrheic dermatitis
Langerhans cell histiocytosis

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• The diagnosis is confirmed by light microscopic identification of mites, larvae, ova, or scybala (fecal pellets) in skin scrapings (see Media File 12).
• In rare cases, mites are identified in biopsy specimens obtained to rule out other dermatoses. Characteristic histopathology in the absence of actual mites also may suggest the diagnosis.

Other Tests

• Elevated immunoglobulin E titers and eosinophilia may be demonstrated in some patients with scabies.
• Clinically inapparent infection can be detected by amplification of Sarcoptes DNA in epidermal scale by polymerase chain reaction.²
• Immunosuppression, either medication or disease related, may be associated with crusted scabies.

Procedures

• Skin scraping: Place a drop of mineral oil on a glass slide, touch a No. 15 blade or a 7-mm curette to the oil, and scrape infested skin sites, preferably primary lesions such as vesicles, juicy papules, and burrows (see ³).
• • The skin scrapings are placed on a glass slide, covered with a coverslip, and examined under a light microscope at 40X magnification.
  • Multiple scrapings may be required to identify mites or their products. Persistence is key to accurate diagnosis.
• Burrow ink test: The tip of a fountain pen is rubbed along the site of a possible burrow. The ink penetrates the burrow, distinguishing it from the surrounding tissue. The excess ink is wiped off with an alcohol pad. This technique is particularly useful in children and individuals with very few burrows.
• Alternative to burrow ink test: Topical tetracycline solution is an alternative to the burrow ink test. After application and removal of the excess tetracycline solution with alcohol, the burrow is examined under a Wood's light. The remaining tetracycline within the burrows fluoresces a greenish color. This method is preferred because tetracycline is a colorless solution and large areas of skin can be examined.
• Crusted scabies: Add 10% potassium hydroxide (KOH) to the skin scraping. This dissolves excess keratin and permits adequate microscopic examination.

Histologic Findings

The histologic features of scabies are distinctive enough to suggest the diagnosis, although they are common to a variety of arthropod reactions. If a burrow is excised, mites, larvae, ova, and feces may be identified within the stratum corneum. A superficial and deep dermal infiltrate composed of lymphocytes, histiocytes, mast cells, and eosinophils is characteristic. Spongiosis and vesicle formation with exocytosis of eosinophils and occasional neutrophils is present. Biopsy of older lesions is nondiagnostic, demonstrating only excoriation and scale crusts.

Crusted scabies demonstrates massive hyperkeratosis of the stratum corneum with innumerable mites in all stages of development. Psoriasiform hyperplasia of the underlying epidermis with spongiotic foci and occasional epidermal microabscesses is present. The dermis shows a superficial and deep chronic inflammatory infiltrate with admixed interstitial eosinophils.

Nodular scabies reveals a dense, mixed, superficial, and deep dermal inflammatory cell infiltrate. Lymphoid follicles may be present, and the infiltrate occasionally extends into the subcutaneous fat. Mite parts may be seen on serial sectioning in up to 20% of cases.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

• Treatment includes administration of a scabicidal agent, an antipruritic agent such as a sedating antihistamine, and an appropriate antimicrobial agent if secondarily infected.
• Provision of detailed verbal and written instructions is critical for compliance and complete eradication.
• All family members and close contacts must be evaluated and treated, even if they do not have symptoms. Pets do not require treatment. All carpets and upholstered furniture should be vacuumed and vacuum bags immediately discarded.
• Instruct patients to launder clothing, bed linens, and towels used within the last week in hot water the day after treatment is initiated and again in 1 week. Items that cannot be washed may be professionally dry cleaned or sealed in plastic bags for 1 week.
• Patients with crusted scabies or their caregivers should be instructed to remove excess scale to allow penetration of the topical scabicidal agent and decrease the burden of infestation. This can be achieved with warm water soaks followed by application of a keratolytic agent such as 5% salicylic acid in petrolatum or Lac-Hydrin cream. (Salicylic acid should be avoided if large body surface areas are involved because of the potential risk of salicylate poisoning.) The scales are then mechanically debrided with a tongue depressor or similar nonsharp device.

Consultations

Assessment of immune function may be indicated in individuals presenting with crusted scabies.

Activity

Affected individuals should avoid skin-to-skin contact with others. Decontamination of clothing, bed linens, and other personal items must coincide with medical treatment. Patients with typical scabies may return to school/work 24 hours after the first treatment.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

The mainstay of treatment is the application of topical antiscabietic agents, with repeat application in 7 days. An oral agent, ivermectin, is also available and effective.^{4, 5}

Ivermectin is a synthetic macrocyclic lactone belonging to the avermectin group of antibiotics. It has no antibiotic activity but is active against a number of endoparasites and ectoparasites of humans and animals.⁶ Ivermectin is effective in most cases of typical scabies at a dose of 200-250 mcg/kg given at diagnosis and repeated in 7-14 days. Crusted scabies may require 3 or more doses given at 1- to 2-week intervals. Ivermectin is an ideal agent in cases for which topical therapy is difficult or impractical, such as in widespread institutional infestations and bedridden patients.⁵

Ivermectin is contraindicated in patients with allergic sensitization or nervous system disorders and in women who are pregnant or breastfeeding. Children younger than 5 years or less than 15 kg should not be treated with ivermectin.

Symptomatic treatment may require oral antihistamines and topical antipruritics/anesthetics such as menthol (Sarna) and pramoxine (Prax). More severe symptoms may require a short course of topical or oral steroids. Secondary infections may require antibiotics and should be prescribed based on culture and sensitivity data.

Drug Category: Scabicides/antiparasitics

Drug Name	Lindane (Kwell)
Description	In 1% lotion or cream. Stimulates nervous system of parasite, causing seizures and death. Previously standard treatment for scabies, but now considered second line, to be used if other agents fail or are not tolerated. Not very safe in children or neonates because of transcutaneous absorption leading to neurotoxicity. Overall, permethrin is a safer choice.
Adult Dose	Apply thin layer from chin to toes; use on dry skin and shower off 10 h later; repeat in 1 wk
Pediatric Dose	Not for use in neonates or infants Children: Apply thin film topically over entire body, including hairline, neck, scalp, temple, and forehead; leave on 6-8 h before washing off with water; may repeat in 1 wk if necessary; not to exceed 30 g per application
Contraindications	Documented hypersensitivity to lindane products; premature infants; seizure disorders; crusted scabies; other skin conditions (eg, atopic dermatitis, psoriasis) that may increase systemic absorption
Interactions	Oil-based hairdressings may increase toxicity of lindane
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	May cause CNS toxicity; caution if history of seizures; do not apply to eyes, face, or mucous membranes; caution if history of keratinization/ichthyosis disorders

Drug Name	Precipitated sulfur in petrolatum
Description	In 6% concentration.
Adult Dose	Applied to entire body below head on 3 successive nights; bathe 24 h after each application
Pediatric Dose	Administer as in adults, including head and neck
Contraindications	Documented hypersensitivity
Interactions	None reported
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	Available evidence is inconclusive or is inadequate for determining fetal risk when used in pregnant women or women of childbearing potential; weigh potential benefits of drug treatment against potential risks before prescribing during pregnancy

Drug Name	Crotamiton (Eurax)
Description	A 10% cream or lotion for treatment of scabies. Mechanism of action unknown.
Adult Dose	Apply a thin layer onto skin of entire body from neck to toes; repeat application in 24 h; take cleansing bath 48 h after last application
Pediatric Dose	Not FDA approved in pediatric patients
Contraindications	Documented hypersensitivity
Interactions	None reported
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, mucous membranes, or swollen, raw, or oozing skin; less effective than lindane; toxicity unknown; discontinue if severe skin irritation develops

Drug Name	Ivermectin (Stromectol)
Description	Binds selectively with glutamate-gated chloride ion channels in invertebrate nerve and muscle cells, causing cell death. Half-life is 16 h; metabolized in liver. Available in 3- and 6-mg tab.
Adult Dose	200-250 mcg/kg PO at diagnosis; repeat in 7-14 d; crusted scabies may require 3 doses <120 lb: 12 mg 120-200 lb: 18 mg >200 lb: 24 mg
Pediatric Dose	<5 years or <15 kg: Not established >5 years: Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	May interact with other ligand-gated chloride channels such as those gated by GABA
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 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

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Deterrence/Prevention

All household members and close personal contacts older than 2 months and not pregnant should be treated, even if they have no symptoms or signs of infestation. Detailed directions regarding treatment and environmental control measures should be provided verbally and in writing.

Patients must be evaluated within 2-4 weeks after treatment to ensure compliance and adequate response to therapy. Patients may experience pruritus up to 2 weeks after successful treatment. If itching persists beyond this time, the patient must be reevaluated to ensure correct diagnosis, adequate treatment, and simultaneous treatment of contacts and environment. A second treatment course may be indicated.

Rarely, individuals with a history of atopy may require a tapered dose of prednisone for the treatment of severe pruritus. Intranodular injection of dilute corticosteroids may be necessary in cases of nodular scabies.
 
Because of the heavy mite burden, cases of crusted scabies may require repeated applications of topical scabicides or simultaneous treatment with a topical agent such as permethrin and oral ivermectin.

Complications

• Treatment failures are uncommon if guidelines are followed.
• Residual pruritus may require antihistamines or a short course of topical or oral corticosteroids.
• Secondary infection requires the use of antibiotics based on culture and sensitivity data.
• Scabietic nodules may require intranodular corticosteroid injection for complete resolution.
• Flaring or reactivation of preexisting eczema or atopic dermatitis requires the use of standard eczema treatments.

Prognosis

Prognosis is excellent with proper diagnosis and treatment in otherwise healthy individuals. Immunocompromised or institutionalized individuals are at an increased risk for crusted scabies, which is associated with a less favorable outcome.

Patient Education

For excellent patient education resources, visit eMedicine's Infections Center, eMedicine's patient education article Scabies, and the American Academy of Dermatology.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Failure to inform patients about the potential neurotoxicity of lindane and the lack of toxicity data available for crotamiton

Special Concerns

• Neonates and pregnant women should only be treated if the benefit exceeds the risk and if the diagnosis is confirmed by a positive skin scraping or biopsy result.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Scabies mite scraped from a burrow (original magnification, 400X).
	View Full Size Image
Media type:  Photo

Media file 2:  A typical linear burrow on the flexor forearm. Courtesy of Kenneth E. Greer, MD.
	View Full Size Image
Media type:  Photo

Media file 3:  A subtle linear burrow accompanied by erythematous papules on the sole of the foot in a child with scabies. Courtesy of Kenneth E. Greer, MD.
	View Full Size Image
Media type:  Photo

Media file 4:  Erythematous papules and papulovesicles on the flexor wrist. Courtesy of Kenneth E. Greer, MD.
	View Full Size Image
Media type:  Photo

Media file 5:  Scabies on the penile shaft and glans. Courtesy of William D. James, MD.
	View Full Size Image
Media type:  Photo

Media file 6:  Scabietic papules on the penile shaft and scrotum. Courtesy of Kenneth E. Greer, MD.
	View Full Size Image
Media type:  Photo

Media file 7:  Widespread eruption on the back of an infant with scabies. Courtesy of Kenneth E. Greer, MD.
	View Full Size Image
Media type:  Photo

Media file 8:  Nodular scabies in an infant. Courtesy of Kenneth E. Greer, MD.
	View Full Size Image
Media type:  Photo

Media file 9:  Nodular scabies. Courtesy of Kenneth E. Greer, MD.
	View Full Size Image
Media type:  Photo

Media file 10:  Crusted scabies. Courtesy of William D. James, MD.
	View Full Size Image
Media type:  Photo

Media file 11:  Crusted scabies. Courtesy of Kenneth E. Greer, MD.
	View Full Size Image
Media type:  Photo

Media file 12:  Scabies preparation demonstrating a mite and ova. Courtesy of William D. James, MD.
	View Full Size Image
Media type:  Photo

Media file 13:  Scabies. Erythematous vesicles and papules are present on torso extremities, some with adjacent linear excoriations.
	View Full Size Image
Media type:  Photo

Media file 14:  In routine scabies, a single mite is seen. Eosinophilic spongiosis may be present (hematoxylin and eosin; original magnification, 400X).
	View Full Size Image
Media type:  Photo

Media file 15:  Scabies mite in the stratum corneum. Courtesy of William D. James, MD.
	View Full Size Image
Media type:  Photo

Media file 16:  In crusted scabies, sections show multiple mites (arrows) within the hyperkeratotic stratum corneum. The epidermis is spongiotic (hematoxylin and eosin; original magnification, 100X).
	View Full Size Image
Media type:  Photo

Media file 17:  Scabies. Courtesy of William D. James, MD.
	View Full Size Image
Media type:  Photo

Media file 18:  Scabies in the interdigital web spaces. Courtesy of William D. James, MD.
	View Full Size Image
Media type:  Photo

Media file 19:  Papulovesicles and nodules on the palm in a patient with scabies. Courtesy of Kenneth E. Greer, MD.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

1. Haubrich WS. Medical Meanings: A Glossary of Word Origins. Philadelphia, Pa: American College of Physicians; 1997:200.
2. Bezold G, Lange M, Schiener R, Palmedo G, Sander CA, Kerscher M, et al. Hidden scabies: diagnosis by polymerase chain reaction. Br J Dermatol. Mar 2001;144(3):614-8. [Medline].
3. Johnston G, Sladden M. Scabies: diagnosis and treatment. BMJ. Sep 17 2005;331(7517):619-22. [Medline].
4. Aubin F, Humbert P. Ivermectin for crusted (Norwegian) scabies. N Engl J Med. Mar 2 1995;332(9):612. [Medline].
5. Huffam SE, Currie BJ. Ivermectin for Sarcoptes scabiei hyperinfestation. Int J Infect Dis. Jan-Mar 1998;2(3):152-4. [Medline].
6. Elgart GW, Meinking TL. Ivermectin. Dermatol Clin. Apr 2003;21(2):277-82. [Medline].
7. Brodell RT, Helms SE. Bedside testing: the diagnostic cornerstone of dermatology. Compr Ther. Mar 1997;23(3):211-7. [Medline].
8. Burgess I. Sarcoptes scabiei and scabies. Adv Parasitol. 1994;33:235-92. [Medline].
9. Burkhart CG, Burkhart CN, Burkhart KM. An epidemiologic and therapeutic reassessment of scabies. Cutis. Apr 2000;65(4):233-40. [Medline].
10. Fitzpatrick TB, Austen KF, Wolff K, et al, eds. Dertmatology in General Medicine. 4^th ed. New York, NY: McGraw-Hill; 1993:1812-3.
11. Elgart ML. Scabies. Dermatol Clin. Apr 1990;8(2):253-63. [Medline].
12. Fitzpatrick TB, Johnson RA, Wolff K. Inset Bites and Infestations. In: Fitzpatrick TJ, Johnson RA, Wolff K, Polano MK, Suurmond R, eds. Color Atlas and Synopsis of Clinical Dermatology. 3^rd ed. New York, NY: McGraw-Hill; 1997:836-61.
13. Guldbakke KK, Khachemoune A. Crusted scabies: a clinical review. J Drugs Dermatol. Mar 2006;5(3):221-7. [Medline].
14. Karthikeyan K. Treatment of scabies: newer perspectives. Postgrad Med J. Jan 2005;81(951):7-11. [Medline].
15. McCarthy JS, Kemp DJ, Walton SF, Currie BJ. Scabies: more than just an irritation. Postgrad Med J. Jul 2004;80(945):382-7. [Medline].
16. Molinaro MJ, Schwartz RA, Janniger CK. Scabies. Cutis. Dec 1995;56(6):317-21. [Medline].
17. Orkin M, Maibach HI. Scabies treatment: current considerations. Curr Probl Dermatol. 1996;24:151-6. [Medline].
18. Paller AS. Scabies in infants and small children. Semin Dermatol. Mar 1993;12(1):3-8. [Medline].
19. Schleicher SM, Stewart P. Scabies: the mite that roars. Emerg Med. 1997;6:54-8.

Article Last Updated: Jan 9, 2008