Dermatologic Manifestations of Scabies 

  • Author: Kelly M Cordoro, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Dec 9, 2009
 

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.

For a pediatric perspective, see the eMedicine article Scabies.

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Pathophysiology

Human scabies is caused by the S scabiei mite, var hominis, an obligate human parasite and is shown in the image below.

Scabies mite scraped from a burrow (original magniScabies mite scraped from a burrow (original magnification, 400X).

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.

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Epidemiology

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.[2] 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 for scabies.

Sex

No predilection is recognized for scabies.

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.

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Contributor Information and Disclosures
Author

Kelly M Cordoro, MD  Assistant Professor of Pediatric and Adult Dermatology, Department of Dermatology, University of California, San Francisco School of Medicine

Kelly M Cordoro, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Association of Professors of Dermatology, Dermatology Foundation, Medical Society of Virginia, National Psoriasis Foundation, Society for Pediatric Dermatology, and Women's Dermatologic Society

Disclosure: Nothing to disclose.

Coauthor(s)

Barbara B Wilson, MD  Edward P Cawley Associate Professor, Department of Dermatology, University of Virginia School of Medicine

Barbara B Wilson, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Medical Society of Virginia, and Sigma Xi

Disclosure: Nothing to disclose.

Catharine Lisa Kauffman, MD, FACP  Georgetown Dermatology and Georgetown Dermpath

Catharine Lisa Kauffman, MD, FACP is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Royal Society of Medicine, Society for Investigative Dermatology, and Women's Dermatologic Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Daniel J Hogan, MD  Clinical Professor of Internal Medicine (Dermatology), NOVA Southeastern University; Investigator, Hill Top Research, Florida Research Center

Daniel J Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, and Canadian Dermatology Association

Disclosure: Nothing to disclose.

Richard P Vinson, MD  Assistant Clinical Professor, Department of Dermatology, Texas Tech University School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Paul Krusinski, MD  Director of Dermatology, Professor, Department of Internal Medicine, Fletcher Allen Health Care, University of Vermont

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Joel M Gelfand, MD, MSCE  Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania

Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology

Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

Chief Editor

Dirk M Elston, MD  Director, Department of Dermatology, Geisinger Medical Center

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

References
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Scabies mite scraped from a burrow (original magnification, 400X).
A typical linear burrow on the flexor forearm. Courtesy of Kenneth E. Greer, MD.
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.
Erythematous papules and papulovesicles on the flexor wrist. Courtesy of Kenneth E. Greer, MD.
Scabies on the penile shaft and glans. Courtesy of William D. James, MD.
Scabietic papules on the penile shaft and scrotum. Courtesy of Kenneth E. Greer, MD.
Widespread eruption on the back of an infant with scabies. Courtesy of Kenneth E. Greer, MD.
Nodular scabies in an infant. Courtesy of Kenneth E. Greer, MD.
Nodular scabies. Courtesy of Kenneth E. Greer, MD.
Crusted scabies. Courtesy of William D. James, MD.
Crusted scabies. Courtesy of Kenneth E. Greer, MD.
Scabies preparation demonstrating a mite and ova. Courtesy of William D. James, MD.
Scabies. Erythematous vesicles and papules are present on torso extremities, some with adjacent linear excoriations.
In routine scabies, a single mite is seen. Eosinophilic spongiosis may be present (hematoxylin and eosin; original magnification, 400X).
Scabies mite in the stratum corneum. Courtesy of William D. James, MD.
In crusted scabies, sections show multiple mites (arrows) within the hyperkeratotic stratum corneum. The epidermis is spongiotic (hematoxylin and eosin; original magnification, 100X).
Scabies. Courtesy of William D. James, MD.
Scabies in the interdigital web spaces. Courtesy of William D. James, MD.
Papulovesicles and nodules on the palm in a patient with scabies. Courtesy of Kenneth E. Greer, MD.
 
 
 
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