Scabies

Scabies
Author: Megan Barry, MD; Chief Editor: William D J ames, MD more...

Updated: Sep 16, 2013
Practice Essentials
Human scabies is an intensely pruritic skin infestation caused by the host-specific mite Sarcoptes scabiei hominis.
Approximately 300 million cases of scabies are reported worldwide each year.
Signs and symptoms
Burrows are a pathognomonic sign and represent the intraepidermal tunnel created by the moving female mite. They
appear as serpiginous, grayish, threadlike elevations in the superficial epidermis, ranging from 2-10 mm long.
High-yield locations for burrows include the following:
Webbed spaces of the fingers
Flexor surfaces of the wrists
Elbows
Axillae
Belt line
Feet
Scrotum (men)
Areolae (women)
In geriatric patients, scabies demonstrates a propensity for the back, often appearing as excoriations. In infants and
small children, burrows are commonly located on the palms and soles.
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.
Nodular scabies
Nodules occur in 7-10% of patients with scabies, particularly young children. In neonates unable to scratch, pinkish
brown nodules ranging in size from 2-20 mm in diameter may develop.
Crusted scabies
In crusted scabies, lesions are often hyperkeratotic and 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
the usual locations for lesions, but all sites are vulnerable.
Secondary lesions
These lesions result from scratching, secondary infection, and/or the hosts immune response against the scabies
mites and their products. Characteristic findings include the following
[1, 2, 3]
:
Excoriations
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Widespread eczematous dermatitis
Honey-colored crusting
Postinflammatory hyperpigmentation
Erythroderma
Prurigo nodules
Frank pyoderma
See Presentation for more detail.
Diagnosis
The diagnosis of scabies can often be made clinically in patients with a pruritic rash and characteristic linear
burrows. The diagnosis is confirmed by light microscopic identification of mites, larvae, ova, or scybala (feces) in skin
scrapings.
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 of scabies.
Clinically inapparent infection can be detected by amplification of Sarcoptes DNA in epidermal scale by polymerase
chain reaction (PCR) assay.
[4]
In addition, elevated immunoglobulin E (IgE) titers and eosinophilia may be
demonstrated in some patients with scabies.
See Workup for more detail.
Management
Scabies treatment includes administration of a scabicidal agent (eg, permethrin, lindane, or ivermectin), as well as an
appropriate antimicrobial agent if a secondary infection has developed.
Pruritus may be partially alleviated with an oral antihistamine, such as hydroxyzine hydrochloride (Atarax),
diphenhydramine hydrochloride (Benadryl), or cyproheptadine hydrochloride (Periactin). In rare cases, prednisone
may be used to treat severe pruritus.
Because of their heavy mite burden, patients with crusted scabies may require repeated applications of topical
scabicides or treatment that simultaneously uses oral ivermectin and a topical agent, such as permethrin.
See Treatment and Medication for more detail.
Image library
Scabies mite scraped from a burrow (original magnification, 400X).
Background
Human scabies is an intensely pruritic skin infestation caused by the host-specific mite Sarcoptes scabiei var
hominis. 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 term "7-year itch" was first used with reference to persistent, undiagnosed infestations with
scabies (see the image below). (See Presentation, Workup, Treatment, and Medication.)
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Scabies mite scraped from a burrow (original magnification, 400X).
Scabies is a global public health problem, affecting persons of all ages, races, and socioeconomic groups.
Worldwide, an estimated 300 million cases occur annually.
[5]
Overcrowding, delayed diagnosis and treatment, and
poor public education contribute to the prevalence of scabies in industrial and developing nations. (See Etiology and
Epidemiology.)
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, human immunodeficiency virus (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. (See Pathophysiology, Etiology, Epidemiology, and DDx.)
Patient education
For patient education information, see the Infections Center and Children's Health Center, as well as Scabies and
Skin Rashes in Children.
Additional information can be obtained from the Centers for Disease Control and Prevention, Parasites - Scabies site
and from the American Academy of Dermatology.
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. The mite does not penetrate deeper than the superficial layer of the
epidermis, the stratum corneum.
A person infested with mites can spread scabies even if he/she is asymptomatic.
[6]
There may be a prolonged
interval (up to 10 wk) between the primary infection, when the patient becomes contagious, and the onset of clinical
manifestations.
[7]
Scabies 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 hominis mite that infects humans is female and is large enough (0.3-0.4 mm long) to be seen with the
naked eye. (The male is about half this size.) The mite has 4 pairs of legs and crawls at a rate of 2.5 cm/min; it is
unable to fly or jump.
[8]
Although its life cycle occurs completely on the host, the mite is 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 20C, S scabiei are immobile, although they can survive such temperatures for extended
periods. (See the image below.)
Scabies preparation demonstrating a mite and ova. Courtesy of William D. J ames, MD.
Mite life cycle
3 of 14 5/22/2014 1:28 PM
The scabies mite is an obligate parasite that 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, although they can irritate
human skin as well. However, they are unable to reproduce in humans and cause only a transient dermatitis.
The female S scabiei var hominis mite lays 60-90 eggs in her 30-day lifespan, although less than 10% of the eggs
result in mature mites. The average patient is infected with 10-15 live adult female mites at any given time. Life cycle
stages are as follows (see the images below)
[6]
:
Eggs incubate and hatch in 3-4 days (90% of the hatched mites die) 1.
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 days)
2.
Larvae molt into nymphs (4 pairs of legs), which molt once into larger nymphs before becoming adults 3.
Mating takes place once, and the female is fertile for the rest of her life; the male dies soon after mating 4.
The female makes a serpentine burrow using proteolytic enzymes to dissolve the stratum corneum of the
epidermis, laying eggs in the process; she continues to lengthen her burrow and lay eggs for the rest of her
life, surviving 1-2 months
5.
Transmission of impregnated females from person-to-person occurs through direct or indirect skin contact
Scabies mite in the stratum corneum. Courtesy of William D. J ames, MD.
In routine scabies, a single mite is seen. Eosinophilic spongiosis may be present (hematoxylin and eosin; original
magnification, 400X).
In crusted scabies, sections show multiple mites (arrows) within the hyperkeratotic stratum corneum. The epidermis is
spongiotic (hematoxylin and eosin; original magnification, 100X).
Classic scabies
In classic scabies infection, typically 10-15 mites (range, 3-50) live on the host.
[8]
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 (feces) occurs. The time required to induce immunity in
primary infestations probably accounts for the 4-week asymptomatic latent period. With reinfestation, the sensitized
individual may develop a rapid reaction (within hours). The resultant skin eruption and its associated intense pruritus
are the hallmarks of classic scabies. (See the images below.)
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Scabies. Erythematous vesicles and papules are present on torso extremities, some with adjacent linear excoriations.
Scabies. Courtesy of William D. J ames, MD.
An immunologic study analyzing the cellular infiltrate types and patterns in scabies lesions concluded that T4-cell
dominance is the cause of persistent itching, while an increase in T8 cells reduces pruritus.
[9]
Crusted scabies
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 the disease. In this variant, hundreds to millions of mites infest the host
individual, who is usually immunocompromised, elderly, or physically or mentally disabled and impaired.
(Assessment of immune function may be indicated in individuals presenting with crusted scabies.)
[10, 11]
Crusted scabies can be easily confused with severe dermatitis or psoriasis because widespread, crusted lesions
appear with thick, hyperkeratotic scales over the elbows, knees, palms, and soles. The diagnosis of crusted scabies
should be considered when suspected dermatitis or suspected psoriasis does not respond to usual treatments. (See
the images below.)
[2]
Crusted scabies. Courtesy of William D. J ames, MD.
5 of 14 5/22/2014 1:28 PM
Crusted scabies. Courtesy of Kenneth E. Greer, MD.
Serum immunoglobulin E (IgE) and IgG levels are extremely high in patients with crusted scabies, yet the immune
reaction does not seem to be protective. Cell-mediated immunity in classic scabies demonstrates T4-cell
predominance in the dermal infiltrate, while one study suggests a T8-cell predominance in crusted scabies.
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 have been described in which immunocompetent patients have developed the crusted variant
without clear explanation.
Etiology
Human scabies is caused by the host-specific mite S scabiei hominis, an obligate human parasite. It is a member of
the family Sarcoptidae, which belongs to the order Astigmata, in the subclass Acari, class Arachnida.
Human infestation with S scabiei varieties of animal origin can occur. 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 foxes, among other animals.
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 hominis. Contacts
of patients with scabies contracted from an animal source require no treatment.
Risk factors
Prevalence rates for scabies 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, human immunodeficiency virus (HIV) disease, and old age are at particular risk
for the crusted variant.
A 2009 study conducted in an impoverished rural community in Brazil identified the following major risk factors for
scabies in that community
[12]
:
Young age
Presence of many children in the household
Illiteracy
Low family income
Poor housing
Sharing clothes and towels
Irregular use of showers
Epidemiology
International occurrence
Approximately 300 million cases of scabies are reported worldwide each year. Natural disasters, war, and poverty
lead to overcrowding and increased rates of transmission.
[13, 14]
In industrialized countries, scabies epidemics occur primarily in institutional settings, such as prisons, and in
long-term care facilities, including hospitals and nursing homes.
[15, 16, 17]
Scabies occurs more commonly in fall and
winter months in these countries. Prevalence rates for scabies in developing nations are higher than those in
6 of 14 5/22/2014 1:28 PM
industrialized countries.
A survey of children in a welfare home in Pulau Pinang, Malaysia found that the infestation rate for scabies was
highest among children aged 10-12 years.
[18]
The disease was more commonly evident in boys (50%) than in girls
(16%). The overall prevalence rate for scabies was 31%.
Of 200 dermatology outpatients in Sirte, Libya, with scabies, the following distribution was found
[19]
:
Females - 59%
Children - 37.5%
Military personnel - 18%
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, since these accounts have 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.
Scabies is clearly an endemic disease in many tropical and subtropical regions, being 1 of the 6 major epidermal
parasitic skin diseases (EPSD) that are prevalent in resource-poor populations, as reported in the Bulletin of the
World Health Organization in February 2009.
[20]
Prevalence rates are extremely high in aboriginal tribes in Australia,
Africa, South America,
[21]
and other developing regions of the world. Incidence in parts of Central and South America
approach 100%.
[20]
Age-related demographics
In a 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.
[22]
In parts of Bangladesh, the number of children with scabies exceeds the number with diarrheal and respiratory
diseases combined.
[20]
Prognosis
With proper diagnosis and treatment, the prognosis in otherwise healthy individuals with classic scabies is excellent.
If one medication is ineffective, the sequential use of agents can be curative. Immunocompromised or
institutionalized individuals are at an increased risk for crusted scabies, which is associated with a less favorable
outcome.
Persistent symptoms in scabies may last up to 2-4 weeks after treatment. Anxiety or a hypersensitivity state may
prolong symptoms even after the mites have been destroyed.
[23]
Residual pruritus may require antihistamines or a
short course of topical or oral steroids. If symptoms last longer than 2-4 weeks, treat the patient with another dose of
scabicides.
[6, 8, 7]
Symptoms may also persist as a result of the following:
Treatment failure
Allergic dermatitis due to the topical medicine used
Ordinary household mites that cause a cross reactivity, driving persistent symptoms
Acarophobia - Delusional parasitosis; requires psychiatric intervention
Secondary infection requiring antibiotics
Morbidity/mortality
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.
Common pyodermas include impetigo andcellulitis, which in rare cases cause sepsis.
[24]
The staphylococci or
7 of 14 5/22/2014 1:28 PM
streptococci in the lesions can also lead to pyelonephritis, abscesses, pyogenic pneumonia, sepsis, and death.
A retrospective, matched-cohort study by Chung et al comparing more than 5000 patients with scabies with more
than 25,000 randomly selected subjects found an association between scabies and increased risk of chronic kidney
disease. It was determined that the likelihood of being diagnosed with chronic kidney disease during the studys
5-year follow-up period was 1.4 times greater in males with scabies than in those without it, and that it was 1.27
times greater in females with scabies than in females without it.
[25]
Complications can also result if a scabies infestation exacerbates underlying eczema, psoriasis, transient
acantholytic dermatosis (Grover disease), or another preexisting dermatosis. Even with appropriate treatment,
scabies can leave in its wake residual eczematous dermatitis and/or postscabietic pruritus, which can be debilitating
and recalcitrant.
[26]
In remote Aboriginal communities in Australia, where scabies is endemic, extremely high levels of renal failure and
rheumatic heart disease appear to be related to repeated scabies infestations and secondary streptococcal
infections.
Crusted scabies carries a higher mortality rate than the classic form of the disease, because of the frequency of
secondary bacterial infections resulting in sepsis.
Contributor Information and Discl osures
Author
Megan Barry, MD Resident Physician, Department of Dermatology, University of Virginia School of Medicine
Disclosure: Nothing to disclose.
Coauthor(s)
Catharine Li sa 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
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
Eugene Rozen, MD Resident Physician, Department of Emergency Medicine, Detroit Receiving Hospital
Adam J Rosh, MD Assistant Professor, Program Director, Emergency Medicine Residency, Department of
Emergency Medicine, Detroit Receiving Hospital, Wayne State University School of Medicine
Adam J Rosh, MD is a member of the following medical societies: American Academy of Emergency Medicine,
American College of Emergency Physicians, and Society for Academic Emergency Medicine
8 of 14 5/22/2014 1:28 PM
Chief Editor
Will iam D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director,
Department of Dermatology, University of Pennsylvania School of Medicine
William D J ames, MD is a member of the following medical societies: American Academy of Dermatology and
Society for Investigative Dermatology
Additional Contributors
Will iam D Binder, MD Clinical Instructor in Emergency Medicine, Brown University Medical School; Consulting
Staff, Instructor, Department of Emergency Medicine, Massachusetts General Hospital
Jennifer R Casatelli, MD Consulting Staff, Department of Pediatrics, Watson Clinic of Lakeland, Lakeland
Regional Medical Center
Kevin P Connelly, DO Clinical Assistant Professor, Department of Pediatrics, Division of General Pediatrics and
Emergency Care, Virginia Commonwealth University School of Medicine; Medical Director, Paws for Health Pet
Visitation Program of the Richmond SPCA; Pediatric Emergency Physician, Emergency Consultants Inc,
Chippenham Medical Center
Kevin P Connelly, DO is a member of the following medical societies: American Academy of Pediatrics, American
College of Osteopathic Pediatricians, and American Osteopathic Association
Kelly M Cordoro, MD Assistant Professor of Clinical Dermatology and Pediatrics, 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, andWomen's
Dermatologic Society
Dirk M Elston, MD Director, Ackerman Academy of Dermatopathology, New York
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Kenneth E Greer, MD Former Professor, Department of Dermatology, University of Virginia School of Medicine;
Former Chairman, Department of Dermatology, University of Virginia Medical Center
Ulri ch Hengge, MD, MBA Professor, Department of Dermatology, Heinrich-Heine-University Dsseldorf,
Germany
Daniel J Hogan, MD Clinical Professor of Internal Medicine (Dermatology), Nova Southeastern University
College of Osteopathic Medicine; 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
9 of 14 5/22/2014 1:28 PM
Cami la K Janniger, MD Clinical Professor of Dermatology, Clinical Associate Professor of Pediatrics, Chief of
Pediatric Dermatology, University of Medicine and Dentistry of New J ersey-New J ersey Medical School
Camila K J anniger, MD is a member of the following medical societies: American Academy of Dermatology
Paul Krusinski, MD Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal
Medicine, University of Vermont College of Medicine
Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American
College of Physicians, and Society for Investigative Dermatology
Mudra Kumar, MD, MBBS, MRCP Associate Professor, Department of Pediatrics, University of South Florida
College of Medicine
Mudra Kumar, MD, MBBS, MRCP is a member of the following medical societies: American Academy of
Pediatrics and American Society of Hematology
Audra Malerba, MD Staff Physician, Department of Family Medicine, Long Beach Medical Center, New York
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
Giuseppe Micali, MD Head, Professor, Department of Dermatology, University of Catania School of Medicine,
Italy
Giuseppe Micali, MD is a member of the following medical societies: American Academy of Dermatology
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
Adam J Rosh, MD Assistant Professor, Department of Emergency Medicine, Detroit Receiving Hospital, Wayne
State University School of Medicine
Adam J Rosh, MD is a member of the following medical societies: American Academy of Emergency Medicine,
American College of Emergency Physicians, and Society for Academic Emergency Medicine
Joseph A Salomone III, MD Associate Professor and Attending Staff, Truman Medical Centers, University of
Missouri-Kansas City School of Medicine; EMS Medical Director, Kansas City, Missouri
J oseph A Salomone III, MD is a member of the following medical societies: American Academy of Emergency
10 of 14 5/22/2014 1:28 PM
Medicine, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Robert A Schwartz, MD, MPH Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine,
and Preventive Medicine and Community Health, University of Medicine and Dentistry of New J ersey-New J ersey
Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American
Academy of Dermatology, American College of Physicians, and Sigma Xi
Joseph Sciammarella, MD, FACP, FACEP, FAAMA Major, MC, USAR Attending Physician, Department of
Emergency Medicine, Mercy Medical Center, Rockville Centre, New York
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College
of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Jeter (Jay) Pritchard Taylor III, MD Compliance Officer, Attending Physician, Emergency Medicine Residency,
Department of Emergency Medicine, Palmetto Health Richland, University of South Carolina School of Medicine;
Medical Director, Department of Emergency Medicine, Palmetto Health Baptist
J eter (J ay) 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
Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health
Sciences Center, Paul L Foster 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
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of
Pharmacy; Editor-in-Chief, Medscape Drug Reference
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