eMedicine Specialties > Emergency Medicine > Infectious Diseases

Scabies

Author: William D Binder, MD, Clinical Instructor in Emergency Medicine, Brown University Medical School; Consulting Staff, Instructor, Department of Emergency Medicine, Massachusetts General Hospital
Coauthor(s): Joseph Sciammarella, MD, FACP, FACEP, Major, Medical Corps, US Army Reserve; Attending Physician, Emergency Medicine, Weatherby Locums; President and Director of Education, Health Training/Consulting, Inc
Contributor Information and Disclosures

Updated: Jun 19, 2006

Introduction

Background

Scabies is a common parasitic infection of global proportion. Worldwide, an estimated 300 million cases occur annually. The arthropod Sarcoptes scabiei var hominis causes an intensely pruritic and highly contagious skin infestation, which affects males and females of all socioeconomic stratas and all ethnic groups.

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Scabies 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. 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

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 infest human skin as well. However, they are unable to reproduce in humans and only cause a transient dermatitis.

The S scabiei var hominis mite that infects humans is female and can just be seen with the naked eye (0.3-0.4 mm long). The male is about one half this size. The male fertilizes the female on human skin and then dies. Newly mated females burrow into human skin, using proteolytic enzymes to dissolve the stratum corneum of the epidermis. The mite has 4 pairs of legs and tracheal breaths and thus does not penetrate deeper than the outer layer of the epidermis.

The female deposits eggs in the burrows, and then the eggs incubate and hatch after 3-5 days (range up to 8 d). About 90% of the hatched mites die, but those that survive go through various molting stages and reach maturity after a little more than 2 weeks. The female adults, who never leave their burrows, die after 1-2 months.

In a classic scabies infection, anywhere from 5-15 mites (range, 3-50) live on the host. 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 reaction rapidly (within hours). The resultant skin eruption, and its associated intense pruritus, is the hallmark of classic 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 scabies. In this variant, hundreds to millions of mites infest the host individual, who is usually immunocompromised, elderly, or physically and/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).

Frequency and epidemiology

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. Indeed, while epidemics have been reported (1919-1925, 1936-1949, 1964-1979), it is clearly an endemic disease in many tropical and subtropical regions. Prevalence rates are extremely high in aboriginal tribes in Australia, in Africa, in South America, and in 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.

Worldwide, the prevalence of scabies has been estimated at 300 million cases annually, although this figure may be an overestimate. 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. In one epidemiologic study in the United Kingdom, scabies was shown to have a higher frequency of occurrence in winter months than in summer months, and it more commonly affected women and children. In this study, the disease was found to be more prevalent in urban regions.

While scabies appears to be more common in the younger population, it certainly occurs in all ages, all ethnic groups, all socioeconomic levels, and in both sexes. It is not directly related to hygiene, but it is associated with poverty and crowding.

Mode of transmission

Mites are unable to fly or jump. They crawl at a rate of 2.5 cm/min. 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 about 48 hours 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.

Transmission is predominantly through direct skin-to-skin contact, and for this reason, scabies has been considered a sexually transmitted disease. Indirect contact through fomites such as infested bedding or clothing is possible, although not usual. However, the greater the number of parasites on a person, as in crusted scabies, the more likely that indirect contact will abet transmission of the disease.

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 chemotherapy lead to a decrease of scabies by 96% and a parallel drop in an indicator of renal disease. In remote Aboriginal communities in Australia where scabies is endemic, the repeated infestations 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.

Other complications of scabies include impetigo, furunculosis, and cellulites. The staphylococci and/or streptococci in the lesions can lead to pyelonephritis, 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.
  • While unusual in the neonate, scabies has been reported in this age group.

Physical

  • Primary lesions
    • A short elevated serpiginous (S-shaped) track in the superficial epidermis, known as a burrow, is pathognomonic of scabies infestation.
    • Burrows or runs appear as a thin (approximately the width of a human hair), short (perhaps 2-3 mm in length), gray brown, wavy channel on the skin.
    • 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 or occur independently.
    • Nodular scabies may erupt on covered parts of the body (see below) 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 (psoriasiformlike lesions) 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
    • Ordinarily, burrows are best detected in the web spaces of the fingers, flexor aspects of the wrists, antecubital fossa, axilla, umbilicus, buttocks, and feet.
    • 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 almost pathognomonic of scabies.
    • Compared to 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.
    • Nodular scabies presents exclusively on covered parts of the bodies, such as the scrotum, penis, buttocks, groin, axillary folds, and upper back.
    • Geriatric scabies demonstrates a propensity for the back, often appearing as excoriations.

Causes

  • Scabies is caused by the mite S scabiei var hominis, an arthropod of the order Acarina.
  • 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.
  • Humans can be affected by animal scabies. Transient pruritic popular or vesicular erythremic lesions may occur after 24 hours of an exposure to an infested animal. The rapid sensitivity differs from primary infections in humans with the human variety of S scabiei. 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.

More on Scabies

Overview: Scabies
Differential Diagnoses & Workup: Scabies
Treatment & Medication: Scabies
Follow-up: Scabies
Multimedia: Scabies
References

References

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Further Reading

Keywords

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

Contributor Information and Disclosures

Author

William D Binder, MD, Clinical Instructor in Emergency Medicine, Brown University Medical School; Consulting Staff, Instructor, Department of Emergency Medicine, Massachusetts General Hospital
Disclosure: Nothing to disclose.

Coauthor(s)

Joseph Sciammarella, MD, FACP, FACEP, Major, Medical Corps, US Army Reserve; Attending Physician, Emergency Medicine, Weatherby Locums; President and Director of Education, Health Training/Consulting, Inc
Joseph Sciammarella, MD, FACP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Physicians, and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Joseph A Salomone, III, MD, Associate Professor, Department of Emergency Medicine, Truman Medical Center, University of Missouri at Kansas City School of Medicine
Joseph A Salomone, III, MD is a member of the following medical societies: American Academy of Emergency Medicine, Society for Academic Emergency Medicine, and Southern Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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
Disclosure: Nothing to disclose.

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
Disclosure: Nothing to disclose.

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
Disclosure: Nothing to disclose.

 
 
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