eMedicine Specialties > Emergency Medicine > Infectious Diseases

Scabies

Author: Amy L McCroskey, MD, Resident Physician, Department of Emergency Medicine, Wayne State University Detroit Medical Center, Detroit Receiving Hospital
Coauthor(s): Adam J Rosh, MD, MS, Assistant Professor, Department of Emergency Medicine, Wayne State University/Detroit Receiving Hospital
Contributor Information and Disclosures

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.

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).

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

• 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.

• 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

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