Introduction
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.
The Medscape CME course, Preventing and Controlling Emerging and Reemerging Transmissible Diseases in the Homeless, may be of interest, as may Scabies: Molecular Perspectives and Therapeutic Implications in the Face of Emerging Drug Resistance, an article posted on Medscape.
For a pediatric perspective, see the eMedicine article Scabies.
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
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.
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Further Reading
Keywords
human scabies, seven-year itch, 7-year itch, itch mites, pruritic eruption, Sarcoptes scabiei, S scabiei, Sarcoptes scabiei var hominis, S scabiei var hominis, skin infestation, skin mite, pruritic skin disease, pruritus, crusted scabies, Norwegian scabies, mite infestation
