Scabies

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.)

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.

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.

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, 8] 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.[9] 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 20°C, 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. James, MD.

Mite life cycle

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] :

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 days)

3. Larvae molt into nymphs (4 pairs of legs), which molt once into larger nymphs before becoming adults

4. Mating takes place once, and the female is fertile for the rest of her life; the male dies soon after mating

5. 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

6. Transmission of impregnated females from person-to-person occurs through direct or indirect skin contact

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.[9] 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.)

Scabies. Erythematous vesicles and papules are present on torso extremities, some with adjacent linear excoriations.

Scabies. Courtesy of William D. James, 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.[10]

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.)[11, 12]  Some data suggest a higher incidence of autoimmune diseases in patients with scabies.[13]

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. James, MD.

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.

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[14] :

• Young age

• Presence of many children in the household

• Illiteracy

• Low family income

• Poor housing

• Sharing clothes and towels

• Irregular use of showers

An estimated 200 million people are affected by scabies at any given time, with prevalence rates ranging from 0.2% to 71%.[15] Natural disasters, war, and poverty lead to overcrowding and increased rates of transmission.[16, 17]

In industrialized countries, scabies epidemics occur primarily in institutional settings, such as prisons, and in long-term care facilities, including hospitals and nursing homes.[18, 19, 20] Scabies occurs more commonly in fall and winter months in these countries. Prevalence rates for scabies in developing nations are higher than those in 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.[21] 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[22] :

• 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.[23] Prevalence rates are extremely high in aboriginal tribes in Australia, Africa, South America,[24] and other developing regions of the world. Incidence in parts of Central and South America approach 100%.[23] One report suggests the highest reported rates of the crusted scabies in the world is in remote Aboriginal communities of northern Australia.[25]

Age-related demographics

The World Health Organization reports a prevalence rate of 5-10% in children in resource-poor tropical countries.[15]

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.[26]

In parts of Bangladesh, the number of children with scabies exceeds the number with diarrheal and respiratory diseases combined.[23]

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.[27] 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, 9, 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.[28, 29] Superinfection with S pyogenes can precipitate acute poststreptococcal glomerulonephritis, chronic renal failure, and even rheumatic fever.

Common pyodermas include impetigo and cellulitis, which in rare cases cause sepsis.[30] The staphylococci or 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 study’s 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.[31]

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.[32]

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. Patients with crusted scabies often contribute to widespread infestation in long-term care facilities, and delays in diagnosis contribute to the spread.[33]

Additional information can be obtained from the Centers for Disease Control and Prevention, Parasites - Scabies site and from the American Academy of Dermatology.

Patient history can reliably suggest the presence of scabies. Lesion distribution and intractable pruritus that is worse at night, as well as scabies symptoms in close contacts (including multiple family members), 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 following parts of the body (see the images below):

• Flexor aspects of the wrists

• Interdigital web spaces of the hands

• Dorsal feet

• Axillae

• Elbows

• Waist

• Buttocks

• Genitalia

  Erythematous papules and papulovesicles on the flexor wrist. Courtesy of Kenneth E. Greer, MD.

  Scabies in the interdigital web spaces. Courtesy of William D. James, MD.

  Scabies on buttocks. Courtesy of William D. James, MD.

Pruritic papules and vesicles on the scrotum and penis in men and areolae in women are highly characteristic.

Infants and young children may develop lesions diffusely, but unlike in adults, lesions are common on the face, scalp, neck, palms, and soles.[34]

All cutaneous sites are susceptible in immunocompromised and elderly patients, who often have a history of a widespread, pruritic, eczematous eruption. The same is true in patients with existing dermatologic, particularly atopic, diseases, in whom scabies may exacerbate or complicate these conditions.[34]

Patients who have had scabies misdiagnosed may have been treated with topical corticosteroids. This delays the correct diagnosis as the lesions may take on the incognito form in which lesions might appear as vesicles, pustules, or nodules and whose distribution could become diffuse.[35, 36]

Signs and symptoms of pruritus tend to crescendo progressively over 2-3 weeks before compelling the patient to seek medical attention. (However, debilitated or immunocompromised patients may not have the urge to scratch.[37] )

Scabies appears to occur in clusters. If there is an outbreak in the community, consider scabies in an individual presenting with rash and itching.

Clinical findings include primary and secondary lesions. Primary lesions are the first manifestation of the infestation and 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.[38]

Primary scabies lesions

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, as seen in the image below.

A typical linear burrow on the flexor forearm. Courtesy of Kenneth E. Greer, MD.

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 following:

• Webbed spaces of the fingers

• Flexor surfaces of the wrists

• Elbows

• Axillae

• Belt line

• Feet

• Scrotum (men)

• Areolae (women)

Classic scabies typically has a distribution involving the axillae, elbow flexures, wrists and hands, and genital area. This is commonly known as the circle of Hebra.

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, as in the image below. In immunocompromised patients, bullous lesions may be observed.

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.

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, as in the image below.

Papulovesicles and nodules on the palm in a patient with scabies. Courtesy of Kenneth E. Greer, MD.

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 the images below.)

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.

Scabies on penis. Courtesy of Hon Pak, MD.

Unlike adults, children commonly present with facial and neck involvement. In very young children and infants, a widespread, eczematous eruption primarily on the trunk is common, as in the image below. In addition, infants may have 1- to 3-mm papules, vesicles, and pustules on the palms and soles.

Widespread eruption on the back of an infant with scabies. Courtesy of Kenneth E. Greer, MD.

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, as demonstrated in the images below. Mites are rarely found within the nodules.

Nodular scabies in an infant. Courtesy of Kenneth E. Greer, MD.

Nodular scabies. Courtesy of Kenneth E. Greer, MD.

Crusted scabies

Crusted scabies, previously referred to as Norwegian scabies, manifests with marked thickening and crusting of the skin. Lesions are often hyperkeratotic and crusted and cover large areas. Marked scaling is common, and pruritus may be minimal or absent. Nail dystrophy (subungual hyperkeratosis) and scalp lesions may be present.

The hands and arms are the usual locations for lesions, but all sites are vulnerable. Mites can number in the thousands to millions in this form of scabies. (See the images below.)

Crusted scabies. Courtesy of William D. James, MD.

Crusted scabies. Courtesy of Kenneth E. Greer, MD.

Secondary scabies lesions

These lesions result from scratching, secondary infection, and/or the host’s immune response against the scabies mites and their products. Characteristic findings include the following[1, 2, 3] :

• Excoriations (see the image below)

• Widespread eczema

• Honey-colored crusting

• Postinflammatory hyperpigmentation

• Erythroderma

• Prurigo nodules

• Frank pyoderma

Scabies. Erythematous vesicles and papules are present on torso extremities, some with adjacent linear excoriations.

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 IgE titers and eosinophilia may be demonstrated in some patients with scabies.

A simple, cheap, sensitive, and specific test for routine diagnosis of active scabies is desirable.[42] The expression and purification of S scabiei recombinant antigens have identified numerous molecules with diagnostic potential. Current studies are assessing the accuracy of these recombinant proteins in identifying antibodies in individuals with active scabies and in differentiating them from individuals with past exposure.

Burrow ink test

A burrow can be located by rubbing a washable felt-tip marker across the suspected site and removing the ink with an alcohol wipe. When a burrow is present, the ink penetrates the stratum corneum and delineates the site. This technique is particularly useful in children and in individuals with very few burrows.

Tetracycline

Topical tetracycline solution is an alternative to the burrow ink test. After application and removal of the excess tetracycline solution with alcohol, the burrow is examined under a Wood light. The remaining tetracycline within the burrow fluoresces a greenish color. This method is preferred because tetracycline is a colorless solution and large areas of skin can be examined.

Definitive testing relies on the identification of mites or their eggs, eggshell fragments, or scybala.[22] This is best undertaken by placing a drop of mineral oil directly over the burrow on the skin and then superficially scraping longitudinally and laterally across the skin with a scalpel blade. (Avoid causing bleeding.) Scraping 15 or more burrows often produces only 1 or 2 eggs or mites, except in a case of crusted scabies, in which many mites will be present.[43]

The sample is placed on a microscope slide and examined under low and high power. Potassium hydroxide should not be used, since it can dissolve mite pellets. Failure to find mites is common and does not rule out the diagnosis of scabies.

Superficial cyanoacrylate biopsy (SCAB) combined with conventional transillumination light microscopy reveals the anatomic features of the scabies mite in detail. It can also distinguish living mites from dead ones, because living mites are mobile on the slide.[44] Scabies mites are seen in the images below.

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

Scabies preparation demonstrating a mite and ova. Courtesy of William D. James, MD.

Crusted scabies

Add 10% potassium hydroxide to the skin scraping. This dissolves excess keratin and permits adequate microscopic examination.

Strips of tape are applied to areas suspected of being burrows and then rapidly pulled off. These are then applied to microscope slides and examined. The adhesive tape test is easy to perform and had high positive and negative predictive values, making it a good screening test. The sensitivity of skin scraping was judged to be low.

Dermatoscopy-guided tape testing may be beneficial and should be evaluated.[45] Dermatoscopy was compared with the microscopic examination of a skin scraping and with the adhesive tape test, in patients with a presumptive diagnosis of scabies.[46] The sensitivity of dermatoscopy was 0.83, which was significantly higher than that of the adhesive tape test.

The histologic features of scabies are distinctive enough to suggest the diagnosis, although they are common to a variety of arthropod reactions. If a burrow is excised, mites, larvae, ova, and feces may be identified within the stratum corneum, as in the images below.

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).

A superficial and deep dermal infiltrate composed of lymphocytes, histiocytes, mast cells, and eosinophils is characteristic. Spongiosis and vesicle formation with exocytosis of eosinophils and occasional neutrophils are present, as in the image below. Biopsy of older lesions is nondiagnostic, demonstrating only excoriation and scale crusts.

In routine scabies, a single mite is seen. Eosinophilic spongiosis may be present (hematoxylin and eosin; original magnification, 400X).

Crusted scabies

Crusted scabies demonstrates massive hyperkeratosis of the stratum corneum, with innumerable mites in all stages of development. Psoriasiform hyperplasia of the underlying epidermis with spongiotic foci and occasional epidermal microabscesses is present. The dermis shows a superficial and deep, chronic inflammatory infiltrate with admixed interstitial eosinophils.

Nodular scabies

Nodular scabies reveals a dense, mixed, superficial and deep dermal inflammatory cell infiltrate. Lymphoid follicles may be present, and the infiltrate occasionally extends into the subcutaneous fat. Mite parts may be seen on serial sectioning in up to 20% of cases.

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.[47, 48] A 2019 meta-analysis reports that no single agent ranked most effective with respect to cure and control of adverse effects from the scabies infection. Permethrin, oral ivermectin, and synergized pyrethrins were deemed most effective for cure and symptomatic relief.[49]  A small segment of the population is at increased risk for ivermectin toxicity based on genetic predisposition.[50] Close contacts should be treated, and, during epidemics, large numbers may need to be treated.[51, 52, 53, 54]

In a World Health Organization (WHO)–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%, as well as a decrease in the prevalence of pyoderma (secondary infection) from 40% to 21%. There was also a decline in hematuria, which was a sign of renal damage by group A Streptococcus secondary infection in children.[55] Treatment also decreased occurrence of streptococcal skin disease. Similar successes have been reported in other populations.[56]

Treatment failures are uncommon but do occur. The most common causes of treatment failure include the following[57] :

• Improper application

• Inadequate application

• Reinfestation - Recurrence of the eruption usually means reinfection has occurred, underscoring the importance of treating all members of the household

• Resistance - Resistance to lindane has been widely reported; less frequently, cases of resistance to permethrin have been noted; resistance to ivermectin is still rare but has been reported in patients who received multiple doses of the drug over several years[57]

Neonates and pregnant women should be treated for scabies only if the benefit exceeds the risk and if the diagnosis is confirmed by a positive skin scraping or biopsy result.

Crusted scabies may require several treatments with scabicides and sometimes several different medications used sequentially.[27] Scabetic nodules may require intranodular steroid injection.

Activity

Individuals affected by scabies should avoid skin-to-skin contact with others. Patients with typical scabies may return to school or work 24 hours after the first treatment.[58]

Consultations

Consultation with a dermatologist or an infectious disease specialist may be required for severe, refractory scabies or for disseminated scabies in patients who are immunocompromised.

A scabicidal agent, such as permethrin, lindane, or ivermectin, is administered to destroy S scabiei mites, with an appropriate antimicrobial agent used as well if a secondary infection has developed. Moxidectin and afoxolaner are emerging as promising new agents. Botanical oils have also been used, but they present a risk of allergic contact dermatitis. Despite the development of resistance, permethrin retains good efficacy.[59, 60, 61, 62]

Itching may persist for up to a month, even following successful treatment. Pruritus may be partially alleviated with an oral antihistamine, such as hydroxyzine hydrochloride (Atarax), diphenhydramine hydrochloride (Benadryl), or cyproheptadine hydrochloride (Periactin). Rarely, individuals with a history of atopy may require a tapered dose of prednisone for the treatment of severe pruritus. Intranodular injection of dilute corticosteroids may be necessary in cases of nodular scabies.

If available, videodermatoscopy can be used to enhance the monitoring of clinical response to scabies treatment and allows for optimal timing of drug application.[63] This may minimize the risk of overtreatment, reduce the potential for side effects, and enhance patient compliance. This is not a widespread technique. With videodermoscopy, a handheld device is used to illuminate, magnify, and record video of the skin.

Crusted scabies

Patients with crusted scabies or their caregivers should be instructed to remove excess scale in order to allow penetration of the topical scabicidal agent and decrease the burden of infestation. This can be achieved with warm water soaks followed by application of a keratolytic agent, such as 5% salicylic acid in petrolatum or Lac-Hydrin cream. (Salicylic acid should be avoided if large body surface areas are involved because of the potential risk of salicylate poisoning.) The scales are then mechanically debrided with a tongue depressor or similar unsharp device.

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

Follow-up

Patients with scabies may need to be reexamined at 2 weeks and again at 1 month after treatment. If a patient has persistent lesions at the 1-month check-up, reinfection or persistent infection should be suspected. In this case, treatment should be reinitiated. The patient’s family or any close contacts should also be examined to check for a source of reinfection. Patients with crusted scabies, especially, should be followed after treatment and may require repeated courses of treatment.

All household members and close personal contacts older than 2 months and not pregnant should be treated for scabies, even if they have no symptoms or signs of infestation. (Pets do not require treatment.) Detailed directions regarding treatment and environmental control measures should be provided verbally and in writing.[57]

Instruct patients to launder clothing, bed linens, and towels used within the last week in hot water (60°C or higher) and to machine dry them, the day after treatment is initiated and again in 1 week. Items that cannot be washed may be professionally dry cleaned or sealed in plastic bags for 1 week. All carpets and upholstered furniture should be vacuumed and the vacuum bags immediately discarded.

Mass screening and treatment of all affected individuals give the greatest reductions in scabies prevalence,[22] but once these efforts end, prevalence rates quickly escalate. One approach to this problem is to provide more frequent treatment to a predetermined, randomly chosen number of affected individuals. Sometimes, as a result of nonlinearity, treatment densities do not have to be impractically high to produce significant reductions in scabies burden. Single-dose oral treatment may be effective in mass infestations.[64]

The US Centers for Disease Control and Prevention offer the following suggested guidelines for the treatment of scabies[65] :

• Treatment should be given to both the infested person a nd to household members and sexual contacts, particularly those who have had prolonged direct skin-to-skin contact with the infested person.
• All persons should be treated at the same time to prevent reinfestation.
• Bedding, clothing, and towels used by infested persons or close contacts anytime during the 3 days before treatment should be decontaminated by washing in hot water and drying in a hot dryer, by dry-cleaning, or by sealing in a plastic bag for at least 72 hours. Scabies mites generally do not survive more than 2-3 days away from human skin.
• Use of insecticide sprays and fumigants is not recommended.
• Scabicides are available only with a prescription. No over-the-counter (nonprescription) products have been tested and approved to treat scabies.
• For classic scabies, one or more of the following may be used: permethrin cream 5%, crotamiton lotion 10% and crotamiton cream 10%, sulfur (5-10%) ointment, lindane lotion 1%, or ivermectin.
• For crusted scabies, both oral and topical agents should be used together.

Japanese guidelines cite phenothrin lotion and oral ivermectin as first-line therapy.[66]  German guidelines list permethrin as first-line therapy.[67]  Some German authors have published data suggesting that outcomes are similar with currently available agents.[68]

The mainstay of scabies treatment is the application of topical scabicidal agents, with repeat application in 7 days. The treatment of choice is permethrin 5% lotion. A 2007 Cochrane Review found that topical permethrin appeared to be the most effective treatment for scabies.[69]  Alternative drug therapy includes precipitated sulfur 6% in petrolatum, lindane, benzyl benzoate, crotamiton, and ivermectin; a possible new option is albendazole.[70, 71, 72, 73]  Regarding ivermectin,  a second course of treatment is often recommended 7-10 days later because of some developing larvae that may survive the initial treatment.[74]

Pruritus can be treated with an oral antihistamine, such as hydroxyzine hydrochloride (Atarax), diphenhydramine hydrochloride (Benadryl), or cyproheptadine hydrochloride (Periactin). More severe symptoms may require a short course of topical or oral steroids.

Secondary infections may require antibiotics, which should be prescribed based on culture and sensitivity data.

Scabies outbreaks in nursing homes and cases of crusted scabies may require combination therapy consisting of topical application of permethrin and 2 oral doses of ivermectin at 200 μg/kg (administered 1 wk apart).[75] Bullous scabies may respond to ivermectin therapy.[76]

Observations, however, have noted emerging drug resistance to oral ivermectin and 5% permethrin.[77] Drug resistance is emerging as a concern with repeated administration. Clinical resistance has not been documented for permethrin use, but it has been documented in 2 people with crusted scabies who had repeated regimens of multiple doses of ivermectin.[7] Thus, the need to define molecular mechanisms of drug resistance in scabies mites is urgent, as is the development and assessment of alternative therapeutic options.[78]

Benzyl benzoate,an ester of benzoic acid and benzyl alcohol, is neurotoxic to mites and has been used. It is not available in the United States[9]  and is not FDA approved as a scabicide, although it is used in Europe.[57] There is an unmet need for new acaricide molecules with greater efficacy and improved pharmacological profiles to tackle scabies and its morbidity. One such molecule may be afoxolaner (AFX). It shows efficacy against fleas, ticks, and mites in dogs, as well as scabies. Controlled studies of the efficacy of scabies treatments can be difficult to set up, as scabies mites cannot be maintained or propagated in vitro away from their host for more than a few days.[79]

Class Summary

Treatment options include either topical or oral medication. Topical options include permethrin cream (drug of choice), lindane, benzyl benzoate, crotamiton lotion and cream, sulfur, topical ivermectin, tea tree oil, or oil of the leaves of Lippia multiflora Moldenke, a shrub found growing in West African savanna. Oral options include ivermectin, although it has not been approved by US Food and Drug Administration (FDA) for the treatment of scabies. A second course of treatment is often recommended 7-10 days later because of some developing larvae that may survive the initial treatment.

The Centers for Disease Control and Prevention (CDC) recommends treatment with either permethrin lindane or ivermectin. Permethrin is the drug of choice in the United States and the United Kingdom, but it is not available in France. In some studies, it has been shown to be more effective than a single dose of oral ivermectin, although it has equivalent efficacy when 2 doses of ivermectin are used at time zero and 2 weeks later. In severe cases, a topical medication may be used with oral medication (ivermectin).

A 2007 Cochrane Review found that topical permethrin appeared to be the most effective treatment for scabies.

Drug resistance is emerging as a concern with repeated administration. Clinical resistance has not been documented for permethrin use, but it has been documented in 2 people with crusted scabies who had repeated regimens of multiple doses of ivermectin.

Permethrin (Acticin, Elimite)

A neurotoxin that causes paralysis and death in ectoparasites, permethrin 5% cream is the drug of choice for scabies treatment, especially in infants over age 2 months and small children. It is more effective than crotamiton in treating symptoms and reducing chances of secondary bacterial infection.

The lotion should be applied over the entire body, including the face and scalp in infants. It should be left on for 8-12 hours and then rinsed. Reapplication 1 week later is advised; however, no controlled studies have demonstrated that 2 applications are more effective than 1.

Lindane

This is available in 1% lotion or cream. Lindane stimulates the nervous system of parasites, causing seizures and death. It was previously the standard treatment for scabies but is now considered a second-line drug, to be used if other agents fail or are not tolerated. Lindane is not safe in children or neonates, because of increased transcutaneous absorption leading to possible neurotoxicity. The systemic absorption rate of lindane is 10 times greater than that of permethrin, and its serum levels are more than 40 times higher. Overall, permethrin is a safer choice.

Sulfur topical (Sulpho-Lac, Sulfo-Lo)

This is the oldest scabicide, although it has not received FDA approval for scabies treatment. Topical sulfur is one of only a few scabicidal agents that can be used safely in very small children (< 2 mo) and in pregnant women. Sulfur is messy, malodorous, stains clothes, and requires repeat applications, thus reducing compliance. Sulfur should be used only when a patient cannot tolerate permethrin, lindane, or ivermectin. It is inexpensive and can be used for mass therapy in resource-poor economies. Creams or ointments ranging from 2-10% (6% preferred) are available.

Crotamiton (Eurax)

Crotamiton is a 10% cream or lotion for the treatment of scabies. Its mechanism of action is unknown, and the drug is associated with frequent treatment failures.

Ivermectin (Stromectol)

Ivermectin binds selectively with glutamate-gated chloride ion channels in invertebrate nerve and muscle cells, causing cell death. It is available in 3- and 6-mg tablets. The drug is currently approved for the treatment of human onchocerciasis and strongyloidiasis. Although it is not approved by the FDA for the treatment of scabies, it is widely administered for this purpose, with the literature supporting its use.

Ivermectin is a synthetic macrocyclic lactone belonging to the avermectin group of antibiotics. It has no antibiotic activity but is active against a number of endoparasites and ectoparasites of humans and animals. Ivermectin is an ideal agent in cases in which topical therapy is difficult or impractical, such as in widespread institutional infestations and bedridden patients. Patients with crusted scabies may require 3 or more doses, given at 1- to 2-week intervals.

Ivermectin is contraindicated in patients with allergic sensitization or nervous system disorders and in women who are pregnant or breastfeeding. Children younger than 5 years or weighing less than 15 kg should not be treated with ivermectin.

One study compared the efficacy of ivermectin with benzyl benzoate lotion in the treatment of scabies and found that ivermectin was at least as effective as the other drug and led to more rapid improvement. The efficacy of benzyl benzoate lotion and permethrin were also evaluated in a retrospective, matched cohort study of pregnant women. No adverse effects on pregnancy outcome were reported in patients using either drug.

Class Summary

These agents are used to treat secondarily infected lesions.

Mupirocin (Bactroban, Centany)

This agent is used to treat infection with Staphylococcus species, beta-hemolytic streptococci, or Streptococcus pyogenes. It inhibits protein and ribonucleic acid (RNA) synthesis by inactivating transfer-RNA synthetase.

Class Summary

These agents may be applied to help control intense pruritus caused by scabies.

Hydrocortisone, topical (Westcort, U-Cort, Ala Cort, Rederm)

This is an adrenocorticosteroid derivative that is suitable for application to skin or external mucous membranes. It has mineralocorticoid and glucocorticoid effects that result in anti-inflammatory activity. Hydrocortisone is considered the lowest-potency topical steroid.