ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Scabies: Epidemiology, clinical features, and diagnosis

Scabies: Epidemiology, clinical features, and diagnosis
Literature review current through: Jan 2024.
This topic last updated: May 24, 2022.

INTRODUCTION — Scabies is an infestation of the skin by the mite Sarcoptes scabiei (picture 1A-B). Classic scabies typically manifests as an intensely pruritic eruption with a characteristic distribution. The sides and webs of the fingers, wrists, axillae, areolae, and genitalia are among the common sites of involvement. Crusted scabies, a less common variant that primarily occurs in the setting of reduced cellular immunity and is associated with a heavy mite burden, is characterized by thick scale, crusts, and fissures. The diagnosis of scabies is confirmed through the detection of scabies mites, eggs, or feces with microscopic examination.

The clinical features and diagnosis of scabies will be reviewed here. The management of scabies is discussed separately. (See "Scabies: Management".)

EPIDEMIOLOGY — Scabies is a relatively common infestation that can affect individuals of any age and socioeconomic status. The worldwide prevalence is estimated to be 200 million people, with wide variation in prevalence among individual geographic regions [1]. A systematic review of population-based studies from various regions of the world (excluding North America) found prevalence estimates ranging from 0.2 to 71 percent, with the highest prevalences in the Pacific region and Latin America [2]. Scabies is particularly common in resource-limited regions.

Crowded conditions increase risk for scabies infestation [3]. Epidemics can occur in institutional settings, such as long-term care facilities and prisons [4].

LIFE CYCLE — S. scabiei var. hominis is a whitish-brown, eight-legged mite (picture 1A-B). Female mites are larger than male mites and measure approximately 0.4 x 0.3 mm [3]. After mating, female mites burrow into the epidermis, a process facilitated by secretion of proteolytic enzymes that cause keratinocyte damage [5]. Female mites continue to extend the burrow and lay two to three eggs per day before dying after four to six weeks [3]. Larvae hatch in three to four days and molt three times within the burrow to reach adulthood.

The mite burden in patients with classic scabies is generally low, limited to an average of 10 to 15 mites during an initial episode and approximately half as many with subsequent infestations [6,7]. In contrast, patients with crusted scabies can have up to millions of mites on the body.

In typical conditions (at room temperature and average humidity), mites can survive off a host for 24 to 36 hours [8]. Survival times can be longer in colder conditions with high relative humidity [8,9].

TRANSMISSION — Transmission of scabies usually occurs through direct and prolonged skin-to-skin contact, as may occur among family members or sexual partners [10]. Casual skin contact is unlikely to result in transmission. Transmission through fomites (eg, clothing, bedclothes, or other objects) used by a person with classic scabies is uncommon; however, fomite transmission is more likely to occur in the setting of crusted scabies due to a much higher parasite burden [3,11]. (See 'Life cycle' above.)

True scabies infestation is not transmitted from animals to humans. The scabies mites responsible for animal scabies (ie, sarcoptic mange) belong to distinct subspecies and typically cannot reproduce in humans. Reactions to such mites are usually self-limited and resolve if contact with the affected animal ceases [3,12].

CLINICAL MANIFESTATIONS — The major clinical variants of scabies are classic scabies and crusted scabies.

Classic scabies — The prominent clinical feature of classic scabies is pruritus. It is often severe and usually worse at night. Pruritus results from a delayed-type hypersensitivity reaction to the mite, mite feces, and mite eggs [6]. Symptoms typically begin three to six weeks after primary infestation [13-15]. However, in previously infested patients, symptoms usually begin within one to three days after infestation, presumably because of prior sensitization [13,14,16].

Typical cutaneous findings are multiple small, erythematous papules, often excoriated (picture 2A-G). Burrows may be visible as 2 to 15 mm, thin, gray, red, or brown, serpiginous lines (picture 3A-B). Burrows are a characteristic finding but often are not visible due to excoriation or secondary infection. Miniature wheals, vesicles, pustules, and, rarely, bullae also may be present.

The distribution of cutaneous findings usually involves more than one of the following areas; rarely, scabies is localized to a single area [17,18] (figure 1):

Sides and webs of the fingers (picture 2A, 2H-I)

Flexor aspects of the wrists (picture 2B-C, 2J)

Extensor aspects of the elbows

Anterior and posterior axillary folds (picture 4)

Periareolar skin (especially in women) (picture 2E)

Periumbilical skin

Waist

Male genitalia (scrotum, penile shaft, and glans) (picture 2D, 2K)

Extensor surface of the knees

Lower buttocks and adjacent thighs (picture 5)

Lateral and posterior aspects of the feet (picture 2F)

The back is relatively free of involvement, and the head is spared except in very young children. Young children and infants often show heavy involvement of the palms and soles and all aspects of the fingers (picture 6A-C). Lesions in children are usually more inflammatory than in adults and often are vesicular or bullous (picture 7A-E).

Nodular scabies is a less common manifestation of classic scabies. Nodular scabies is characterized by persistent, firm, erythematous, extremely pruritic, dome-shaped papules 5 or 6 mm in diameter. The groin, genitalia, buttocks, and axillary folds are the usual sites of involvement (picture 8A-C). The nodules may represent a hypersensitivity reaction to prior or currently active scabies infestation [19,20].  

Crusted scabies — Crusted scabies (also known as scabies crustosa, Norwegian scabies, Boeck scabies, or keratotic scabies) can occur in the presence of conditions that compromise cellular immunity, such as AIDS, human T cell lymphotropic virus type 1 (HTLV-1) infection, leprosy, and lymphoma [21]. This variant may also occur in older adults and patients with Down syndrome [22]. Crusted scabies may also accompany long-term use of topical corticosteroids [23]. High numbers of scabies mites are present. (See "Fever and rash in patients with HIV".)

Crusted scabies begins with poorly defined, erythematous patches that quickly develop prominent scale (picture 9A-G). Any skin area may be affected, but the scalp, hands, and feet are particularly susceptible. If untreated, the disease usually spreads inexorably and may eventually involve the entire integument. Scales become warty, especially over bony prominences. Crusts and fissures appear. The lesions are malodorous. Nails are often thickened, discolored, and dystrophic. Pruritus may be minimal or absent.

Laboratory abnormalities may include eosinophilia and increased immunoglobulin E (IgE) levels [24]. (See "Eosinophil biology and causes of eosinophilia", section on 'Parasites and other infections'.)

COMPLICATIONS — Secondary staphylococcal or streptococcal infections, including impetigo, ecthyma, paronychia, and furunculosis, frequently complicate classic scabies. The fissures associated with crusted scabies provide a portal of entry for bacteria. This may lead to sepsis in older adults and immunocompromised patients [25]. Streptococcal infections may lead to poststreptococcal glomerulonephritis or other complications [26]. Data from an in vitro study suggest that a scabies mite complement inhibitor (SMSB4) may contribute to increased risk for secondary streptococcal infections. (See "Poststreptococcal glomerulonephritis".)

Rarely, patients with scabies develop generalized urticaria. Occurrences of urticaria as the initial manifestation of scabies have been reported [27,28].

HISTOPATHOLOGY — The histopathologic findings can vary based upon lesion morphology. Common histologic findings include epidermal spongiosis and a mixed infiltrate in the dermis with eosinophils, lymphocytes, and histiocytes. In crusted scabies, the stratum corneum is markedly thickened.

Scabies, mites, eggs, or feces may be visualized if captured in the biopsy specimen and are most likely to be visualized in patients with crusted scabies, given the high number of mites present. Pink, pigtail-like structures may be present in the stratum corneum and may represent egg fragments [29].

DIAGNOSIS — The diagnosis of scabies is confirmed through the detection of the scabies mite, eggs, or fecal pellets (also known as "scybala") through microscopic examination. However, since these findings are not always readily detected given the low number of mites in patients with classic scabies and microscopic examination is not always feasible, a presumptive diagnosis is sometimes made based upon a consistent history and physical examination [30,31].

Dermoscopy is a helpful adjunctive diagnostic tool. Skin biopsies are not usually necessary and are reserved for difficult cases in which other disorders need to be excluded. (See 'Differential diagnosis' below.)

History and physical examination — The diagnosis of classic scabies should be suspected in patients with one or more of the following [32,33]:

Widespread itching that is worse at night, spares the head (except in infants and young children), and seems to be out of proportion to visible changes in the skin

A pruritic eruption with characteristic lesions and distribution (figure 1)

Other household members with similar symptoms

A diagnosis of crusted scabies should be suspected when the following features are present:

Thick, crusted, fissured plaques

Older adult or immunosuppressed patient

Burrows often are not evident on physical examination but, when seen, strongly support the diagnosis (picture 3A-B, 9F).

Examination for mites — The definitive method to confirm diagnosis of scabies is a scabies preparation. Scabies preparations are used to detect mites, mite eggs, or mite fecal pellets. Dermoscopic examination can identify sites of scabies mites or burrows and can facilitate placement of the scraping. Because of the low mite burden in classic scabies, negative results do not exclude the diagnosis [11,34,35]. (See 'Scabies preparation' below and 'Dermoscopy' below.)

Scabies preparation — Performance of a skin scraping involves the sampling and microscopic examination of the epidermis from sites that may harbor scabies mites. In adults, the areas most likely to yield mites are between the fingers, sides of hands, flexural wrists, elbows, axillae, groin, breasts, and feet. Sites on the palms, soles, or torso may offer the highest yield in infants and young children. The sensitivity of scabies preparation ranges from 46 to 90 percent; the specificity is 100 percent [36].

Scrapings should be performed on skin lesions in multiple sites; burrows or erythematous papules are ideal. Anesthesia is not necessary. A blade (typically a number 15 blade) is used to vigorously scrape across the surface of the lesion sufficiently to remove a portion of the epidermis without inducing significant bleeding. A 3 mm disposable curette is an alternative tool that may be helpful for performing a scraping on children [37]. Prior to scraping, a small amount of mineral oil is usually applied to the site or the blade to aid in removal of mites, scale, and debris.

The specimen should be applied to a glass slide. Additional mineral oil can be added prior to placement of the coverslip. Application of potassium hydroxide (KOH) to the slide may be helpful for examination of specimens from suspected crusted scabies; the KOH will dissolve excess keratotic debris [36]. The clinician then examines the specimen for scabies mites, eggs, or feces (picture 1A-D). In crusted scabies, large numbers of mites and eggs may be seen [22].

Alternatively, a scabies preparation can be performed using a piece of transparent tape with a strong adhesive (eg, clear packing tape) rather than a blade [34,38]. This procedure is called "the adhesive tape test." The tape is firmly applied to a skin lesion and then is rapidly pulled off. After applying the tape to a glass slide, the clinician utilizes a microscope to examine the tape for mites and eggs. An advantage of the adhesive tape test is the lack of need for specialized equipment other than a microscope. The procedure may also be useful in children who cannot tolerate skin scrapings.

Dermoscopy — Dermoscopy (examination of the skin surface with a handheld dermatoscope to allow visualization of specific structures related to the epidermis, dermal-epidermal junction, and papillary dermis) may be a useful tool in scabies [34,35]. The test can be used to visualize mites and burrows in vivo and to guide the placement of confirmatory skin scrapings [39]. A disadvantage of dermoscopy as a sole diagnostic test is lower specificity compared with scabies preparation [36]. In addition, mites are frequently difficult or impossible to detect via dermoscopy in patients with highly pigmented skin [34]. (See "Overview of dermoscopy".)

The characteristic finding on dermoscopic examination is a dark, triangular shape that represents the head of the mite within a burrow ("delta wing" sign) (picture 10A-B). In addition, burrows are more easily visualized with dermoscopy. A noodle-like pattern representing aggregates of burrows has been described in crusted scabies [40].

Laboratory tests — Blood tests are generally not indicated for the diagnosis of scabies. However, eosinophilia has been reported, particularly in crusted scabies, and investigation of the cause of persistent eosinophilia has led to the diagnosis of scabies in challenging cases [24,41]. (See 'Crusted scabies' above and "Eosinophil biology and causes of eosinophilia", section on 'Parasites and other infections'.)

DIFFERENTIAL DIAGNOSIS — Lesions of classic scabies are often excoriated, obscuring their appearance. The differential diagnosis is broad, and scabies can appear similar to common pruritic disorders, such as atopic dermatitis, contact dermatitis, nummular eczema, and arthropod bites. (See "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis", section on 'Clinical manifestations' and "Clinical features and diagnosis of allergic contact dermatitis" and "Nummular eczema" and "Insect and other arthropod bites".)

Close attention to the patient's history (eg, pruritus in close contacts) and physical examination (eg, distribution and morphology of lesions) is helpful for differentiating scabies from these diagnoses. Dermoscopic examination can be used to identify features that strongly suggest scabies. When positive, a scabies preparation confirms a scabies diagnosis. (See 'Clinical manifestations' above and 'Diagnosis' above.)

Less common disorders in the differential diagnosis of classic scabies include dermatitis herpetiformis and bullous pemphigoid:

Dermatitis herpetiformis – Dermatitis herpetiformis is an autoimmune blistering disorder associated with gluten sensitivity. Classic clinical manifestations include intensely pruritic, inflammatory papules and vesicles with predilection for the forearms, knees, scalp, and buttocks (picture 11A-B). The diagnosis is confirmed through skin biopsy and direct immunofluorescence microscopy demonstrating granular deposits of immunoglobulin A in the dermal papillae. (See "Dermatitis herpetiformis".)

Bullous pemphigoid – Bullous pemphigoid is an autoimmune blistering disorder that usually occurs in older adults. A prodromic phase characterized by pruritic, eczematous, papular, or urticaria-like skin lesions can precede the development of the classic features of tense bullae on an erythematous, urticarial, or noninflammatory base (picture 12). The diagnosis is confirmed through a skin biopsy and direct immunofluorescence microscopy demonstrating linear deposition of immunoglobulin G and/or C3 along the basement membrane zone. (See "Clinical features and diagnosis of bullous pemphigoid and mucous membrane pemphigoid".)

In particular, the clinical differential diagnosis of classic scabies in infants should include acropustulosis of infancy and Langerhans cell histiocytosis:

Infantile acropustulosis (acropustulosis of infancy) – Infantile acropustulosis is a benign, recurrent, vesiculopustular eruption characterized by pruritic vesiculopustules (picture 13). The extremities, especially the palms and soles, are the primary sites of involvement. Diagnosis is based upon the clinical features and the absence of additional findings suggestive of scabies. Burrows are absent, and a scabies preparation will be negative. (See "Vesicular, pustular, and bullous lesions in the newborn and infant", section on 'Infantile acropustulosis'.)

Langerhans cell histiocytosis – Langerhans cell histiocytosis is a rare histiocytic disorder that can have associated skin manifestations. Infants or young children may present with red-orange or yellow-brown, scaly papules, erosions, or petechiae, often on the groin, intertriginous skin, and scalp (picture 14A-B). A skin biopsy is necessary to confirm the diagnosis. (See "Clinical manifestations, pathologic features, and diagnosis of Langerhans cell histiocytosis".)

The differential diagnosis of crusted scabies includes other disorders characterized by hyperkeratotic patches or plaques, including psoriasis, seborrheic dermatitis, Darier disease (picture 15A-B), and palmoplantar keratoderma. A scabies preparation differentiates crusted scabies from these disorders. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis" and "Seborrheic dermatitis in adolescents and adults" and "Cradle cap and seborrheic dermatitis in infants" and "Darier disease" and "The genodermatoses: An overview", section on 'Palmoplantar keratodermas'.)

Occasional patients with pruritus secondary to other causes strongly believe that they have scabies in the absence of true infestation. The clinical evaluation aids in distinguishing these patients from patients with scabies. The clinical evaluation can also help to identify the subgroup of patients who may have delusional parasitosis, a psychiatric disorder characterized by a fixed, false belief of infection with parasites or other organisms. (See "Pruritus: Etiology and patient evaluation", section on 'Evaluation' and "Delusional infestation: Epidemiology, clinical presentation, assessment, and diagnosis".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Scabies (The Basics)")

Beyond the Basics topics (see "Patient education: Scabies (Beyond the Basics)")

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Scabies".)

SUMMARY AND RECOMMENDATIONS

Epidemiology – Scabies is a common infestation of the skin caused by Sarcoptes scabiei (picture 1A-B). Scabies can affect individuals of any age and socioeconomic status. Crowded conditions increase risk for scabies infestation. (See 'Epidemiology' above.)

Scabies mites – Scabies mites typically cannot be seen with the naked eye. The size of the larger female mite is approximately 0.4 x 0.3 mm. Female scabies mites create burrows in the skin where they lay two to three eggs per day. (See 'Life cycle' above.)

Clinical variants – The two major clinical variants of scabies are classic scabies and crusted scabies. Classic scabies, the most common presentation, is associated with a relatively low mite burden (approximately 10 to 15 mites on the body). Crusted scabies usually occurs in older adults or immunocompromised individuals and is associated with a much higher mite burden (up to millions of mites on the body). (See 'Life cycle' above and 'Clinical manifestations' above.)

Transmission – Transmission of scabies usually occurs through direct and prolonged skin-to-skin contact, as may occur among family members or sexual partners. Casual skin contact is unlikely to lead to transmission. Transmission via fomites is uncommon in classic scabies but is more likely to occur in crusted scabies. (See 'Transmission' above.)

Clinical manifestations:

Classic scabies – The characteristic clinical findings of classic scabies are intense pruritus and multiple small, erythematous papules that are often excoriated (picture 2A-G). Burrows, which appear as 2 to 15 mm, thin, serpiginous lines, may be visible (picture 3A-B). The fingers, wrists, elbows, axillae, areolae, periumbilical skin, waist, male genitalia, knees, buttocks, and feet are common sites of involvement (figure 1). The head is usually spared except in very young children. Heavy involvement of the palms, soles, and fingers is common in very young children (picture 6A-C). Larger papules (nodular scabies) are a less common manifestation (picture 8A-C). (See 'Classic scabies' above.)

Crusted scabies – Crusted scabies typically manifests as poorly defined, erythematous patches that develop prominent scale, crusts, and fissures (picture 9A-G). Nail dystrophy is common. Pruritus may be minimal or absent. (See 'Crusted scabies' above.)

Diagnosis – A diagnosis of scabies may be strongly suspected based upon the patient history and physical examination. The diagnosis is confirmed through detection of scabies mites, eggs, or feces through microscopic examination (scabies preparation) (picture 1A-D). A negative scabies preparation does not exclude the diagnosis. Dermoscopic examination is a helpful adjunctive diagnostic tool (picture 10A-B). (See 'Diagnosis' above.)

  1. GBD 2015 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet 2016; 388:1545.
  2. Romani L, Steer AC, Whitfeld MJ, Kaldor JM. Prevalence of scabies and impetigo worldwide: a systematic review. Lancet Infect Dis 2015; 15:960.
  3. Heukelbach J, Feldmeier H. Scabies. Lancet 2006; 367:1767.
  4. www.cdc.gov/parasites/scabies/epi.html (Accessed on August 11, 2017).
  5. Fimiani M, Mazzatenta C, Alessandrini C, et al. The behaviour of Sarcoptes scabiei var. hominis in human skin: an ultrastructural study. J Submicrosc Cytol Pathol 1997; 29:105.
  6. Currie BJ, McCarthy JS. Permethrin and ivermectin for scabies. N Engl J Med 2010; 362:717.
  7. Johnston G, Sladden M. Scabies: diagnosis and treatment. BMJ 2005; 331:619.
  8. Arlian LG, Runyan RA, Achar S, Estes SA. Survival and infectivity of Sarcoptes scabiei var. canis and var. hominis. J Am Acad Dermatol 1984; 11:210.
  9. Arlian LG, Vyszenski-Moher DL, Pole MJ. Survival of adults and development stages of Sarcoptes scabiei var. canis when off the host. Exp Appl Acarol 1989; 6:181.
  10. Fuller LC. Epidemiology of scabies. Curr Opin Infect Dis 2013; 26:123.
  11. Chosidow O. Clinical practices. Scabies. N Engl J Med 2006; 354:1718.
  12. www.cdc.gov/parasites/scabies/index.html (Accessed on August 11, 2017).
  13. Chosidow O. Scabies and pediculosis. Lancet 2000; 355:819.
  14. Vorou R, Remoudaki HD, Maltezou HC. Nosocomial scabies. J Hosp Infect 2007; 65:9.
  15. Walton SF, Oprescu FI. Immunology of scabies and translational outcomes: identifying the missing links. Curr Opin Infect Dis 2013; 26:116.
  16. McCarthy JS, Kemp DJ, Walton SF, Currie BJ. Scabies: more than just an irritation. Postgrad Med J 2004; 80:382.
  17. Pomares C, Marty P, Delaunay P. Isolated itching of the genitals. Am J Trop Med Hyg 2014; 90:589.
  18. Eshagh K, DeKlotz CM, Friedlander SF. Infant with a papular eruption localized to the back. JAMA Pediatr 2014; 168:379.
  19. Suh KS, Han SH, Lee KH, et al. Mites and burrows are frequently found in nodular scabies by dermoscopy and histopathology. J Am Acad Dermatol 2014; 71:1022.
  20. Czeschik JC, Huptas L, Schadendorf D, Hillen U. Nodular scabies: hypersensitivity reaction or infection? J Dtsch Dermatol Ges 2011; 9:840.
  21. Kartono F, Lee EW, Lanum D, et al. Crusted Norwegian scabies in an adult with Langerhans cell histiocytosis: mishaps leading to systemic chemotherapy. Arch Dermatol 2007; 143:626.
  22. Wong SS, Woo PC, Yuen KY. Unusual laboratory findings in a case of Norwegian scabies provided a clue to diagnosis. J Clin Microbiol 2005; 43:2542.
  23. Bilan P, Colin-Gorski AM, Chapelon E, et al. [Crusted scabies induced by topical corticosteroids: A case report]. Arch Pediatr 2015; 22:1292.
  24. Roberts LJ, Huffam SE, Walton SF, Currie BJ. Crusted scabies: clinical and immunological findings in seventy-eight patients and a review of the literature. J Infect 2005; 50:375.
  25. Lin S, Farber J, Lado L. A case report of crusted scabies with methicillin-resistant Staphylococcus aureus bacteremia. J Am Geriatr Soc 2009; 57:1713.
  26. Swe PM, Christian LD, Lu HC, et al. Complement inhibition by Sarcoptes scabiei protects Streptococcus pyogenes - An in vitro study to unravel the molecular mechanisms behind the poorly understood predilection of S. pyogenes to infect mite-induced skin lesions. PLoS Negl Trop Dis 2017; 11:e0005437.
  27. Witkowski JA, Parish LC. Scabies: a cause of generalized urticaria. Cutis 1984; 33:277.
  28. Chapel TA, Krugel L, Chapel J, Segal A. Scabies presenting as urticaria. JAMA 1981; 246:1440.
  29. Kristjansson AK, Smith MK, Gould JW, Gilliam AC. Pink pigtails are a clue for the diagnosis of scabies. J Am Acad Dermatol 2007; 57:174.
  30. Osti MH, Sokana O, Gorae C, et al. The diagnosis of scabies by non-expert examiners: A study of diagnostic accuracy. PLoS Negl Trop Dis 2019; 13:e0007635.
  31. Engelman D, Yoshizumi J, Hay RJ, et al. The 2020 International Alliance for the Control of Scabies Consensus Criteria for the Diagnosis of Scabies. Br J Dermatol 2020; 183:808.
  32. Mahé A, Faye O, N'Diaye HT, et al. Definition of an algorithm for the management of common skin diseases at primary health care level in sub-Saharan Africa. Trans R Soc Trop Med Hyg 2005; 99:39.
  33. Heukelbach J, Wilcke T, Winter B, Feldmeier H. Epidemiology and morbidity of scabies and pediculosis capitis in resource-poor communities in Brazil. Br J Dermatol 2005; 153:150.
  34. Walter B, Heukelbach J, Fengler G, et al. Comparison of dermoscopy, skin scraping, and the adhesive tape test for the diagnosis of scabies in a resource-poor setting. Arch Dermatol 2011; 147:468.
  35. Dupuy A, Dehen L, Bourrat E, et al. Accuracy of standard dermoscopy for diagnosing scabies. J Am Acad Dermatol 2007; 56:53.
  36. Micheletti RG, Dominguez AR, Wanat KA. Bedside diagnostics in dermatology: Parasitic and noninfectious diseases. J Am Acad Dermatol 2017; 77:221.
  37. Jacks SK, Lewis EA, Witman PM. The curette prep: a modification of the traditional scabies preparation. Pediatr Dermatol 2012; 29:544.
  38. Katsumata K, Katsumata K. Simple method of detecting sarcoptes scabiei var hominis mites among bedridden elderly patients suffering from severe scabies infestation using an adhesive-tape. Intern Med 2006; 45:857.
  39. Prins C, Stucki L, French L, et al. Dermoscopy for the in vivo detection of sarcoptes scabiei. Dermatology 2004; 208:241.
  40. Chavez-Alvarez S, Villarreal-Martinez A, Argenziano G, et al. Noodle pattern: a new dermoscopic pattern for crusted scabies (Norwegian scabies). J Eur Acad Dermatol Venereol 2018; 32:e46.
  41. Sluzevich JC, Sheth AP, Lucky AW. Persistent eosinophilia as a presenting sign of scabies in patients with disorders of keratinization. Arch Dermatol 2007; 143:670.
Topic 4038 Version 28.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟