Could it be…SCABIES?
3-year-old boy (http://cme.medscape.com/viewarticle/582674_2) presents to his pediatrician with a history of worsening erythema and pruritus on the thenar aspect of his right hand. Examination of the hand reveals a few grouped, blanchable, erythematous papules. His history is significant for a vacation in which the family had stayed in multiple hotels.
A skin scraping was performed and examined under microscopy. The scraping demonstrated mites, ova, and scybala (fecal debris) consistent with a diagnosis of scabies. Scabies is a parasitic infestation of the skin caused by the arthropod Sarcoptes scabiei var. hominis, a very small parasite measuring 0.3 to 0.9 mm in size. Variants of the scabies mite that affect other animals (such as dogs, cats, pigs, etc.) are unable to reproduce in humans, but they can cause a transient dermatitis. Scabies was well known to the Greeks and Romans. The word scabies is derived from the Latin word “scabere,” which means to scratch. The Italian biologist Giovanni Cosimo Bonomo described the mite and linked it to the disease in the 17th century; however, it wasn’t until the 19th century that the skeptical scientific community finally accepted that scabies was caused by the mite Sarcoptes scabiei.[1,2]
In the 21st century, scabies continues to be a worldwide health problem. Its prevalence is higher in developing countries, where overcrowding and poverty lead to an increase in transmission. Scabies is transmitted by prolonged skin-to-skin contact with an infected person. Children (especially those of poor or underserved communities), sexually active individuals, and institutionalized patients are all at increased risk for acquiring the disease, because these groups have an increased chance of human contact. Scabies is also considered a sexually transmitted disease. It is infrequently acquired through the use of infested clothes, bed linen, and towels. A scabies infestation occurs when an impregnated female parasite enters the skin, tunnels into the stratum corneum, and excavates burrows to live and deposit its eggs. The larvae hatch and begin to move 3-10 days later. The female mite can sometimes be observed at the end of the burrow. Male mites usually roam on the surface of the skin, but female mites may also surface occasionally (especially at night), at which time they can be washed or scratched off.[1,2,3]
Intense pruritus is a classic symptom of scabies, and it is usually more severe at night. Symptoms are caused by a delayed type IV hypersensitivity reaction to the mites, ova, and scybala (feces) under the skin. The symptoms occur 4-6 weeks after the initial infection. Antibodies may form against the parasite causing this reaction; therefore, previously sensitized patients may have symptoms within hours of reinfection.[1,2]
Scabies can mimic numerous skin conditions, such as insect bites, atopic and contact dermatitis, and herpetic dermatitis (among others). Not uncommonly, scabies is misdiagnosed as one of these other skin conditions, allowing transmission to continue to occur until the correct diagnosis is established. Scabies can be diagnosed by visualizing the burrows or “tracks” left by the female mite as she moves through the stratus corneum of the skin. Initially, these burrows may appear as short, zigzagging, and hardly noticeable scratchlike marks with a slightly shiny hue, and they may be connected to an erythematous papule. This papule harbors the female mite and feces. As a result of the intense pruritus associated with scabies, the burrows may be difficult to differentiate from the scratch marks produced by the patient. Adult patients may show lesions between their fingers or on their wrists, axillae, areolae, elbows, knees, genitals, and buttocks. Alternately, children may have any part of their skin affected. The diagnosis can be confirmed by finding the mite, ova, or fecal debris of a lesion scraping under microscopy. The skin scraping is obtained by scraping infested primary lesions, such as vesicles or burrows, and placing the scraping on a glass slide; multiple scrapings may be necessary to positively make the diagnosis. In rare cases, skin biopsies may be obtained to both positively identify the mite or characteristic histopathology and to rule out other dermatoses.[1]
Related to scratching, patients with scabies may also become superinfected with Streptococcus pyogenes and Staphylococcus aureus. The complication of superinfection can lead to specific infections, such as impetigo, cellulitis, acute poststreptococcal glomerulonephritis, rheumatic fever, and even sepsis. Immunosuppressed patients may present with a severe form of scabies known as crusted scabies or Norwegian scabies. This is a widespread hyperkeratotic rash, with thick scaling and crusting and, at times, minimal to no pruritus. During this type of infection, up to millions of mites may survive for up to 1 week. In nonimmunocompromised hosts, an average of 5-15 mites cause infestation and survive for only 2-3 days. Crusted scabies appears to be the result of a high number of infiltrating CD8+ T lymphocytes in the dermis, with minimal helper T lymphocytes (CD4+), which is the opposite to that of a normal immune reaction to scabies. This detail may account for the body’s inability to mount an appropriate immune response against the scabies mites.[1,2]
The cornerstone of medical treatment for scabies consists of administering a scabicidal agent in combination with an antipruritic agent. An antimicrobial agent may be added if the lesions have become infected with bacteria. Topical scabicidal agents include permethrin 5%, lindane, malathion, sulfur in petrolatum (usually 6%), crotamiton, and benzyl benzoate. Of these agents, permethrin is the most commonly used in the United States, and it is recommended as a first-line therapy by the Centers for Disease Control and Prevention (CDC). Permethrin is applied from chin to toes and for a period of 10-12 hours, after which it should be washed off. The treatment is repeated in 1 week. Hypersensitivity reactions to permethrin have been documented, and there seems to be minimal systemic toxicity caused by minimal skin absorption. Permethrin is the recommended drug of choice for infants (age >2 mo), children, and pregnant (Class B) and nursing mothers. Antihistamines and topical antibiotics may be used as well to decrease pruritus and treat any skin infection. Ivermectin, an oral scabicide, is used in the United States for refractory patients or patients who cannot tolerate topical treatments (although it is not yet approved by the US Food and Drug Administration [FDA]). Preventing scabies reinfestation in family members and close contacts to the affected person is paramount; therefore, all household members should be treated regardless of their symptoms (or lack thereof). In addition, all clothing and linen that may have been in contact with the affected person should be washed in hot water and machine-dried. This process should be repeated 1 week later. Carpets and upholstered furniture should be vacuumed, and the vacuum bags should be disposed of. Patients should be reexamined 2 weeks after treatment to ascertain the treatment effectiveness.[1]
In this patient, treatment with topical permethrin 5% cured the infestation; however, he developed an allergic reaction to the permethrin cream that manifested as widespread pruritic, papular, 1-mm lesions on his knees and elbows. His condition responded to a 1-week course of oral antihistamines (diphenhydramine hydrochloride) and topical zinc oxide lotion. Although they were asymptomatic, all household contacts were treated along with the family members who had been on vacation with the patient.
References
- Binder WD, Sciammarella J. Scabies. eMedicine [serial Online]. Last updated: June 2006. Available at: http://www.emedicine.com/emerg/TOPIC517.HTM
- Walton SF, Holt DC, Currie BJ, Kemp DJ. Scabies: new future for a neglected disease. Adv Parasitol. 2004;57:309-76. Abstract
- Clucas DB, Carville KS. Disease burden and health-care clinic attendances for young children in remote aboriginal communities of northern Australia. Bull World Health Organ. 2008;86:275-81. Abstract
