Gregory Juckett, MD, MPH, is Professor of Family Medicine at the West Virginia University School of Medicine, Morgantown, WV.
Dr. Juckett has disclosed no relevant financial relationships.
Address correspondence to: Gregory Juckett, MD, MPH, fax: 304-293-2713; email: email@example.com
Dermatologic problems are the third most common cause of post-travel consultation at GeoSentinel travel clinics, after febrile illness and diarrhea.1 At these sites, typical skin problems in returning travelers included cutaneous larva migrans (9.8%); insect bites (8.2%); abscesses (7.7%); infected insect bites (6.8%); allergic rash (5.5%); dengue fever (3.4%); and leishmaniasis (3.3%).2 Other pyodermas and skin infestations (scabies, myiasis, tungiasis) were also routinely seen.
Skin conditions in returning travelers can be divided into infectious and noninfectious etiologies. Infectious skin conditions may be tropical in origin (25%), although the majority are cosmopolitan (75%).3 Rash with fever should always be distinguished from rash without, since the former implies potentially serious illness. Although most skin conditions in travelers are self-limited, dengue and chikungunya fevers, rickettsial diseases, hemorrhagic fevers and meningococcemia may be life threatening.
Travel rashes may be acquired from exposure to sun, heat, insects, marine life and/or an array of infectious causes: viruses, bacteria, fungi and parasites. Taking a detailed travel history is therefore a critical first step, since many of these diagnoses are dependent on specific exposures and locales. What was the exposure (location and environment), when did the rash begin, where did it spread, and how has it changed?
The predominant skin symptom is an important clue: Itching suggests an allergic etiology; tenderness at the site suggests infection. Another clue is how the rash progresses. Centrifugal rashes start on the trunk and spread to the extremities (varicella), whereas centripetal rashes (dengue fever, rickettsial infections) do the opposite. Topical treatment by the patient may alter the appearance of the rash (tinea incognito with steroid use) or even exacerbate it (Neosporin contact dermatitis). An oral medication history is also essential, as travelers frequently experience drug eruptions or photosensitivity reactions.
Determining the identity of the primary skin lesion based on its appearance and size (macule/patch, papule/plaque, etc.) and any secondary characteristics (scaling, hypopigmentation, lichenification, etc.) will help narrow the differential diagnosis (Sidebar, see page 364). Pattern recognition is key. One author suggests identifying eight different categories of skin lesions as starting points: ulcers; pruritic lesions; papules; nodules; vesicles; pigment change; linear lesions; and rash with fever.3
impetigo sores (vesicle/ulcer); HSV (vesicle/ulcer); CL; rickettsial infection (eschar); cutaneous anthrax (eschar).Vesicles/Bullae:
contact dermatitis; bullous impetigo; sunburn; HSV; varicella.Pruritic Lesions:
contact dermatitis; eczema; insect bites; CLM; scabies; swimmer’s itch; sea bather’s eruption; tinea infections; urticaria.Papules:
molluscum contagiosum; insect bites; acne; pyodermas; myiasis (early); tungiasis; miliaria.Nodules:
boils; myiasis (late).Pigment change:
pityriasis versicolor; vitiligo; pityriasis alba (following eczema); phytophotodermatitis; fire coral injuries; post-inflammatory hyperpigmentation.Linear lesions:
CLM; contact dermatitis; phytophotodermatitis (streaks); jelly fish stings; larva currens (strongyloides).Fever:
dengue; chikungunya; other viral exanthems; rickettsial infections (eschar); typhoid/enteric fever (rose spots); leptospirosis (jaundice; erythema nodosum; petechiae); brucellosis (erythema nodosum); drug eruption.
Note some categories overlap (adapted in part from O’Brien classification)
CLM = cutameous larva migrants (creeping eruption); CL = cutaneous leishmaniasis.
Types of Infections
Dengue or “break-bone” fever is the most common arbovirus (arthropodborne viral infection) in the world, the others being yellow fever, Japanese encephalitis, and tick-borne encephalitis. Most dengue infections in travelers are acquired in Asia, increasingly followed by the Americas, with a minority of cases from Africa.4 Day-biting Aedes aegypti or A. albopictus mosquitoes spread dengue, which is now at a 20-year high throughout the Caribbean and Central America, including recent non-travel-related cases in the Florida Keys and Texas.
Image courtesy of the Public Health Image Library/ James GathanyThe Aedes albopictus mosquito, also known as the Asian tiger mosquito, has been found to be a vector of dengue fever.
Symptoms include headache, fever, retro-orbital pain, severe myalgias/arthralgias and a pink centripetal maculopapular rash in 50% of patients.5 The characteristic rash, usually appearing around the time of defervescence, initially resembles a sunburn and blanches with pressure. Typically, small islands of normal skin are spared (“white islands in a red sea”). It usually resolves after 2 to 4 days with moderate itching and desquamation.
A clinically similar illness, also associated with rash and joint pain, is chikungunya fever, which can be distinguished from dengue by serology. Arthritis pain with chikungunya tends to persist much longer (several months) and the disease is much more prevalent in Asia, where it co-exists with dengue, than in the Americas. It is also spread by day-biting Aedes mosquitoes. A major outbreak in India and Indian Ocean islands occurred in 2005.6 Management of both conditions is symptomatic; the only practical prevention for travelers is to use mosquito repellents.
Other viral exanthems, mostly non-specific rashes associated with various viral infections, are common and usually self-limited. Enteroviruses (predominating in summer) and various winter-time respiratory viruses (eg, adenoviruses) are likely culprits in travelers.
Molluscum contagiosum is a common childhood infection presenting as shiny pearly-pink skin papules, often with a characteristic central dimple. It is easily spread by any skin contact and may also be acquired sexually. Treatment is through destroying the lesions by ablation, cryotherapy or, in the case of multiple lesions, by imiquimod cream.7
Cold sores (herpes simplex virus 1) are easily provoked by sun exposure or respiratory illness in travelers. Genital herpes (HSV-2) may follow ill-advised sexual encounters in adolescents. Both infections often follow adolescent or college-age spring break trips. Both HSV-1 and HSV-2 appear as clustered vesicles in their respective areas and are managed by acyclovir or related antivirals, such as valcyclovir.
Bacterial Skin Infections
Pyodermas, either from Staphylococcus aureus or Streptococcus pyogenes, are the most common bacterial skin infections in travelers. Staph infections may manifest as impetigo contagiosum (honey-colored crusts and sores); bullous impetigo (blisters and erosions); folliculitis; furuncles (boils); or carbuncles (aggregates of furuncles). Strep infections present also as impetigo contagiosum; ecthyma infectiosum (punched-out sores); erysipelas; or cellulitis. Erysipelas appears raised with well-demarcated margins, whereas cellulitis has none of these features. Localized impetigo usually responds to mupiricin ointment, but systemic beta-lactam antibiotics are usually necessary for deeper or widespread infections. Methicillin-resistant Staphylococcus aureus (MRSA) infections respond to sulfamethoxazole-trimethoprim, clindamycin or vancomycin. In the event of a fluctuant skin abscess, incision and drainage usually cure the infection.
Rickettsial infections classically present with fever, centripetal maculopapular rash and headache. A small papule at the site of an infected bite develops into a black eschar or scab (tache noire). Travelers to Asia may acquire scrub typhus (Orienta tsutsugamushi), spread by infected trombiculid mites or “chiggers.” A black eschar with regional lymphadenopathy and fever is a classic presentation. Neurologic symptoms (obtunded mental state, deafness), meningitis and vasculitis may follow with up to 50% mortality if untreated.8 The similar African tick typhus (R. africae) is the commonest rickettsial infection in South Africa. Other tick typhus species with similar symptoms occur in the Mediterranean (Rickettsia conorii), Australia (R. australis) and the Americas (Rocky Mountain Spotted Fever or Brazilian Spotted Fever, both from R. rickettsiae). Travelers returning from endemic areas with headache, fever and rash warrant prompt empiric treatment with doxycycline 100 mg twice a day for 14 days. Doxycycline is usually avoided in children under 8 years of age but exceptions are usually made for life-threatening rickettsial infections. The usual pediatric dose is 2.2 mg/kg orally every 12 hours (maximum 100 mg per dose).
Typhoid or enteric fever (Salmonella typhi or paratyphi), characterized by sustained high fever, abdominal discomfort and sometimes “pea-soup” diarrhea, may be associated with faint “rose spots,” actually bacterial emboli, visible only in lightskinned individuals. These 2- to 3-mm macules are usually on the abdomen or lower chest and last 3 to 4 days.9 Travelers visiting friends and relatives (“VFR” travelers) in South Asia are at particular risk, and typhoid vaccines, even when used, are only 50% to 80% protective.9 Diagnosis is through culture of the blood or bone marrow. Although ciprofloxacin has been the usual treatment, increasing quinolone resistance may warrant ceftriaxone therapy.9
Cutaneous anthrax (Bacillis anthracis) is characterized by a larger, painless black eschar at the site of inoculation surrounded by swollen red tissue (“malignant pustule”). Spores may infect animal hides, and some infections have been linked to imported skins used in drumming workshops.10 The importation of animal hides from several countries (eg, Haiti) is prohibited for this reason. Human-to-human spread of cutaneous anthrax is not known to occur. Ciprofloxacin is curative.
The hot, humid conditions of the tropics favor the development of fungal infections. Tinea corporis (“ringworm”) infections usually appear as scaly, round, itchy patches with central clearing and serpiginous margins. Tinea pedis (“athlete’s foot”) causes itching and scaling of the feet. Groin tinea or T. crurus (“jock itch”) commonly affects post-pubescent males and may be mimicked by erythrasma, a bacterial infection that fluoresces coralred with Wood’s lamp. Tinea imbricata from Trichophyton concentricum produces complex shingled patterns and is acquired in the South Pacific and humid areas of South and Southeast Asia. Most tinea infections fail to fluoresce (Trichosporum spp.), although Microsporum spp. lesions will fluoresce green with Wood’s lamp.11 Diagnosis of fungal infection may also be confirmed by seeing hyphae on microscopic exam of skin scrapings (best from the lesion border) with a drop of 20% potassium hydroxide (KOH). Treatment is usually with 2 weeks of a topical antifungal cream, although systemic treatment is necessary for tinea capitis (scalp ringworm) and tinea imbricata.
Tinea versicolor (Malassezia furfura) is a superficial fungal infection presenting as hypo- or hyperpigmented scaly macules on the neck, chest and upper back, fluorescing yellow-white under Wood’s lamp. Vacation tanning accentuates the hypo-pigmentation. Skin scrapings reveal a characteristic “spaghettiand-meatball” hyphae/spore pattern. Best treatment is with a short course of oral ketoconazole because topical treatments usually result in recurrence.
Visceral larval migrans (VLM), or “creeping eruption,” caused by the dog hookworm (Ancylostoma brasiliense), is the most common dermatologic diagnosis in returning travelers.2 A disproportionate number of cases come from the Caribbean, where dog feces on the beach are the usual source of infection.2 The hookworm larvae enter the vacationer’s feet or buttocks, causing an itchy serpiginous rash as the larvae migrate within the skin. Fortunately, the infection is self-limited because the larvae eventually die without developing. The simplest treatment is oral single-dose albendazole or ivermectin.
Myiasis is a human botfly infestation producing a tender skin boil. Close examination usually reveals a small central pore or breathing hole for the motile maggot inside. The human botfly (Dermatobium hominis) from Latin America attaches its eggs to mosquitoes that seek out mammalian hosts. Usually only a few lesions can be found on exposed skin and they take 6 to 12 weeks to develop.12
One type of botfly in Africa, the Tumbu fly (Cordylobia anthropophaga), lays its eggs on laundry drying outdoors. Hence, there are many lesions on sites covered by clothing containing these larvae, which develop rapidly, typically within 9 days.12 For both botfly and Tumbu fly infestation, surgical extraction for either species can be aided by prior application of an occlusive substance (bacon fatback or petroleum jelly), which induces upward migration of the larvae, typically within 24 hours.13 Dermatobium infection can be reduced through use of insect repellents while Cordylobia eggs can be killed by ironing clothes before wearing them. A recent hotspot for Dermatobium infections has been the Bolivian Amazon.14
Tungiasis (Tunga penetrans) describes a sand flea infestation of the feet. This small burrowing flea of Africa, west India and South America produces itchy subcutaneous, dark 5- to 8-mm nodules that may be observed to extrude tiny eggs.15 The lesions last about a month and often become secondarily infected. Treatment involves excision. Proper footwear is protective.
Types of Exposures
Insect bites are ubiquitous in the tropics, but for most patients, result only in transiently temporary pruritic papules. However, bite severity depends on patient sensitivity. Bites on the ankles are usually due to fleas. Persistent, red pruritic papules on the trunk may be due to bed bugs (often in clusters of three: “breakfast, lunch and dinner” sign) or chiggers (found on belt or sock-lines). Insect repellents containing either N, Ndiethyl-meta-toluamide (DEET) 35% or picaridin (known overseas as icaridin) 15% to 20% reduce the number of bites, whereas antihistamines relieve much of the itching.16 Permethrin spray may be used to protect clothing. Most insect bites presenting after travel are complicated by secondary infection and may thus require antibiotics.
Scabies or itch mites (Sarcoptes scabiei) may afflict travelers 4 to 6 weeks after skin exposure when the mite population reaches symptomatic levels.17 An allergic response to the burrowing of female mites results in extremely itchy papules in the finger webs, wrists, axillae, breasts, buttocks, and genitals. Usually the face is spared, except in heavier infestations. Pruritus may become intolerable at night, resulting in insomnia. Sexually acquired scabies presents as nodules on the penis or scrotum. Therefore, sexual partners, as well as family members, should be treated along with the patient.
The most effective scabies treatment is permethrin 5% cream applied from the neck down and left overnight.18 Next morning, the cream is showered off and all bedding and clothing should be washed. Treatment may be repeated in 7 to 14 days to ensure eradication.19 Gamma-benzene hexachloride lotion (Lindane) is more toxic than permethrin and is being abandoned for safety and environmental reasons. In more hygienic conditions, oral ivermectin 200 mcg/kg may be given as a single dose and, if possible, repeated in 2 weeks, but this therapy is not FDA approved.20 Itching from the dead mites may persist for several weeks after any of these treatments.
Head lice infestation or pediculosis (Pediculus humanis capitus) is easily acquired through contact with infected children. An itchy scalp is typical and nits may be observed attached to hair behind the ears and on the nape of the neck. Nits hatch in a week, with lice maturing in only 15 days. Nits attached more than 5 mm out on the hair shaft are usually nonviable, so school “no-nit” policies are unnecessary.21
Pubic lice (“crabs”) may be acquired from sexual contact and are confirmed by finding nits on pubic hair. Although permethrin and pyrethroid shampoos (Nix, Rid) have been the mainstay of treatment, increasing drug resistance has led to the development of newer therapies. Isopropyl myristate 50% (Resultz) dehydrates the lice by damaging their exoskeleton. Spinosad (Natroba topical solution), a natural insecticide derived from the soil bacterium Saccharopolyspora spinosa, was just approved by the FDA for children older than age 4 years. Malathion 0.5% lotion is a much more toxic second-line therapy for resistant infections approved only for children older than 6 years. Oral ivermectin also seems to work at the same dosage for scabies. All family members and any close contacts should be treated, even if asymptomatic.
Cutaneous leishmaniasis is a parasitic skin infection spread by sand fly bites: Phlebotomus sand flies in the Old World (Europe, Africa, and Asia) or Lutzomyia in the New (the Americas). Travelers describe a bite papule developing into a persistent painless ulcer with raised margins. The lesion’s edge should be biopsied and sent for pathology and polymerase chain reaction (PCR) testing. PCR is the diagnostic method of choice because it identifies the species involved.22
Treatment, usually with pentavalent antimony or with intravenous amphotericin, is problematic but will speed lesion healing. Most untreated lesions usually heal with scarring, but this may take 12 to 18 months. New World L. braziliensis ulcers appear to resolve but may recur years later as mucocutaneous leishmaniasis, thus the decision to treat with antimonial drugs or amphotericin often hinges on the likelihood of L. braziliensis re-infection.22
Because many travelers engage in water sports, aquatic exposures pose a particular risk. Bacterial infections may result from marine skin abrasions, often contact with shellfish or coral. Serious cellulitis from Vibrio vulnificus, V. parahemolyticus and Aeromonas may follow. V. vulnificus is especially dangerous, causing high mortality in patients with liver disease. If blood pressure drops and hemorrhagic bullous necrotic cutaneous lesions develop, approximately 50% of V. vulnificus patients die within 48 hours.23 Treatment of early marine infections in healthy patients can be initiated with doxycycline, but more susceptible patients require doxycycline and a third-generation cephalosporin.
Leptospirosis is primarily a febrile illness with jaundice, but it may provoke an erythema nodosum rash or even mimic hemorrhagic fever.24Mycobacterium marinum infection presents as a persistent hand or foot nodule. Pseudomonas aeruginosa, found in contaminated pools or hot tubs, causes self-limited “hot-tub” folliculitis with most lesions found in areas covered by bathing suits.
Coral injuries are especially troublesome in snorkelers and divers, often taking months to heal. Fire coral (Millepora), actually a hydrozoan rather than a true coral, is capable of stinging on touch, producing long-lasting areas of residual hyperpigmentation.
Sea bather’s eruption is the result of microscopic Linuche jellyfish larvae or “sea lice” trapped under a swimsuit. The itchy maculopapular rash develops hours after exposure and is treated symptomatically. “Swimmer’s itch” describes a fresh-water dermatitis on exposed skin caused by avian schistosome larvae (cercaria). Fortunately, these larvae are poorly adapted to humans, so the rash is selflimited. However, human schistosomiasis may also begin with a swimmer’s itch from fresh-water exposure in the tropics. Most human schistosomiasis is acquired in Africa, and in one series, 45% of cases reported cutaneous symptoms.25
Drug-related rashes accounted for nearly 1% of rashes in returning travelers.2 Pruritic urticarial rashes are the most common, but maculopapular rash, fixed drug eruptions, erythema multiforme, Stevens-Johnson syndrome and even anaphylaxis may occur. The incidence of antimalarial skin reactions in travelers to Africa was 8% for chloroquineproguanil; 3% for doxycycline; 2% for Malarone; and 1% for mefloquine.26
Photosensitivity-type drug reactions require additional UVA exposure so the rash is limited to exposed areas. Photosensitizing drugs include tetracyclines (doxycycline); quinolones (ciprofloxacin); antimalarials (chloroquine); sulfonamides; sulfonylureas; phenothiazines; and acne medications. Discontinuation of the offending drug and use of antihistamines to control itching are often all the treatment that is required. More severe reactions respond to prednisone.
Environmental Skin Conditions
Contact dermatitis is an allergic contact reaction from plants or other allergens in the environment. Although poison ivy, poison oak and poison sumac (all in the genus Toxicodendron) are the usual US suspects, many other plants can trigger this response. Mango sap, present in the unpeeled fruit, crossreacts with urushiol (the allergenic component in poison ivy sap), causing a pruritic, erythematous rash. Other sensitizing plants include poisonwood (Metopium toxiferum); cashew fruit (Anacardium); Japanese lacquer trees (Toxicodendron); African poison ivy (Smodingium); and Indian marking nut (Semecarpus anacardium).
Phytophotodermatitis describes a plant sensitivity reaction requiring UVA light exposure. Lemon or lime juice on the skin frequently produces a hyperpigmented persistent rash where the juice dripped on an exposed extremity. Other culprits include figs, rue, and giant hogweed (Heracleum).27
Sunburn ruins many trips, especially if the burn occurs during the first few days. Usually, this is the result of sunscreen being applied in insufficient quantities or not being reapplied after swimming. Ideally, 1 oz of 30+ SPF sunscreen is needed (if wearing a bathing suit) at least 30 minutes before exposure. Direct sun during peak intensity, between the hours of 10 a.m. and 3 p.m., should be avoided. Symptoms of sunburn range from erythema to intense blistering. Chills, fever, and dehydration may accompany severe cases (“sun poisoning”). Treatment involves anti-inflammatory agents such as aspirin or nonsteroidal anti-inflammatory agents, cool compresses, aloe vera lotion, topical steroids and, rarely, prednisone. Topical anesthetics should be avoided because they often induce sensitization. Although some of these treatments provide symptomatic relief, none of them appear to shorten recovery time or reduce epithelial cell damage.28 Continued protection from further sun exposure is mandatory.
Solar urticaria (sun-induced hives) is a pruritic eruption induced by sunlight in susceptible individuals. Polymorphous light eruption, appearing as a variable itchy maculopapular eruption, is a sensitivity reaction to intense UVA exposure in an un-acclimated individual. Rash and pruritus occur shortly after exposure. The condition usually subsides later in the summer after the skin becomes desensitized to sunlight.
Excess sweating also produces skin problems. Pitted keratolysis or “sweaty socks syndrome” is caused by the bacteria Kytococcus (Micrococcus) sedentarius and appears as tiny crater-like pits on weight-bearing areas of the foot. A foul smell is associated. Keeping the feet dry or using topical antibiotics is curative. Miliaria rubra, better known as “prickly heat,” is a self-limited intensely pruritic skin reaction caused by trapped sweat. Multiple tiny erythematous papules are noted under clothing. Miliaria profunda describes a more persistent form that occurs only in hot, humid climates. Treatment involves removal of clothing, air conditioning, and cool compresses.
Rashes in returning pediatric travelers require a careful history and exam to exclude multiple infectious and environmental causes. Many of these are nontropical conditions, but it is important to know what the patient may have been exposed to in their travels. Identifying the primary lesion, time of rash onset, key symptoms (itching or tenderness), and the presence or absence of fever will assist in making an accurate diagnosis.
- Freedman DO, Weld LH, Kozarsky PE, et al. Spectrum of disease and relation to place of exposure among ill returned travelers. N Engl J Med. 2006; 354:119. doi:10.1056/NEJMoa051331 [CrossRef]
- Lederman ER, Weld LH, Elyazar IR, et al. Dermatologic conditions of the ill returned traveler: an analysis from the GeoSentinel Surveillance Network. Int J Infect Dis. 2008; 12:593. doi:10.1016/j.ijid.2007.12.008 [CrossRef]
- O’Brien B. A Practical approach to common skin problems in returning travelers. Travel Medicine and Infectious Disease. 2009;7:125–146. doi:10.1016/j.tmaid.2009.03.003 [CrossRef]
- Jelinek T, Muhlberger N, Harms G, et al. Epidemiology and clinical features of imported dengue fever in Europe: sentinel surveillance data from TropNetEurop. Clin Infect Dis. 2002;35:1047–1052. doi:10.1086/342906 [CrossRef]
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- Ampaiwan C, Wathanee C, Viroj P, et al. The use of dengue nonstructural protein 1 antigen for the early diagnosis during the febrile stage in patients with dengue infection. The Pediatric Infectious Disease Journal. 2008;27(1):43–48. doi:10.1097/INF.0b013e318150666d [CrossRef]
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- Watt G, Strickman D. Life-threatening scrub typhus in a traveler returning from Thailand. Clin Infect Dis. 1994; 18: 624–626. doi:10.1093/clinids/18.4.624 [CrossRef]
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- Centers for Disease Control and Prevention. Cutaneous anthrax associated with drum making using goat hides from West Africa--Connecticut, 2007. MMWR Morb Mortal Wkly Rep. 2008;57(23):628–631.
- Gupta LK, Singhi MK. Wood’s lamp. Indian J Dermatol Venereol Leprol2004;70:131–135.
- Jelinek T, Nothdurft HD, Rieder N, Löscher T. Cutaneous myiasis: review of 13 cases in travelers returning from tropical countries. Int J Dermatol. 1995; 34(9): 624–626. doi:10.1111/j.1365-4362.1995.tb01088.x [CrossRef]
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- Schwartz E, Gur H. Dermatobia hominis myiasis: an emerging disease among travelers to the Amazon basin of Bolivia. J Travel Med. 2002; 9(2): 97–99. doi:10.2310/7060.2002.21503 [CrossRef]
- Franck S, Feldmeier H, Heuklebach J. Tungiasis: more than an exotic nuisance. Travel Medicine and Infectious Disease2003;1: 159–166. doi:10.1016/j.tmaid.2003.09.005 [CrossRef]
- Katz T, Miller J, Herbert A. Insect repellents: historical perspectives and new developments. J Amer Acad Dermatol2008;58(5):865–871. doi:10.1016/j.jaad.2007.10.005 [CrossRef]
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- Strong M, Johnstone PW. Interventions for treating scabies. Cochrane Database Syst Rev. 2007;(3):CD000320.
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