Pediculosis and Scabies 

DAVID C. FLINDERS, M.D., and PETER DE SCHWEINITZ, M.D., Utah Valley Family Practice Residency, Provo, Utah

Am Fam Physician. 2004 Jan 15;69(2):341-348.

Pediculosis and scabies are caused by ectoparasites; patients usually present with itching. Head and pubic lice infestations are diagnosed by the visualization of insects or viable nits (eggs). Primary treatment is topically administered 1 percent permethrin. Malathion is one alternative for treatment failures. The importance of environmental measures to prevent infestation is a matter of controversy. Pubic lice are treated the same as head lice, but this finding should prompt evaluation for other sexually transmitted diseases. Body lice infestation should be suspected when symptoms of generalized itching occur in persons who do not change or wash their clothing or bedding regularly; lice may be found in the seams of their clothing. Topically administered permethrin may help to eradicate body lice, but personal hygiene measures are essential for successful treatment. Classic scabies in adults can be recognized by a pruritic, papular rash with excoriations; in infants, small children, and the immunocompromised, the rash may include vesicles, pustules, or nodules. Primary treatment for scabies is permethrin cream, and environmental measures are important to prevent recurrent infestation. Generalized crusted scabies is best treated with oral ivermectin.

Pediculosis and scabies are closely related skin conditions caused by arthropods. Although these conditions typically cause severe itching, they generally are benign. Pediculosis and scabies have similar treatments.

PediculosisThe three lice species that infest humans are Pediculus humanus capitis—head louse (Figure 1, left), Phthirus pubis —crab or pubic louse (Figure 1, right), and Pediculus humanus corpus—body louse. All three insects are obligate human parasites. Contrary to popular belief, these insects do not hop, jump, or fly. Rather, they are transmitted by person-to-person contact.

FIGURE 1.

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(Left) Pediculus humanus capitis (head louse). The adult female has a slightly larger abdomen than the male. The human body louse is similar in appearance to the head louse.  (Right) Phthirus pubis (pubic, or crab louse).

Despite the introduction of new treatments, the frequency of lice infestation may be increasing. One explanation may be the development of resistance to current treatments.1,2 Fortunately, head and pubic lice do not transmit systemic disease. Hence, treatment is directed at relieving symptoms and preventing reinfestation and transmission.

CLINICAL PRESENTATIONItching is the primary symptom of pediculosis. It is the result of an allergic reaction to louse saliva and takes two or more weeks to develop. By this time, the infestation is well established.

DIAGNOSISHead and pubic lice infestations are diagnosed by finding lice or viable eggs (nits) on examination. Excoriations and pyoderma also may be present.

Lice can be difficult to detect. A bright light, a magnifying lens, and separating the hair aids inspection. However, combing through the hair with a louse comb and examining the teeth of the comb for living lice detects more cases than direct visualization alone. 3 The presence of a single live louse is adequate for the diagnosis of active infestation. The presence of nits only does not necessarily indicate active infestation.4 If only nits are found, they should be examined microscopically for viable embryos (Figure 2).

The diagnosis of body lice may be suggested by the presence of pruritus in homeless persons or in persons who live in situations in which bedding and clothing are not changed regularly. Examination may show generalized excoriations. In addition, body lice should be confirmed in the seams of clothing.

LIFE CYCLE OF HEAD LICEThe head louse begins as an egg laid near the scalp and “glued” firmly to a hair shaft. After three to four days, the embryo's central nervous system is fully developed. It hatches as a nymph in seven to 10 days. Nine to 12 days after hatching, the nymph develops into a sexually mature male or female.

Within 24 hours of mating, the mature female louse begins laying seven to 10 eggs a day. Repeated fertilization is not required. Head lice of both sexes have a life span of as much as 30 days. They survive only 15 to 20 hours off the host.

Nymphs and adult head lice take frequent blood meals, contributing to the symptoms of itching.

TREATMENT OF HEAD LICEMost topical and systemic treatments are toxic to the nervous system of the louse. Because some developing embryos survive initial treatment, a second course of treatment, seven to 10 days after the first course, is recommended to kill newly hatched nymphs.

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FIGURE 2.

(Top left) Microscopic appearance of a viable nit. In moderate climates, viable nits are usually found within 1 cm of the scalp and contain an embryo that occupies most of the nit. A viable embryo should show some movement inside the nit. Often one or two prominent eye spots are visible, and the nit has a rounded distal end, the operculum. (Bottom right) Microscopic appearance of a nonviable nit. The operculum is missing, giving a flat appearance to the distal end. The hatched nit with an absent embryo is nearly transparent. Dandruff, remnants of hair spray, and other debris that may be mistaken for nits are not usually fixed firmly to the hair shaft and do not have the typical appearance of a nit.

Topical AgentsIn the United States, several topical agents are available for the treatment of head lice infestation. All over-the-counter agents approved by the U.S. Food and Drug Administration (FDA) belong to the pyrethrum group of insecticides (pyrethroids). Both 4 percent piperonyl butoxide–0.33 percent pyrethrins (e.g., Rid, Pronto) and 1 percent permethrin (Nix) are safe and effective. Experts consider permethrin the treatment of choice.5

The pyrethrum insecticides are pregnancy category B drugs. Their safety in breastfeeding is unknown.

A 0.5 percent malathion lotion (Ovide) is available by prescription. 6 It is highly effective in the treatment of resistant head lice infestation in the United States. Because of its odor, flammability, and potential for causing respiratory depression if ingested, malathion is considered a second-line agent. Malathion should not be used in neonates and infants; its safety in nursing mothers and children under six years of age is uncertain. Malathion is a pregnancy category B drug.

Two recent evidence-based reviews found that malathion, permethrin, and pyrethrum insecticides were equally effective in treating head lice infestations.7,8 [Reference 8—Evidence level A, randomized controlled trial]

A 1 percent lindane shampoo is also used to treat resistant head lice infestations. However, lindane shampoo is used infrequently now because of concerns about neurotoxicity, resistance, and slow killing time.

Topical agents are more likely to be effective when they are applied to dry hair. 9 Successful treatment requires strict adherence to directions for application. The importance of

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environmental measures is controversial. A recent study10 failed to show that nit removal improved treatment efficacy. Screening of household contacts and treatment of those infested or sharing the same bed as the index case may reduce reinfestation. Treatment should be repeated after seven to 10 days if live lice are present.

Oral AgentsIvermectin (Stromectol), in an oral dose of 200 mcg per kg, effectively kills nymphs and lice, but not eggs. To kill newly hatched nymphs, a second dose should be given seven to 10 days after the first dose. Treatment with this agent occasionally is associated with mild, transient side effects such as rash or pruritus, but no serious adverse reactions have been reported.

Pediculosis is not an FDA-labeled indication for ivermectin. In the United States, the drug is not labeled for use in children weighing less than 15 kg (33 lb). Ivermectin is a pregnancy category C drug, and safety in breastfeeding is unknown.

Trimethoprim-sulfamethoxazole (Bactrim, Septra) has been used in the treatment of head lice infestation, although frequent allergic reactions and treatment failure limit its efficacy.11 Trimethoprim-sulfamethoxazole is not toxic to the louse; instead, it acts by killing essential bacterial flora in the insect's gastrointestinal tract.

Treatment FailureCauses of treatment failure are listed in Table 1. Resistance should be suspected if live lice are still present 12 to 24 hours after treatment and no other cause for failure can be found. Resistant infestations should be treated with an agent from a different insecticide class (e.g., malathion when a pyrethrin or permethrin product was initially used). Treatment with a second agent in the same class (e.g., pyrethrin for permethrin) will result in another failure. Higher concentrations or longer application times for the same agent kill few additional resistant lice.2

Alternative TherapyPatients who do not wish to use topical insecticides or systemic agents to treat head lice infestation may try alternative treatments. Many over-the-counter herbal shampoos and pomades are available, but they have not been tested for efficacy. Cure through physical removal alone has demonstrated a 38 percent cure rate in one study.12 Head shaving is also effective.

Lice, including nits, are difficult to kill by suffocation. Applying olive oil or petrolatum ointment and covering the head with a shower cap for four to six hours a day for three or four consecutive days may succeed. However, olive oil and petrolatum ointment are difficult to remove from the hair after treatment. Petrolatum ointment, however, is the preferred treatment for infestations of the eyelashes and eyebrows.

Environmental MeasuresAlthough nit removal after treatment is often difficult and controversial, some think it may improve efficacy and reduce the risk of transmission before a second treatment. Use of a 50

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percent vinegar and water rinse after shampooing may help slightly with nit removal.13 Thorough wet-combing with a nit comb aids in nit removal. Use of a hair conditioner makes wet-combing easier.

Bedding and recently worn clothing may be decontaminated by hot-water washing (60°C [140°F]) and heated drying, or by dry cleaning. Brushes, combs, and hair ornaments may be soaked in hot water for 10 minutes. The importance of these measures, however, is controversial. Concurrent treatment of infested personal contacts and persons sharing the same bed may prevent reinfestation. Extensive environmental measures, such as spraying pediculicides on furniture, are unnecessary. Mass school-wide screening and “no nit” policies for school reentry have not been shown to be effective.

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FIGURE 3.

Sarcoptes scabiei, or scabies mite.

Reprinted with permission from National Pediculosis Association, accessed November 2003 fromhttp://www.headlice.org.

PUBIC LICEPubic lice are readily transmitted sexually. Perhaps they occasionally may be transmitted through contaminated clothing or towels, although this is controversial. The presence of pubic lice should prompt an evaluation for other common sexually transmitted diseases, such as chlamydial infection and gonorrhea. Treatment is the same as for head lice. Sexual contacts also should be treated if infested.

BODY LICEPatients with body lice infestations should wash their entire body thoroughly and then put on clean clothing. If the infestation is severe, topically administered permethrin, pyrethrin, or malathion also may help. Oral ivermectin is an alternative to topical treatment. Clothing and bedding should be decontaminated by hot-water washing (60°C) and heated drying, or by dry cleaning.

Body lice may transmit typhus and trench fever. Outbreaks of trench fever have occurred in homeless persons in the United States.14

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ScabiesScabies is caused by the parasitic mite Sarcoptes scabiei (Figure 3). Although intense pruritus, papular rash, and excoriations are characteristic, variable forms exist and may mimic other conditions.

CLINICAL PRESENTATIONIn adults, classic scabies presents as a pruritic, papular rash with excoriations. The itching in scabies is caused by a delayed hypersensitivity reaction to mites, eggs, and fecal pellets. Papules and burrows generally follow a characteristic distribution, with the head and neck typically spared (Figure 4).

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FIGURE 4.

Characteristic distribution of lesions in adults with classic scabies. Burrows are more common on hands and wrists, whereas papular or nodular lesions generally are present elsewhere.

In infants and small children, the scabies rash may include vesicles, pustules, or nodules, and the head and neck may not be spared. The lesions are generally distributed but are concentrated especially on hands and feet and in body folds (Figure 5).

Scabies should be suspected when an elderly patient has an intensely pruritic condition. In the elderly, scabies lesions may be bullous. The rash often is misdiagnosed and treated with a topically administered steroid, which leads to crusting and diffuse erythema. Papules are often scant. Excoriations are frequently prominent on the buttocks and back.

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FIGURE 5.

Papular scabies rash in a child's axilla. Papular lesions often are present under the breasts, around the belt line, and on the penis.

Immunocompromised patients with scabies may have crusting of lesions, and itching may be absent. The crusting may be localized or generalized. Patients with human immunodeficiency virus infection sometimes have papular or even nodular eruptions.

LIFE CYCLE OF SCABIES MITELike pediculosis, scabies is caused by an obligate human parasite that is transmitted by human-to-human contact. Scabies mites can survive up to four days off the host. During that time, reinfestation is possible. The female mite burrows under the skin and, before dying, lays 10 to 25 eggs. Three days later, the eggs hatch. The larvae move to the skin surface and mature into adults after 14 to 17 days.

DIAGNOSISThe combination of a history of pruritus (especially at night), a classic rash, and itching in household or sexual contacts is adequate for the diagnosis of scabies. Mites seen on microscopic examination of skin scrapings confirm the diagnosis.

Skin scrapings obtained from the leading edge of the burrow and under the fingernails are most likely to produce a mite. Slicing through the stratum corneum with a no. 15 scalpel blade and examining the burrow under magnification also may visualize mites. For the diagnosis of scabies, skin scrapings have high specificity but low sensitivity. Punch biopsy of a burrow is often unsuccessful in identifying mites or eggs. If treatment fails to improve symptoms after two to three weeks, skin scrapings are essential for diagnosis.

TREATMENT OF CLASSIC SCABIESTopical AgentsIn adults and children over five years of age, 5 percent permethrin cream (Elimite) is standard therapy for scabies. This agent is highly effective, minimally absorbed, and minimally toxic. Adverse effects include itching and stinging on application. After the patient bathes or showers, 5 percent permethrin cream is applied to the entire body from the neck down. The

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cream is washed off after eight to 14 hours. Unless new lesions develop within 10 days, retreatment is unnecessary.

The 5 percent permethrin cream may be used in infants more than two months of age. In children less than five years of age, the cream must be applied to the head and neck, as well as the body.

Permethrin is a pregnancy category B drug and has been used without apparent ill effects in pregnant women. Its safety in breastfeeding is unknown. When a nursing mother has to be treated with permethrin, it would be appropriate for her to bottle-feed her infant and discard pumped breast milk until residual cream has been washed off thoroughly.

Previously, 1 percent lindane lotion was the standard treatment for classic scabies. Although lindane is generally effective, treatment resistance has occurred.15  The chief advantage of lindane is its low cost (Table 2). The primary disadvantage is the potential for neurotoxicity, if misused, which may be increased in patients with major breaks in their skin (e.g., those with crusted scabies) or in infants and small children. Lindane lotion is applied like permethrin cream, but it is washed off after six hours and reapplied one week later.

A 10 percent crotamiton cream (Eurax) can be applied to scabies nodules in children. The cream should be left on the nodules for 24 hours, washed off, and then reapplied for an additional 24 hours.16

In newborns and pregnant or lactating women with classic scabies, 5 or 10 percent precipitated sulfur in petrolatum is probably effective.17 However, there are no controlled trials of efficacy or safety. This agent is inexpensive and can be made by a compounding pharmacy. It should be applied to the entire body (including the head and neck in newborns) for 24 hours and then reapplied every 24 hours for the next two days. A bath should be taken before each application and 24 hours after the last application. All clothing and bed linens should be changed when treatment is completed. Environmental control is essential for successful treatment.

When a scabicide is prescribed, the patient (or a parent or other caregiver) should be informed that itching may persist for up to four weeks after successful treatment. It may take that long for the skin to slough residual mite debris and for the allergic reaction to subside. Itching may be managed with antihistamines and, if necessary, the addition of a topical steroid. However, steroids should not be prescribed before the completion of primary therapy.

Environmental MeasuresOnce scabies has been diagnosed, the physician should explain its basic epidemiology. Otherwise, medication alone might be relied on to eradicate the infestation. If environmental control measures are not instituted, treatment failure will occur, because mites are able to survive and reinfest the patient. Thus, it is critical to decontaminate all linens, towels, and clothing used in the previous four days by hot-water washing (60°C) and heated drying. Items that cannot be washed in hot water should be dry cleaned or sealed in a plastic bag for five

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days. Even if household and sexual contacts have no symptoms, they should follow the same cleaning procedures. Treatment must be simultaneous for all.

GENERALIZED CRUSTED SCABIESTwo issues must be considered in the topical treatment of generalized crusted (Norwegian) scabies. First, crusting diminishes the penetration of medication into burrows. Second, crusting may alter systemic absorption of scabicides because of changes in normal skin integrity.

Topical AgentsAlthough effectiveness is reduced, 5 percent permethrin cream may be used safely in patients with crusted scabies. Keratolytics aid treatment by improving the penetration of permethrin into burrows.

TABLE 2Scabies Treatments

The rightsholder did not grant rights to reproduce this item in electronic media. For the missing item, see the original print version of this publication.

IvermectinOral ivermectin is a new and promising treatment for crusted scabies. Because of its effectiveness and convenience, ivermectin is becoming the agent of choice in crusted scabies treatment, community eradication programs, and general scabies therapy. Studies have demonstrated its safety and efficacy.18,19 In one study,20 a single dose of this agent (200 mcg per kg) eradicated scabies in 70 percent of patients; optimal dosage and timing of the second dose vary.21

Ivermectin is not labeled for the treatment of scabies. Although infants elsewhere in the world reportedly are treated with ivermectin, the FDA has not labeled this drug for use in children weighing less than 15 kg (33 lb). Ivermectin is a pregnancy category C drug. It is excreted in low concentrations in breast milk. In third-world countries, it has been used to treat onchocerciasis in pregnant and nursing women, with no teratogenic effects observed.20

In pregnant or lactating women and in newborns, 5 or 10 percent precipitated sulfur in petrolatum is a safe, effective treatment for generalized crusted scabies. Treatment is as described for classic scabies.

REFERENCE1. Meinking TL, Entzel P, Villar ME, Vicaria M, Lemard GA, Porcelain SL. Comparative efficacy of treatments for pediculosis capitis infestations. Arch Dermatol. 2001;137:287–92....

This article is one in a series coordinated by Daniel L. Stulberg, M.D., director of dermatology curriculum at the Utah Valley Family Practice Residency Program, Provo, Utah.

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Cutaneous larva migrans

Cutaneous larva migrans (CLM) is the most frequent travel-associated skin disease of tropical origin. 1,2 This

dermatosis first described as CLM by Lee in 1874 was later attributed to the subcutaneous migration

of Ancylostoma larvae by White and Dove in 1929.3,4 Since then, this skin disease has also been called

creeping eruption, creeping verminous dermatitis, sand worm eruption, or plumber’s itch, which adds to the

confusion. It has been suggested to name this disease hookworm-related cutaneous larva migrans (HrCLM).5

Although frequent, this tropical dermatosis is not sufficiently well known by Western physicians, and this can

delay diagnosis and effective treatment. Indeed, misdiagnosis or inappropriate treatment affects 22% to 58%

of the travelers with CLM.6–8 In one case report, the time lag between the onset of disease and the diagnosis

was 22 months.9

Five large (>40 patients each) published studies of imported cases of CLM in returning travelers have greatly

helped improve knowledge of this disease.2,6–8,10 This is particularly true as regards its natural history and

response to treatment in short-term travelers without possibility of recontamination.

We reviewed the epidemiological, clinical, and therapeutic data drawn from studies of CLM in travelers. The

aim of this review was to contribute to a better definition and description of the disease known as HrCLM

Epidemiological data

HrCLM is one of the leading causes of dermatologic disorders observed in ill returned travelers. 1,2,11 Risk

factors for developing HrCLM have specifically been investigated in one outbreak in Canadian tourists: less

frequent use of protective footwear while walking on the beach was significantly associated with a higher risk

of developing the disease, with a risk ratio of 4. Moreover, affected patients were somewhat younger than

unaffected travelers (36.9 vs 41.2 yr, p= 0.014). There was no correlation between the reported amount of

time spent on the beach and the risk of developing CLM. Considering animals in the neighborhood, 90% of

the travelers in that study reported seeing cats on the beach and around the hotel area, and only 1.5% noticed

dogs.

Geographical distribution

Published cases in Western countries mainly concern tourists returning from tropical areas.6–8 The hookworms

responsible for CLM are distributed worldwide, but infection is more frequent in the tropical and subtropical

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countries of Southeast Asia, Africa, South America, Caribbean, and the southeastern part of the United

States.8 In a prospective analysis of parasitic infections in Canadian travelers and immigrants, CLM was one

of the leading causes of infections and was primarily acquired in beach destinations such as Jamaica,

Barbados, Brazil, Thailand, and Mexico.11 HrCLM is rare in temperate countries, but a few autochthonous

cases have been reported from Europe, North America, and New Zealand. 13–18 HrCLM is common in the

economically deprived communities of some areas in Brazil, but the clinicoepidemiologic pattern is different

from that observed in travelers.19,20

Pathophysiology

HrCLM is caused by the penetration of the skin by cat, dog, or other mammal nematode larvae. The main

culprit species are Ancylostoma braziliense and Ancylostoma caninum, but other animal hookworms

like Uncinaria stenocephala and Bunostomum phlebotomum are possible agents of HrCLM.6,8,10,21 The adult

hookworms live in animal intestines, and their eggs are spread on the soil during defecation. Egg hatching

and larva survival are facilitated by moist grounds like beaches. After two molts in the soil, larvae become

infectious and acquire the ability to penetrate the host skin.8,13 The infection is usually acquired via contact

with soil or sand contaminated with feces of infected cats or dogs, which explains why bare feet are the

predominant site of penetration by the parasite larvae. In contrast to cats and dogs, humans are incidental

hosts, and the larvae are unable to complete their natural cycle; thus, they are not able to deeply penetrate the

human skin and consequently migrate within it for weeks.8 During skin penetration, the secretion of

hyaluronidase by hookworm larvae facilitates passage through the epidermis and dermis. 22 Usually, the typical

eruption develops within a few days, and the larva itself is usually located 1 to 2 cm ahead of the

eruption.6 Without appropriate treatment, the larva dies and is resorbed within weeks or months of

invasion.23 Most of the time, the infection is restricted to the skin, but migration to the lung has been reported

and is responsible for pulmonary eosinophilic infiltrate.

Clinical presentation

The clinical features of HrCLM have been accurately described in five large series of travelers admitted to

tropical medicine clinics2,6–8,10and in two outbreaks (Table   1 ).12,26 The incubation period of HrCLM is usually a

few days and rarely goes beyond 1 month. Cutaneous lesions appeared after return in 51% to 55% of the

travelers, and the mean time of onset after return ranged from 5 to 16 days. 2,7,8 In a German study, the time of

onset ranged from 16 weeks before return to 28 weeks after return (mean: 1.5 d after return). In the two

above-mentioned outbreaks of CLM, the median time from the start of the trip to the development of the

eruption ranged from 10 to 15 days.12,26However, some extremely long incubation periods have been reported,

lasting for 4 to 7 months.6,7

Date 1993 1994 1995 2000 2001 2000

1st author Davies8 Jelinek6 Caumes2 Bouchaud7 Blackwell10 Tremblay12

Study type Retrospective Retrospective case Prospective Prospective Retrospective Outbreak,

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case study study

study of

travel- associ

ated

dermatitis

study case study

retrospective

(questionnaire-

based study)

Study site Canada Germany France France England Canada

Population

Canadian

(97%),

immigrant

(3%)

German (100%)French

(100%)

French

(100%)

Europeans (98%),

immigrant (2%)

Canadians

(100%)

Number of

patients60 98 67 64 44 32

Male-to-female

ratio0.8 1.2 — 1.4 1 1

Mean age 29.2 (5–73) 32 — 33 (1.5–73) 28.9 (3.5–70) —

Country visited

Caribbean

(75%), Brazil

(8.3%),

Mexico (5%)

Southeast Asia

(31.6%), Caribbean

(19.4%), South

America (13.4%),

East Africa (10.2%),

Indian subcontinent

(10.2%), Central

America (8.2%),

West Africa (5.1%)

—

Caribbean

(39%), Asia

(25%), Latin

America

(19%), Africa

(17%)

Africa (32%),

Caribbean (30%),

Southeast Asia

(25%), Central

America (11%),

South America

(2%)

Barbados

Mean duration of

travel (days)

14.4 ± 13.5 d

(with a mode

of 7 d)

6 (1–72) — 28 (6–90) — 7

Barefoot walk or

sandy beach

exposure

95% — — — 95% beach 100% beach

Misdiagnosed or

inappropriately

treated prior to

diagnosis (%)

58 22 — 55 27.5 46.7

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Mean/median time

from arrival in the

tropics to onset of

symptoms

15 d (2–50)

(mean)— —

21 (5–135)

(median)—

15.5 (5–34)

(median)

Mean/median time

of onset of

symptoms from

departure from the

tropics

5 (0–30)

(mean)—

8 (0–28)

(median)

16 (1–120)

(mean)— —

Onset after return

(%)45 75 51 55 — —

Median duration

of symptoms— 5.6 wk (1–36) — 4 wk 8 wk (1–104) 24.5 d (7–49)

Anatomic location (%)

 Feet 87 62 66 48 39 100

 Buttocks 5 13 3 23 18 —

 Thigh (upper

legs)5 9 — 16 — —

 Lower legs 1.7 3 — — 12 —

 Trunk 3.3 (breast) 7 —17 (abdomen

+ chest)16 —

 Upper extremities 1.7 7 — — 14 —

 Face 0 0 — 1.5 2 —

Pruritus (%) 98 — 100 100 95 100

Serpiginous lesion

(%)96.7 — 99 — 93 96.9

Swelling (%) 17 — 6 — — —

Vesiculobullous

lesion (%)10 — 9 — 4.5 40.6

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Pain 10 — — — — —

Mean/median

number of lesions

per person

1.7 (1–6)

(mean)—

1 (1–24)

(median)

3 (1–15)

(mean)— —

Hookworm

folliculitis (%)— — 3 — — —

Superinfection 0% — — 5 (8%) 2 (5%) —

Table 1.  Main clinical features of cutaneous larva migrans in eight series (>15 patients) of travelers returning from endemic countries

The striking symptom of HrCLM is pruritus localized at the site of the eruption. It is reported in 98% to 100%

of patients.7,8 After effective treatment, the pruritus has been shown to disappear much sooner than the

eruption (on average 7.2 d earlier).12

The most frequent and characteristic sign of HrCLM is “creeping dermatitis,” a clinical sign defined as an

erythematous, linear, or serpiginous track that is approximately 3 mm wide and may be up to 15 to 20 mm in

length.27 The creeping track, associated with the larva migration, may extend a few millimeters to a few

centimeters daily.8 The mean number of lesions per person varies from 1 to 3.2,7,8

Two other major clinical signs are edema and vesiculobullous lesions along the course of the larva. Local

swelling is reported in 6% to 17% of patients and vesiculobullous lesions in 4% to 40%.2,8,10,12

Potentially, all unprotected parts of the skin in contact with contaminated soil may be involved. However, the

most frequent anatomic locations of HrCLM lesions are the feet in more than 50% of individuals, followed by

the buttocks and thighs.2,6,8,12 Other sites may include the elbow, breast, legs, and face.7,8

Without any treatment, the eruption usually lasts between 2 and 8 weeks, but it may be longer. In one case

report, an active disease was reported for almost 2 years.9

Hookworm folliculitis is a particular form of HrCLM. The largest series included seven travelers and

consisted of numerous (20–100) follicular, erythematous, and pruritic papules and pustules, located mainly on

the buttocks and associated with numerous relatively short tracks, generally arising from follicular lesions 28.

Hookworm larvae can be histologically found trapped in the sebaceous follicular canal.

Complications

Local complications are led by secondary bacterial infection of the involved skin area (impetiginization). It

occurs in up to 8% of cases.7,8

Systemic complications are uncommon and mainly involve the lungs, consisting of cases of eosinophilic

pneumonitis associated with CLM.25,30–32 Although the pathogenesis is not completely understood,

the Ancylostoma larva has been identified in the sputum in one case report.24

One case of visceral larva migrans caused by A caninum has been reported,33 together with one larval invasion

of skeletal muscles in a man who also had pulmonary symptoms.34 One case of erythema multiforme in which

HrCLM was considered as one of the triggering events has also been reported.

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Diagnosis

HrCLM is usually a clinical diagnosis based on the typical clinical presentation in the context of recent travel

to a tropical or a subtropical country and beach exposure. 5,6,8 Clinical characteristics of the creeping trail

(length, width, speed of migration, location, duration) easily help differentiate HrCLM from other causes of

creeping dermatitis.27

Blood tests are not necessary for diagnosis and are not currently recommended; no specific serological or

culture methods are currently available. Theoretically, total blood count could detect eosinophilia; this feature

was reported in 20% of the 40 patients tested among a series of 98 CLM in German travelers. 6 Nonetheless, in

the particular case of hookworm folliculitis, skin biopsy specimens may reveal nematode larvae in the

follicular canal.29 In addition, this is the only clinical form of HrCLM that gives the opportunity to diagnose

via a skin smear of a pustular lesion. Additionally, it allows the identification of the larvae of the culprit

nematode.

Differential diagnoses

The differential diagnoses include all the dermatoses that give rise to creeping dermatitis, ie, serpiginous or

linear migrating cutaneous lesions. Thus, noncreeping, linear or serpiginous dermatoses such as

phytophotodermatosis, jellyfish stings, zoster, or lichenoid eruptions are easily ruled out. Nonetheless, there

are numerous causes of creeping eruption, and, with the notable exception of creeping hair mostly described

in Japan,36,37 all of them are of parasitic origin.5,38

From a parasitological point of view, differential diagnoses include diseases in which creeping eruption may

be due to the larvae of nematodes (other than hookworms), adult nematodes, larval forms of trematodes, fly

maggots, and arthropods (Table   2 ).27

Parasite

Form of the

causal

parasite

Distribution Transmission Cutaneous signs Diagnosis

ELISA = enzyme-linked immunosorbent assay.

*

Causes of the cutaneous larva migrans syndrome sensu stricto.26

Nematode’s larvae

 Gnathostomiasis

(Gnathostoma spp.)

Larva of

animal

nematodes*

Southeast

Asia, Latin

America

Eating raw or

nearly raw fish

Creeping eruption,

migratory swelling,

nodules

Serological,

parasitological (if

the larva exists in

the skin)

 Animal hookworms,

Pelodera strongyloides,

Larva of

animal

Tropical and

subtropical

Skin penetration Cutaneous trail,

pruritus, bullae,

Parasitological (in

case of

14

Parasite

Form of the

causal

parasite

Distribution Transmission Cutaneous signs Diagnosis

zoonoticStrongyloides spp. nematodes* folliculitis folliculitis)

 Spirurina spp.39

Larva of

animal

nematodes*

Asia

Eating raw or

nearly raw fish

and shellfish

25 cm long serpiginous

red track with vesicles

Serological

(ELISA)

 Strongyloides stercoralis

Larva of

human

nematodes

Tropical and

subtropicalSkin penetration

Usually one burrow, on

the abdomen or

buttocks; lasts for a few

hours only, recurrences,

larger and fast moving

(larva currens)

Stool test

Adult nematodes

 Loiasis (Loa loa)Adult

nematode

Central

African

forest

Diptera bites

(Chrysops)

Calabar swelling, loa

loa migration under the

skin/conjunctiva

Microfilaremia,

serological

 Dracunculiasis (Dracunculus

medinensis)

Adult

nematode

Sub-Saharan

Africa,

extinction in

view

Drinking

contaminated

water

Limb swelling,

cutaneous ulcer,

serpiginous trail

Clinical,

parasitological

Trematode’s larvae

 Fascioliasis (Fasciola

gigantica)40

Larva of

animal

trematode

Asia

Eating raw

vegetables

(cress,

dandelion)

Dark red and

serpentine, tunnel-like

track

Serological,

parasitological

(after extraction),

stool test

Fly’s maggot

 Migratory myiasis

(Gasterophilus spp.)

Larva of

Diptera

(maggot)

Tropical and

subtropicalSkin penetration Cutaneous trail

Anatomical (after

extraction)

Arthropod

15

Parasite

Form of the

causal

parasite

Distribution Transmission Cutaneous signs Diagnosis

 Scabies (Sarcoptes scabiei)41Adult

arthropodsWorldwide

Skin-to-skin

contact with a

person already

infested with

scabies

Linear burrow, papules,

vesicles

Direct

examination of

skin scrapings

using microscope

Table 2.  Main parasites causing creeping eruption

Animals host other nematode larvae that may infect men, such as Gnathostoma spp.

(gnathostomiasis), Pelodera strongyloides, andSpirurina sp.,5,39,42,43 which are other causes of the CLM

syndrome.27 But other larvae of helminths may cause creeping dermatitis such asStrongyloides

stercoralis (larva currens),44 a human nematode, and Fasciola gigantica (fascioliasis),40 a human trematode. In

the case of hookworm folliculitis, bacterial folliculitis is the main differential diagnosis, but it is nonpruritic.28

From a clinical point of view, differential diagnoses do not include parasites whose larvae do not give rise to

migratory signs when they travel through the skin (cercarial dermatitis, onchocerciasis, dirofilariasis).

Treatment

Oral ivermectin and albendazole have become the first-line treatments as thiabendazole is no longer marketed

and thus is no longer available worldwide.45 Ivermectin is a synthetic derivative of the antiparasitic class of

avermectins.46 Taken in a single dose, ivermectin is well tolerated and highly efficacious, with cure rates of

94% to 100% in all but one of the largest series.7,45,47,48

After ivermectin treatment, symptoms disappear within 1 week: 3 days (1–20) for pruritus and 7 days (1–30)

for creeping dermatitis.7

In case of initial failure or relapse, cure can be obtained with one or two repeated courses of

ivermectin.7,48 Side effects related to ivermectin in this use are rare and not systemic; local bullous reactions

have been reported.7,47

Albendazole, a third-generation, heterocyclic, anthelmintic drug, is also effective and well tolerated. In the

absence of consensual optimal dosage, the regimen should be 400 to 800 mg/d (according to weight) for 3

days.10,45,47,49,50

In the case of hookworm folliculitis, treatment is more difficult than in traditional form and necessitates

repeated courses of oral anthelmintic agents.28 For lightweight children or when oral ivermectin and

albendazole are contraindicated, then the application of a 10% albendazole ointment, twice a day for 10 days,

is a safe and effective alternative treatment.51

Cryotherapy with liquid nitrogen is not recommended. Freezing is ineffective because the larva is usually

located several centimeters beyond the visible end of the trail, and the larvae are capable of surviving

16

temperatures as low as −21°C for more than 5 minutes; moreover, this procedure is painful and can lead to

chronic ulcerations.

Prevention

The best way to prevent HrCLM is to wear protective footwear when walking on the beach because avoiding

tropical beaches frequented by dogs and cats or banning animals from beaches in tropical areas is

impossible.12,52 When lying on tropical beaches potentially frequented by dogs and cats, areas of sand washed

by the tide are preferable to dry sand, and mattresses are preferable to towels.45

Conclusions

HrCLM is a striking example of how travel medicine contributes to improved knowledge of tropical diseases.

Indeed, the description of HrCLM in large series of briefly exposed travelers has contributed to a better

understanding of the incubation period and natural history of the disease. It has helped distinguish it from

other causes of CLM and creeping dermatitis. Finally, it has provided the opportunity to assess the efficacy of

various treatments more reliably than in inhabitants of endemic areas in whom it may be impossible to

distinguish relapses from reinfections.

Declaration of interests

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