Cutaneous Larva Migrans

Cutaneous larva migrans (CLM) is the most common tropically acquired dermatosis whose earliest description dates back more than 100 years. Cutaneous larva migrans manifests as an erythematous, serpiginous, pruritic, cutaneous eruption caused by accidental percutaneous penetration and subsequent migration of larvae of various nematode parasites. Cutaneous larva migrans is most commonly found in tropical and subtropical geographic areas and the southwestern United States. It has become an endemic in the Caribbean, Central America, South America, Southeast Asia, and Africa. However, the ease and the increasing incidence of foreign travel by the world's population have no longer confined cutaneous larva migrans to these areas.[1, 2, 3, 4, 5, 6, 7]

Also see the Medscape Drugs & Diseases article Pediatric Cutaneous Larva Migrans.

In cutaneous larva migrans (CLM), the life cycle of the parasites begins when eggs are passed from animal feces into warm, moist, sandy soil, where the larvae hatch. They initially feed on soil bacteria and molt twice before the infective third stage. By using their proteases, larvae penetrate through follicles, fissures, or intact skin of the new host. After penetrating the stratum corneum, the larvae shed their natural cuticle. Usually, they begin migration within a few days.

In their natural animal hosts, the larvae of cutaneous larva migrans are able to penetrate into the dermis and are transported via the lymphatic and venous systems to the lungs. They break through into the alveoli and migrate to the trachea, where they are swallowed. In the intestine they mature sexually, and the cycle begins again as their eggs are excreted.

Humans are accidental hosts, and the larvae lack the collagenase needed to penetrate the basement membrane and invade the dermis. Therefore, cutaneous larva migrans remains limited to the skin when humans are infected.

The pruritic symptoms occur secondary to an immune response to both the larvae and their products.[8]

Common etiologies and where the parasites of cutaneous larva migrans (CLM) are most commonly found include the following:

• Ancylostoma braziliense (hookworm of wild and domestic dogs and cats) is the most common cause.[9] It can be found in the central and southern United States, Central America, South America, and the Caribbean.[10]

• Ancylostoma caninum (dog hookworm) is found in Australia.

• Uncinaria stenocephala (dog hookworm) is found in Europe.

• Bunostomum phlebotomum (cattle hookworm)

Rare etiologies include the following:

• Ancylostoma ceylonicum

• Ancylostoma tubaeforme (cat hookworm)

• Necator americanus (human hookworm)

• Strongyloides papillosus (parasite of sheep, goats, and cattle)

• Strongyloides westeri (parasite of horses)

• Ancylostoma duodenale

• Pelodera (Rhabditis) strongyloides[11]

• Gnathostorna spinigerum

• Strongyloides stercoralis

• Bunostornum phlebotomum

• Strongyloides myopotami

• Strongyloides procyonis[8]

Frequency

Cutaneous larva migrans is rated second to pinworm among helminth infections in developed countries. Prevalence is high in regions of warm climate, where individuals may be more inclined to walk barefoot (eg, beaches, lower socioeconomic communities) and come in contact with animal feces.[12, 13]

Race

No specific racial predilection exists because cutaneous larva migrans depends on exposure.

Sex

Cutaneous larva migrans demonstrates no specific sexual predilection because cutaneous larva migrans depends on exposure.

Age

Cutaneous larva migrans can affect persons of all ages because it depends on exposure, but it tends to be seen in children more commonly than in adults.

The prognosis for cutaneous larva migrans is excellent. Cutaneous larva migrans is a self-limiting disease. Humans are accidental, dead-end hosts, with the larva dying and the lesions resolving within 4-8 weeks, as long as 1 year in rare cases.

Persons who travel to tropical regions and pet owners should be aware of this condition. For patient education resources, see the patient education article Foreign Travel.

History findings may be as follows:

• Tingling/prickling at the site of exposure within 30 minutes of penetration of larvae, although Archer described a case of late-onset cutaneous larva migrans (CLM)[14]

• Intense pruritus

• Erythematous, often linear lesions that advance

• Often associated with a history of sunbathing, walking barefoot on the beach, or similar activity in a tropical location

Predispositions to contracting cutaneous larva migrans include the following:

• Hobbies and occupations that involve contact with warm, moist, sandy soil

• Tropical/subtropical climate travel

• Barefoot beachgoers/sunbathers

• Children in sandboxes

• Carpenter

• Electrician

• Plumber

• Farmer

• Gardener

• Pest exterminator

Cutaneous signs of cutaneous larva migrans (CLM) include the following:

• Pruritic, erythematous, edematous papules and/or vesicles

• Serpiginous (snakelike), slightly elevated, erythematous tunnels that are 2- to 3-mm wide and track 3-4 cm from the penetration site

• Nonspecific dermatitis

• Vesicles with serous fluid

• Secondary impetiginization

• Tract advancement of 1-2 cm/day

Systemic signs are rarely seen but may include, peripheral eosinophilia (Loeffler syndrome),[15] migratory pulmonary infiltrates, and increased immunoglobulin E (IgE) levels.

Lesions are typically distributed on the distal lower extremities, including the dorsa of the feet and the interdigital spaces of the toes, but can also occur in the anogenital region, the buttocks, the hands, and the knees. Scalp lesions have been reported.[16]

See the images below.

A patient who was sunbathing nude on a beach in Martinique presented with classic erythematous, serpiginous tracts on the left heel.

Cutaneous larva migrans on the right thumb.

Cutaneous larva migrans on the left thigh.

A secondary bacterial infection in patients with cutaneous larva migrans (CLM), usually with Streptococcus pyogenes, may lead to cellulitis.

Allergic reactions may occur.

On rare occasions, Loeffler syndrome has been reported.[15]

Cutaneous larva migrans (CLM) is diagnosed by history and clinical examination. Some patients demonstrate peripheral eosinophilia on a CBC count and increased immunoglobulin E (IgE) levels on total serum immunoglobulin determinations.

A skin biopsy is not necessary for the diagnosis of cutaneous larva migrans (CLM).  A biopsy must be taken 1-2 cm ahead of the leading edge of a tract or else the larva may be missed.

Dermoscopy is an additional tool used to help confirm diagnosis and possibly direct local treatment options. With the use of polarized dermoscopy, one would see an oval structure with a yellow periphery and brown center, representing the body of the larvae.[17]

A biopsy may confirm the presence of tunneling larvae just above the dermoepidermal junction or in the superficial epidermis. The surrounding epidermis reveals spongiosis, intraepidermal vesiculation, with a mixed inflammatory infiltrate and eosinophils.

Even though cutaneous larva migrans (CLM) is self-limited, the intense pruritus and risk for infection mandate treatment. Prevention is key and involves avoidance of direct skin contact with fecally contaminated soil.

Oral albendazole, oral ivermectin, or topical ivermectin are the usual treatment choices,[18, 19, 20] along with perhaps thiabendazole (not available in the United States).[21]

In the United States, albendazole at 400 mg/day for 3 days is recommended. Alternatively, ivermectin can be administered as a 12-mg dose and repeated the next day. Some also recommend trying topical treatment with topical ivermectin or topical thiabendazole compounded in a 10% suspension or 15% cream or topical metronidazole cream, all used four times daily. If effective, the topical therapies are expected to resolve the condition in 1 week.

Outside the United States, thiabendazole has been recommended for the treatment of cutaneous larva migrans, as has oral albendazole or ivermectin.[21] Thiabendazole is not available in the United States.

Consultation with a dermatologist may be warranted.

Oral albendazole, oral ivermectin, or topical ivermectin are the usual treatment choices,[18, 19, 20] along with perhaps thiabendazole (not available in the United States).[21]

Class Summary

Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses.

Ivermectin (Stromectol)

Ivermectin is a semisynthetic macrocyclic lactone antiparasitic agent with broad-spectrum action against nematodes by producing flaccid paralysis through binding of the glutamate-gated chloride ion channels. It may become the drug of choice because of safety, low toxicity, and single dosing, which enhance patient compliance.

Albendazole (Albenza)

Albendazole is a broad-spectrum benzimidazole carbamate anthelmintic that acts by interfering with glucose uptake and disrupting microtubule aggregation. Use it as an alternative to thiabendazole.