Creeping Eruption-Cutaneous Larva Migrans

June 28, 2013

Cutaneous larva migrans (CLM), also known as “creeping eruption,” is the most commonly acquired tropical dermatosis

A 6-year-old boy presented with a 1-month history of an intensely pruritic “rash” that involved the left dorsal foot and left lower leg (Figure). He had a recent history of walking barefoot on a beach in south Florida where dogs are allowed.

The patient’s initial presentation involved an erythematous serpiginous tract on the dorsomedial aspect of the distal left foot. Over the next 4 weeks, the lesion extended from the foot all the way up the lower leg in a serpentine fashion. The migrating lesion stopped just below the knee on the medial aspect of the lower leg.

The advancement of the serpiginous plaque prompted a visit to the emergency department (ED). Suspicious of cutaneous larva migrans (CLM), the ED personnel prescribed an oral anthelmintic drug, albendazole, 400 mg taken daily for 7 days. The patient also was referred to a dermatology office for further evaluation.

At the evaluation, physical examination revealed a systemically well-appearing 6-year-old boy. An erythematous, approximately 3-mm-wide tract extended from the dorsomedial aspect of the distal left foot to the medial aspect of the proximal lower leg. Even though treatment was almost complete, the lesion continued to look active, with papules and erythema.

Continuation of the albendazole prescribed by the ED was recommended. In addition, cryotherapy was used 1 cm from the leading edge of the visible tract. Hydroxyzine, 7.5 mL at bed time, as needed, was advised for the persistent itching. Tips for prevention, including wearing shoes when walking in sandy areas and avoiding beaches cohabited by dogs, were given to the patient’s parents.

A 2-week follow-up visit was arranged. On the visit, the patient reported a resolution of his pruritus. The tract looked hypopigmented and was healing well.

Cutaneous larva migrans (CLM), also known as “creeping eruption,” is the most commonly acquired tropical dermatosis. CLM is caused by the larvae of an animal hookworm. Ancylostoma braziliense hookworm is the most common cause1; others include Ancylostoma caninum and Uncinaria stenocephala.2

These hookworms usually live in the intestines of dogs, cats, and other mammals. When they lay their eggs in the intestines of their host, the eggs are released with the animal feces and are deposited into the soil or sand,1 where the eggs hatch into larvae. The larvae feed on the bacteria present in the soil and, eventually, mature into infectious filariform larvae.2

The infectious larvae use proteases to penetrate intact bare skin or even a thin layer of clothing, such as a bathing suit.3 They burrow into the skin but usually stay confined to the upper dermis because humans are an incidental host.

As a larva migrates through the skin with the help of hyaluronidase secretion, it leaves a raised, erythematous, serpiginous tract, often with vesicles. This trail, or creeping eruption, is pathognomonic for CLM and almost always is associated with severe pruritus.2

CLM is found in tropical climates, such as those in Africa, Latin America, the Caribbean, and southeastern Asia, as well as in the southeastern United States. Diagnosis primarily is based on clinical findings. Laboratory tests are not necessary for diagnosis, although they may reveal a transient peripheral eosinophilia as well as elevated serum IgE levels.

CLM often is self-limited because humans are accidental dead-end hosts. The larvae eventually die off (usually within 4 to 8 weeks), and the lesions resolve uneventfully.

Treatment is suggested because intense pruritus accompanies this disease and increases the risk of excoriation and impetiginization. In rare cases, the larvae may enter the circulation, causing Lffler syndrome. The sequelae include asthma, pulmonary infiltrates, eosinophilia, and fever.3

Treatment options for patients with CLM include cryotherapy, topical or oral thiabendazole, oral albendazole, and oral ivermectin. Cryotherapy may be used to kill the larvae beneath the skin. Because the tissue reaction is delayed 24 to 48 hours, the larvae usually are positioned 1 or 2 cm ahead of the visible tract. Because the larvae cannot be located easily, this method of treatment is not always effective.2,3

Topical application of 10% to 15% thiabendazole is used most frequently for uncomplicated cases of CLM. Patients tolerate it well without systemic adverse effects. Oral thiabendazole is used less frequently because of its common adverse effects, such as nausea, vomiting, and dizziness. Oral albendazole and ivermectin are both effective against CLM and are well tolerated by patients. Oral formulations are preferred for extensive lesions and for patients for whom a trial of topical therapy is not successful.3

In our patient’s case, treatment with albendazole had been initiated by another physician. This therapy was appropriate because the lesion had extended the entire length of the lower leg. Thus, the recommendation was made to continue treatment with albendazole as well as perform cryotherapy.

Take-Home Points
• A pruritic, erythematous tract across the skin (characteristic sign) and residence in or recent travel to a tropical area provides strong evidence for CLM
• Patient report of walking barefoot on the beach or sitting in dirt may provide a clue to the diagnosis
• Although it is self-limited, CLM should be treated
• If the infection is minimal and uncomplicated, begin with a topical anthelminthic drug, such as thiabendazole
• For extensive infection, initiate treatment with an oral anthelminthic drug, such as albendazole or ivermectin
• Cryotherapy can be considered as adjuvant treatment

1. Caumes E. Treatment of cutaneous larva migrans. Clin Infect Dis. 2000;30:811-814.
2. Jelinek T, Maiwald H, Nothdurft HD, Lscher T. Cutaneous larva migrans in travelers: synopsis of histories, symptoms, and treatment of 98 patients. Clin Infect Dis. 1994;19:1062-1066.
3. Brenner MA, Patel MP. Cutaneous larva migrans: the creeping eruption. Cutis. 2003;72:111-115.