Clinical Reference / Therapeutic Strategies / Cutaneous Larva Migrans & Larva Currens

Cutaneous Larva Migrans & Larva Currens


Key Points

Cutaneous Larva Migrans

  • Cutaneous larva migrans presents with serpiginous migratory papules due to the movement of hookworm larvae in the skin.
  • Pruritus is a cardinal feature.
  • The diagnosis is made clinically.
  • Oral ivermectin is the first-line treatment.

Introduction

Cutaneous larva migrans (CLM or creeping eruption) is a condition caused by the presence of hookworm larvae in the skin of humans, an accidental (non-definitive) host for this organism. Generally, unlike in the definitive hosts (dogs or cats), the larva is not able to penetrate the dermis and complete its life cycle of visceral organ involvement and thus remains confined to the epidermis. The larva’s migration through the epidermis prior to dying leads to hypersensitivity with often severe accompanying pruritus. Clinically this condition presents with a papule appearing a few hours to days after larval penetration followed by the appearance of migratory papules and/or vesicles in an arcuate and serpiginous configuration corresponding to the movement of the larva in the skin. The most frequent location is the lower extremities, with anogenital, truncal and upper extremity involvement being less common. The causative organisms are endemic to tropical and subtropical areas including Southeast Asia, the southeastern United States, Caribbean, South America, and Africa.

Larvae of the dog and cat hookworm, Ancylostoma braziliense are the most common cause of this condition. Less common causative organisms include the hookworm Ancylostoma caninum and Uncinaria stenocephala. The larvae hatch in the soil after the eggs are released in the feces of their animal hosts. Individuals at highest risk of being affected include travelers to endemic regions, swimmers and fishermen, children, outdoor laborers and farmers.

Initial Evaluation

Cutaneous Larva Migrans

The diagnosis of cutaneous larva migrans is generally made clinically, based upon the typical morphology of a serpiginous eruption and associated pruritus in a patient with a relevant exposure history. The typical rate of migration of the serpiginous lesion is approximately 1-2 cm per day. Because the location of the organism is not readily apparent and often a few centimeters proximal to the visible eruption, biopsy is not generally helpful diagnostically. While a peripheral eosinophilia is seen in a minority of patients, it is not necessary in confirming the diagnosis.

Differential diagnosis

Larva currens
Gnathostomasis
Loaiasis
Cutaneous pili migrans

Tinea corporis

Allergic contact dermatitis (acute)

Treatment

Cutaneous Larva Migrans

Cutaneous larva migrans is usually a self-limiting condition however, untreated cases, especially if extensive, may last for months to years or become bacterially superinfected. The therapeutic strategy is to eliminate the pathogenic organism. Pruritus symptoms typically resolve within a week after treatment, while the visible rash may take longer to resolve.

First steps

Oral ivermectin 200 mcg/kg once, or two doses on successive days.

Alternative steps

  1. Albendazole 400 mg daily for 3-7 days, depending on the severity of the disease (3 days for single lesions, 5-7 days for multifocal disease). Albendazole is preferred over thiabendazole because of the significantly lower rates of GI upset.
  2. Compounded topical preparations (if available) such as thiabendazole 15% ointment or cream applied three times daily for 5-10 days or 10% albendazole ointment three times daily for 10 days.
  3. Antihistamines may be helpful adjunctively for severe pruritus.

Subsequent steps

  1. About 90% of patients will be cured with the above regimens. Patients failing to improve after the initial dose(s) of ivermectin should have a second or third dose of 200 mcg/kg as required every two weeks.
  2. Patients failing to improve with topical thiabendazole or oral albendazole should be treated with ivermectin.

Pitfalls

  1. Despite the high success rates from the above regimens, at least 5% of patients, especially those with more widespread disease, may require more prolonged or repeated courses of treatment. Relapses may occur up to 30 days following treatment.
  2. Failure of standard therapies to cure CLM may indicate underlying immunosuppression.

Key Points

Larva Currens

  • Larva currens is a fast-moving serpiginous eruption due to skin penetration by larvae of Strongyloides stercoralis.
  • In contrast to cutaneous larva migrans, the larvae travel much more quickly through the skin and are more likely to spread hematogenously to the respiratory system.
  • In immune compromised hosts, autoinfection can lead to elevated larval burden with potential fatal outcome (hyperinfection syndrome).
  • Diagnosis may be made by stool examination, serology, or skin biopsy.
  • Ivermectin for two days is the standard treatment for uncomplicated infection, while dissemination and hyperinfection require longer treatment courses and followup to confirm clearance.

Introduction

Larva currens (“running” larva) is caused by intestinal infection with Strongyloides stercoralis, a parasitic nematode that, uniquely, can complete its entire life cycle within a human host. This organism is endemic to the tropics and subtropics and is acquired via skin penetration by infectious filariform larvae, typically by contact with soil contaminated with human feces. Patients present with serpiginous erythematous papules coalescing into urticarial linear plaques on the feet (most commonly), buttocks, upper thighs, and lower abdomen due to movement within the dermis of these larvae. In contrast to cutaneous larva migrans, the rate of migration is faster at five or more centimeters per hour (compared to 1-2 cm per day in cutaneous larva migrans).

The filariform larvae, after entering the skin, can travel via hematogenous spread to the respiratory system. From there they travel to the upper airways and are swallowed, traveling thereby to the digestive tract where they mature and lay eggs which are excreted in the feces in order to complete the life cycle. In immune compromised hosts, the larvae can undergo autoinfection whereby they re-infect the same host by burrowing into the intestinal wall or peri-anal skin, which can lead to a dramatic increase in the burden of organisms in a single host (known as hyperinfection). In this situation, patients may present with purpuric lesions on the abdomen (classically in a periumbilical distribution) due to massive larval migration within the skin. This situation may present with severe systemic manifestations and septic shock. Eosinophilia is often but not always present.

Initial Evaluation

Larva Currens

Strongyloidiasis is most commonly diagnosed via stool examination for larvae (of note, standard methods are of low sensitivity due to intermittent larval excretion and therefore modified techniques, such as specimen concentration, are used to increase diagnostic yield) or serology (ELISA for IgG). Stool tests become positive approximately three to four weeks after the organism first enters the dermis. In cases of dissemination, larvae may be found in a wide variety of body fluids. Larvae may also be seen in lesional skin biopsies. Eosinophilia is also common, though a nonspecific finding.

Differential diagnosis

Similar to that of cutaneous larva migrans (see Differential diagnosis in Cutaneous Larva Migrans).

Treatment

Larva Currens

First steps

Ivermectin 200 mcg/kg usually given in two doses on two consecutive days.

Alternative steps

Albendazole 400 mg twice daily for 3-7 days.

Subsequent steps

  • In immune compromised patients with disseminated disease, reducing the degree of immune suppression as much as feasible may be helpful, along with multiple doses of ivermectin (one dose per day for one week, e.g., for 3-7 days) until symptoms resolve (and potentially until stool ova and parasite examinations remain negative for at least two weeks).
  • If initial stool exams are positive, stool exams to confirm clearance are recommended approximately two to four weeks after treatment is complete. In patients with hyperinfection, daily stool exams are obtained for at least two weeks after treatment to confirm clearance (alternatively, serology titers may be rechecked at 3-6 months after treatment to confirm clearance).

Pitfalls

  • Albendazole has a lower cure rate in strongyloidiasis and should not be used as first-line therapy.
  • Patients with stronglyloides hyperinfection syndrome are prone to developing potentially fatal gram-negative sepsis due to translocation of gut bacteria—an index of suspicion for this should be maintained, with blood cultures checked and empiric broad spectrum antibiotics used in appropriate cases.

Subsequent steps

Patients failing to improve on short courses of ivermectin should have longer courses or repeat courses at 10- to 14-day intervals.

Clinical Case

Case 1

  • 26-year-old woman, no significant past medical history
  • Review of systems negative
  • Presents for evaluation of one-week history of very itchy rash on foot that seems to be slowly moving, recently returned from backpacking trip in Southeast Asia

Initial evaluation

  • Healthy appearing young woman
  • Serpiginous eruption of papules and vesicles in a linear arrangement on right dorsal foot

Diagnosis: Cutaneous larva migrans

  • Clinical diagnosis based on morphology and exposure history

Treatment

  • Oral ivermectin 200 mcg/kg in a single dose
  • Hydroxyzine 10-20 mg at bedtime for pruritus as needed

Follow-up evaluation

  • Patient reports resolution of itch and partial fading of rash a week later. No further movement of lesions is noted
  • Patient is followed up to ensure complete resolution one month later

References

Criado PR, Belda W Jr, Vasconcellos C, Silva CS. (2012). Cutaneous larva migrans: abad souvenir from the vacation. Dermatol Online J 18(6):11.

Kim JY, Silverman RA. Migrating hair: a case confused with cutaneous larvamigrans. (2010) Pediatr Dermatol, 27(6):628-30.

Ramanathan R, Nutman T. Strongyloides stercoralis infection in theimmunocompromised host. (2008) Curr Infect Dis Rep, 10(2):105-10.

Segarra-Newnham M. Manifestations, diagnosis, and treatment of Strongyloidesstercoralis infection. (2007). Ann Pharmacother, 41(12):1992-2001.

von Kuster LC, Genta RM. Cutaneous manifestations of strongyloidiasis. (1988). Arch Dermatol, 124(12):1826-30.