A 36-year-old male patient with a medical history of asthma, traveled with his wife to Thailand for a 21-day period starting on July 30th. The patient did not attend a pre-travel consultation and therefore did not receive any prophylaxis.
They visited Chiang Rai, Bangkok, Phuket, and Ko Tao, along with surrounding areas. They abstained from swimming in freshwater lakes or rivers but did visit several beaches populated by numerous stray dogs and cats and engaged in diving activities.
Around August 10th, the patient noted the appearance of an itchy rash on his back. He sought advice from his health insurance provider, which resulted in a prescription of antihistamines for 10 days without notable improvement. On August 18th, the rash worsened, with increased itching, folliculitis, and a new lesion on his hand.
Upon his return to Spain on August 20th, he was referred to a tertiary care hospital. Analytically, there were no abnormalities but a mild eosinophilia of 600cells/μL. PCR testing for herpesvirus and monkeypox was performed and yielded negative results, and he was discharged with a diagnosis of “coral dermatitis” along with a new prescription for cetirizine and topical corticosteroids.
Due to lack of improvement, he visited his primary care center, where his family doctor conducted a telemedicine consultation with our department, providing images of the lesions (Fig. 1). What do you consider to be the most likely etiological agent?
Diagnosis and evolution
The patient presented with inflammatory confluent red papules on the right dorsal region, interconnected by serpiginous tracts, leading to the presumptive diagnosis of cutaneous larva migrans (CLM). Similar lesions were observed on his arms (Fig. 1B).
Given the severity of symptoms, we prescribed ivermectin (200mcg/kg for 85kg, totaling 18mg/day for two days) prior to the in-person consultation. Serological tests (HIV, hepatitis, RPR, and Strongyloides spp.) and three stool samples for parasitological analysis were ordered. All tests returned negative. At consultation, the patient reported partial pruritus relief and some lesion improvement. A skin ultrasound with a 15MHz linear probe (Fig. 2) revealed the larval tract as a homogeneous hypoechoic, well-delimited structure with posterior acoustic enhancement. No living larvae were found, likely as a result of prior ivermectin treatment. Due to the persistence of symptoms and the presence of some folliculitis-like lesions, a seven-day course of albendazole 400mg was initiated. One week post-treatment, the patient reported significant improvement and lesion resolution, with full recovery at one month (Fig. 3).
Ultrasound image of the skin 15MHz linear probe: transverse position relative to the track left by larva migrans. The different skin layers – epidermis, dermis, subcutaneous tissue, and muscle – are clearly visible. In the central area, a hypoechoic zone is evident, displaying posterior acoustic enhancement, corresponding to the larva migrans’ migratory path, with associated subepidermal edema. As oral ivermectin treatment had been initiated 48h earlier, only the larval migratory track was captured.
CLM is a clinical syndrome characterized by an erythematous, linear or serpiginous, migrating skin lesion caused by hookworm larvae from cats (Ancylostoma braziliense) or dogs (Ancylostoma caninum). These parasites are globally distributed, with infections more common in tropical/subtropical regions. Eggs are shed in the stool of definitive hosts (dogs, cats), and rhabditiform larvae hatch within 1–2 days. After 5–10 days and two molts, they transform into infective filariform larvae, which can survive in favorable environmental conditions for 3–4 weeks.
Humans are accidental hosts. Filariform larvae can partially penetrate the skin but do not mature due to the absence of collagenase needed to cross the basement membrane. This partial penetration triggers an intense inflammatory response, resulting in pruritic lesions within a few days of exposure. Although the condition is often self-limiting as the parasite dies, it can persist for weeks or months.
Diagnosis is primarily clinical, but complementary tests may aid in differential diagnosis and treatment monitoring. Cutaneous ultrasound can detect living larvae, appearing as a subepidermal hyperechoic dynamic tract surrounded by a hypoechoic halo indicative of acute inflammation. Once larvae are nonviable, a hypoechoic static tract persists, representing the old larval pathway and persistent inflammation, as in our case.1 The differential diagnosis includes other cutaneous infestations such as larva currens (LC) from Strongyloides stercoralis, which a significantly faster migration rate (5–15cm/h) than CLM (1–2cm/day)2; Norwegian scabies, characterized by a more prolonged course; or phytophotodermatoses, which may present as extensive serpiginous dermatitis following sun exposure to plant-based products applied to the skin, typically less symptomatic.
The treatment of choice is ivermectin (200mcg/kg once daily for 1–2 days), with cure rates of 94–100%. Albendazole (400mg/day for three days) is an alternative. Hookworm folliculitis has a poorer response to standard treatment, sometimes requiring additional doses or combination therapy; for extensive folliculitis, a seven-day course of albendazole may be warranted, achieving near-100% cure rates.3 Symptoms usually improve within weeks, with pruritus resolving before dermatitis.
FundingThe authors declare that they have not received any funding sources.
Conflict of interestNone declared.
