Cutaneous larva migrans (creeping eruption)

[1]

Meet the patient

A 28-year-old returns from a week in Phuket with an intensely itchy, snake-like red track inching its way across the dorsum of her foot. She photographed it yesterday and again today — it has moved about half a centimetre overnight. She never had a fever, has no bowel symptoms, and her blood count is normal.[1][3]

The two facts that decide everything else are sitting in that vignette: a contact-site tract advancing millimetres per day, and the absence of eosinophilia or systemic symptoms. Hold those two and the diagnosis, the dose, and the differential all fall into place.[1]

One parasite, one trap, one mantra

Cutaneous larva migrans (CLM) — creeping eruption, hookworm-related CLM, sandworm disease, and historically plumber's itch — is the most common tropically acquired dermatosis in returned travellers, and the single most frequent skin complaint in patients walking into a tropical-disease clinic after a beach holiday.[1][3][6] The culprit is a zoonotic hookworm larva, almost always Ancylostoma braziliense (the dog-and-cat hookworm) with A. caninum second; Uncinaria stenocephala (European dog hookworm) and Bunostomum phlebotomum (cattle hookworm, farm workers) turn up occasionally.[1][2][8]

The trap that defines the disease: in a dog or cat the larva burrows through to the dermis, rides the bloodstream to the lung, is swallowed, and matures in the gut. In a human it gets stuck at the basement membrane — it lacks the species-specific elastase and the laminin/collagen-IV ligands needed to dissolve the dermo-epidermal junction — so it is forced to wander sideways in the stratum corneum, leaving the serpiginous inflammatory trail behind it.[1][3][6][7]

The mantra, said out loud on the viva: centimetres per hour is Strongyloides; millimetres per day is larva migrans.[1][10]

Etymology for viva gold: migrans is Latin for migrare, "to wander" — exactly what the larva does. Ancylostoma is Greek ankylos (curved/hooked) plus stoma (mouth), from the bent, toothed mouth-parts the adult worm uses to hang off the bowel mucosa. Two words, both literal.[3]

How common, and who catches it

CLM is, by a margin, the most common dermatosis in travellers returning from the tropics. The GeoSentinel network and the Parisian Caumes cohort both put it at the top of travel-acquired skin disease, accounting for roughly 9–25% of cases depending on the case mix.[2][3][11] That consistency across continents and decades is the teaching point: a creeping skin lesion after a tropical trip is CLM until proved otherwise.[3][11]

[1]

Where it comes from

The disease follows infected dogs and cats wherever warm, humid sand meets poor sanitation and free-roaming animals:[1]

• Caribbean — Barbados (historically the single most cited exposure), Jamaica, Dominican Republic, the Bahamas, the US Virgin Islands, coastal Mexico.[2][3]
• South America — the northeast Brazilian coast (Bahia, Pernambuco, Ceará), plus Atlantic Colombia and Venezuela.[2]
• West and Central Africa — beach resorts in Senegal, Ghana, Côte d'Ivoire, Cameroon, Gabon.[1][3]
• Southeast Asia — Thailand (Phuket, Koh Samui, Krabi), Malaysia, Indonesia (Bali), the Philippines, Vietnam.[2]
• Indian subcontinent — Goa, Kerala, Pondicherry coasts; also Sri Lanka and the Maldives.[2]
• Southeastern United States — Florida, the Gulf Coast (Alabama, Mississippi, Louisiana, Texas), the Carolinas. A 2026 US Military Health System analysis confirmed CLM is regularly acquired domestically with no international travel — so do not exclude it just because the patient did not fly.[3]
• Mediterranean Europe — sporadic cases on Spanish, Italian, French, and Greek coasts where stray dogs still soil beaches.[2]

How the patient catches it

The reservoir is dog and cat faeces on warm, moist, shaded, sandy or loamy soil. Ova hatch, larvae moult twice, and reach the infective filariform (L3) stage in 5–7 days. Clay, rock, or sun-baked ground rarely transmits — larvae desiccate and ova fail to embryonate.[1][2][6]

• Barefoot on a tropical beach is the single biggest exposure — which is why 50–80% of CLM sits on the feet.[2]
• Lying or sitting on sand explains the buttock, genital, and abdominal lesions in sunbathers.[3]
• Sandboxes contaminated by neighbourhood cats — the classic childhood exposure, especially in the US southeast and southern Europe.[2]
• Occupational soil contact — plumbers, electricians, gardeners, farmers, construction workers. The Victorian "plumber's itch" cases were men crawling under London houses in sandy soil soiled by dogs.[1][6]

Incubation is short — most patients itch within 1–6 days of exposure, sometimes within hours. A light inoculum stretches it out, which is why some patients first notice the track on the plane home or a few days later.[1][3][7]

Why the larva wanders — the pathophysiology

CLM is an evolutionary mismatch: a parasite evolved for a dog or cat that has walked into the wrong host. Three things follow from that mismatch — the life cycle in the natural host, the molecular block in humans, and the immune response that makes the patient itch.[1][3][6][9]

The natural life cycle in the dog and cat

1. Adult hookworms clamp onto the small-intestinal mucosa of dogs and cats and feed on blood; the females shed thousands of ova daily into the faeces.[3]
2. Ova hatch in 1–2 days into rhabditiform (L1) larvae, which feed on soil bacteria and moult twice over 5–7 days to become the infective filariform (L3) larva.[1][3]
3. The L3 larva waits in the top few millimetres of warm moist sand. When a dog or cat lies down it penetrates intact skin, enters the venous system, is carried to the lung, is coughed up and swallowed, and matures into an adult in the small intestine — the cycle closing in 3–4 weeks.[1][6]

The block in humans — why it cannot finish the journey

The larva breaches the stratum corneum easily, releasing collagenases, hyaluronidases, serine proteases, and metalloproteases to slip between keratinocytes. What it cannot do is dissolve the lamina lucida of the dermo-epidermal junction — it lacks the species-specific elastase and the laminin/collagen-IV ligands the natural hookworm uses. So it turns sideways and wanders in the stratum corneum and superficial spinous layer, advancing a few millimetres a day.[1][3][6][7]

Everyone forgets: the visible tract is not a tunnel the larva digs — it is the inflammatory wake left behind the larva, which sits 1–2 cm ahead of the red leading edge. That single fact explains why biopsy of the tract almost always misses the larva (captured in under 5% of biopsies), and why cryotherapy of the leading edge is a waste of a blister.[1]

Migration rate and tract shape — the discriminator

• Classic rate: 2–7 mm per day (sometimes quoted as up to 1–2 cm/day). The advance is visible to the patient and to a serial photograph, which is why patients keep arriving with a ruler in the photo.[1][3][6]
• Tract shape: a raised, erythematous, serpiginous or linear track 2–4 mm wide, sharper at the leading edge, sometimes with a tiny vesicle or pustule over the larva itself.[7]
• Multiple tracts: up to 20% of patients — multiple penetration sites from one exposure.[1]

Why it itches — type I plus type IV

The pruritus is not tissue damage; it is hypersensitivity to larval antigens and enzymes:[1]

• Type I (IgE, immediate): mast-cell degranulation within hours — histamine, tryptase, leukotrienes, prostaglandins — wheal-and-flare and the maddening itch.[3]
• Type IV (T-cell, delayed): over 24–72 hours, Th2 cells and macrophages accumulate around the larva and amplify the erythematous tract.[1][3]
• Eosinophils arrive on eotaxin and IL-5, but the systemic antigen load is small, so peripheral eosinophilia is uncommon in simple CLM. A raised eosinophil count (over 0.5 × 10⁹/L) is a red flag for a different helminth — Strongyloides, Toxocara, filaria, schistosomiasis.[3][6]

The larva dies within 4–8 weeks — it cannot finish its cycle, cannot find a mate, and is overwhelmed by the host. CLM is therefore self-limiting, but nobody waits: the itch is unbearable and a single ivermectin tablet ends it.[1][3][4][9]

Clinical presentation — what you actually see

Incubation and first symptom

The first thing the patient notices is itch at the entry site, within hours to a few days of exposure; a small erythematous papule may mark the bite but is often missed. Then a thread-like eruption begins to move across the skin, leading edge slightly ahead of the inflammation.[1][3][7]

The hallmark — the creeping eruption

The pathognomonic finding is the creeping eruption:[1]

• Serpiginous or linear, often snake-like or question-mark when the larva changes direction.
• Erythematous, raised, 2–4 mm wide, with a sharp leading edge and a fading tail.
• Intensely pruritic, worse at night and in warmth.
• Slowly advancing at 2–7 mm/day — visible on a serial photograph.
• Often trailed by vesicles, pustules, or crusting, especially where it has been scratched.[1][6][7][8]

Where it sits — distribution follows the contact

The body surface that touched the sand is the body surface that gets the tract:[1]

• Feet — half to four-fifths of all lesions; dorsum, sole, lateral border, web spaces. Barefoot walking is the dominant exposure.[2][3]
• Buttocks and perianal area — second most common, from sitting or lying on sand.[2]
• Abdomen, lower back, thighs — sunbathers and sand-playing children.[3]
• Hands and forearms — gardeners, plumbers, electricians, builders.
• Genitalia, breasts, face — uncommon but well described, especially in children and sunbathers.[1][6]

Number, course, complications

• Number: usually 1–3 tracts; 10–20% have multiple, occasionally dozens in a heavy exposure.
• Untreated course: the larva dies in 4–8 weeks, the inflammation settles, the tract fades over weeks, most clear by 2–3 months. The itch never relents until it does.
• Secondary bacterial infection is the commonest complication — 5–25% of patients, driven by scratching, heat, and humidity.[1][3][6]

Differential diagnosis — the creeping-lesion face-off

The two mimics that cost marks — and lives — are larva currens (Strongyloides) and cutaneous gnathostomiasis. Both can look like CLM but neither is treated the same way, and a missed Strongyloides can kill an immunosuppressed patient years later.[3][6][10][12]

[1] [1]

Bedside assessment — the diagnosis is the examination

CLM is a clinical diagnosis made at the bedside on three observations: a recent tropical or beach exposure, a characteristic creeping serpiginous tract on a contact site, and no features pointing elsewhere. There is no lab test that confirms it; the assessment is the test.[1][3][5][7]

Focused history

• Travel: every country, every date, and the timing of symptoms against the trip. Most itch during the trip or within the first week home.[2][3]
• Exposure: barefoot beaches, lying or sitting on sand, sandbox play, occupational soil, stray-animal contact.
• Accommodation: resort, hostel, village, cruise ship.
• Symptoms: onset of itch, first sighting of the tract, rate of advance, nocturnal pattern, any systemic features.
• Background: atopic dermatitis (worse inflammation), immunosuppression (transplant, HIV, chronic steroids, chemo), prior helminths.
• Drugs: any anthelmintic, antihistamine, or topical steroid on board; tetanus status.

Focused examination

• Inspect the whole skin with the patient undressed — CLM can be anywhere, and 10–20% have more than one tract.[1][3]
• Feet, buttocks, abdomen, lower back, thighs in detail. Interdigital spaces, plantar surface, perianal area are easy to miss.
• Mark the leading edge with a surgical pen or photograph it with a ruler. A tract that has advanced 5–20 mm in 24–48 hours is a migrating larva — diagnostic.
• Look for secondary infection: impetiginisation, pustules, cellulitis, regional lymphadenitis.
• Dermoscopy, when available, may show the larva as a translucent comma-shaped or oval structure at the leading edge — a "larva in a burrow" — and can exclude scabies, tinea, and vessels. Not required, but a useful confirmatory adjunct.[7]

Investigations — usually none

Most patients need no investigation before treatment. Labs and imaging are reserved for atypical presentations, the differentials above, and treatment failure.[1][3][5]

Bedside test

• Direct visualisation of the advancing serpiginous tract on a contact site after a relevant exposure. That is enough to treat.
• Serial photography of the leading edge over 24–48 hours when the migration rate is in doubt — very slow, or alarmingly fast and pointing to larva currens.[1]

Laboratory tests — when to send them

• Full blood count: eosinophilia is uncommon in simple CLM (under 10–20% of cases) because the systemic antigen load is small. Significant eosinophilia (over 0.5 × 10⁹/L) means look for another helminth — Strongyloides serology, stool O&P (three samples, or agar-plate culture for Strongyloides), Toxocara serology, filaria serology, schistosomiasis serology if exposure fits.[1][3][6]
• Skin biopsy is rarely needed. When done for uncertainty it shows spongiosis, intraepidermal vesiculation, a mixed infiltrate with eosinophils, and occasionally a larval cross-section — but the larva is ahead of the tract, so it is captured in under 5% of biopsies.[1][7]
• Strongyloides serology (IgG ELISA) is the test to exclude larva currens in a fast-moving or recurrent tract, especially with eosinophilia or abdominal symptoms. Cross-reacts with other helminths, so read it in context.[10]
• Stool O&P is useless for CLM itself (animal hookworms never reach the human gut) but is part of the work-up for concomitant Strongyloides, Ascaris, Trichuris, or human hookworm.
• Gnathostoma serology (where available) for migratory swellings with marked eosinophilia and raw-fish exposure in SE Asia or Mexico.[12]
• HIV serology if the picture raises disseminated strongyloidiasis — long-standing recurrent creeping eruption in a CD4-deficient host.

Imaging

None for uncomplicated CLM. A chest film showing transient Löffler-like infiltrates with eosinophilia points to a coincident helminth (Ascaris, Strongyloides) — not CLM, which never reaches the lung.[3][6]

Management — one tablet ends it

CLM is a medical condition, not a surgical one, and a single dose of ivermectin is the answer in nearly every patient. Before ivermectin arrived in the 1990s the options were cryotherapy of the leading edge (painful, unreliable, fails because the larva is 1–2 cm ahead), topical thiabendazole (effective but messy and often unavailable), and oral albendazole (effective but slower). The modern approach is unambiguous: oral ivermectin 200 µg/kg as a single dose is first-line; oral albendazole is second-line.[1][4][5][9]

[1]

First-line: oral ivermectin

• Dose: ivermectin 200 µg/kg as a single oral dose — one tablet is one course in most patients.[1][4][5][9]
• Cure rate: over 95% in the randomised trials; itch and tract progression stop within 24–48 hours, the tract resolves in 1–2 weeks.[9]
• Mechanism: binds glutamate-gated chloride channels in nematode motor neurons and pharyngeal muscle, paralysing and killing the larva. Mammals lack these channels, which is why it is so well tolerated.
• Repeat dose: 5–10% need a second dose at 1–2 weeks if itch and progression persist — commoner with multiple or heavy-inoculum lesions.[4][5]
• Cautions: pregnancy (limited data), children under 15 kg (or under 5 years in some guidance), and Loa loa co-infection from Central or West Africa, where ivermectin can precipitate encephalopathy in heavily microfilaraemic patients. Take a travel history, and in any West/Central African exposure, screen for Loa loa microfilaraemia before dosing.[3]

Second-line: oral albendazole

• Dose: albendazole 400 mg orally once daily for 3–7 days (some guidelines use 400 mg twice daily for 3 days in heavier disease).[1][4]
• Cure rate: roughly 80–90% after a 3-day course, about 95% after 7 days — slightly slower than ivermectin.
• When to use: pregnancy (better safety data than ivermectin for short second- and third-trimester courses, though conventionally avoided in the first trimester), ivermectin unavailability, or Loa loa co-infection.
• Adverse effects: mild GI upset, transient liver-enzyme rise — watch in hepatic disease.

Historic and topical therapies

• Topical thiabendazole 10–15% suspension or cream 2–4 times daily for 5–10 days was the mainstay before ivermectin. Still useful for a single localised tract or when oral therapy is contraindicated, but messy, often unavailable, and inferior to oral ivermectin.[4][9]
• Topical ivermectin has been used off-label for limited lesions but is not first-line.
• Cryotherapy of the leading edge is a historic approach that targets the visible front of the tract. The classic trap: the larva is 1–2 cm ahead of the visible erythema, so cryotherapy blisters normal skin and misses the parasite. Not recommended unless oral therapy is contraindicated and the lesion is small and single.

Symptomatic and adjunctive measures

• Oral antihistamines (cetirizine 10 mg, loratadine 10 mg, hydroxyzine 25 mg) for itch; a non-sedating one by day and hydroxyzine at night is a sensible combination.
• Topical corticosteroids (mild-to-moderate, e.g. mometasone furoate 0.1%) briefly over an inflamed tract to settle local inflammation — never over infected or impetiginised skin.
• Secondary bacterial infection is treated with oral flucloxacillin (or erythromycin/clarithromycin if penicillin-allergic); consider MRSA if it fails or if there is recent hospital contact. Topical mupirocin or fusidic acid for localised impetiginisation.
• Tetanus immunisation — check and update in any contaminated tropical skin lesion.[1]

Subtypes and special scenarios

A handful of CLM variants behave differently and turn up in exams. Know them by presentation and by management.[1][3][6][12]

[1]

The one co-infection you cannot miss — Strongyloides

A patient who caught CLM barefoot in the tropics may have picked up Strongyloides stercoralis at the same moment, especially in rural and agricultural settings. Strongyloides autoinfects — it can persist for decades and cause fatal hyperinfection when the patient later becomes immunosuppressed. Rule of thumb: a creeping eruption plus eosinophilia, abdominal symptoms, or West/Central African exposure gets Strongyloides serology, and if positive, two consecutive days of ivermectin 200 µg/kg — not the single dose CLM gets.[10]

CLM caught at home — the US southeast

The 2026 US Military Health System analysis confirmed CLM is regularly acquired domestically in the southeastern United States — Florida, the Gulf Coast, the Carolinas — in patients with no international travel. So do not exclude CLM just because the passport is empty; a beach or sandbox exposure in the southern US is enough.[3]

Complications and the way it goes wrong

CLM is rarely dangerous, but the morbidity from relentless itch, secondary infection, and diagnostic delay is real. Three pitfalls deserve a name.[1][3][6]

Secondary bacterial infection

Scratching and humid tropical skin set up:[1]

• Impetiginisation of the tract, honey-coloured crust.
• Cellulitis or erysipelas around the tract, with regional lymphangitis and lymphadenitis.
• Furunculosis when follicular CLM is misread as bacterial folliculitis and treated with antibiotics alone.
• Tetanus — a theoretical risk in a heavily contaminated wound; check and update immunisation.[1]

Misdiagnosis — the confession

[1]

The common mislabels and what each leads to:[1]

• Scabies → repeated scabicidal treatments that do not work.
• Tinea corporis → topical antifungals that do not work.
• Lyme disease → empirical doxycycline.
• Contact dermatitis / insect bite → topical steroids, which dampen inflammation but never kill the larva.
• Larva currens → single-dose ivermectin when two days are needed.[1]

Diagnostic delay runs 1–3 weeks in primary care and can stretch to 8–12 weeks in patients who keep returning with non-resolving "bites" or "eczema".[1][3]

Treatment failure — what to do when one dose is not enough

Failure to respond to single-dose ivermectin within 1–2 weeks should prompt:[1]

1. Re-confirm the diagnosis — look again for larva currens, gnathostomiasis, myiasis, Majocchi's granuloma, sporotrichoid deep fungal infection, cutaneous leishmaniasis.[12]
2. A second dose of ivermectin 200 µg/kg at 1–2 weeks — appropriate for confirmed CLM with multiple or heavy lesions.
3. Switch to oral albendazole 400 mg daily for 7 days if ivermectin is unavailable, contraindicated, or has failed twice.
4. Consider Loa loa co-infection in any West or Central African exposure — ivermectin can precipitate encephalopathy, and albendazole may be the safer choice.

Iatrogenic pitfalls — the three don'ts

• Don't freeze the leading edge. The larva is 1–2 cm ahead; cryotherapy blisters normal skin and misses the parasite.
• Don't use topical steroids alone. They quieten the inflammation but the tract keeps advancing.
• Don't use antibiotics alone for "folliculitis". If the real diagnosis is hookworm folliculitis, antibiotics will not kill the larva and the eruption marches on.[1]

Prognosis and disposition

With ivermectin the prognosis is excellent; the long-term outlook is set by the patient's travel habits, not the worm.[1]

[1]

What changes the outlook

• Inoculum and tract count: multiple or large lesions take longer and may need a second dose.
• Time to treatment: earlier ivermectin means shorter symptoms and less secondary infection.
• Secondary infection: delays resolution and risks scarring.
• Immunosuppression: does not worsen CLM itself — but coexisting Strongyloides in an immunosuppressed host can be lethal. Always screen.
• Re-exposure: the patient who goes back to the same beach gets it again.[1]

Disposition

• Most patients go home with one ivermectin tablet and symptomatic measures; admission is not needed.[1][3]
• Admission is reserved for: extensive secondary infection needing IV antibiotics, suspected Strongyloides hyperinfection in an immunosuppressed host, diagnostic uncertainty needing biopsy, or a severe allergic reaction to ivermectin.
• Follow-up: most need none. Advise return if the tract has not stopped advancing within a week, if new lesions appear, or if secondary infection develops.

Special populations

Children

Common after sandbox play. Principles are the same as adults, but ivermectin is generally avoided under 15 kg (or under 5 years in many guidelines), making albendazole 400 mg daily for 3–7 days the preferred option. Topical thiabendazole helps the child who cannot swallow a tablet. Counsel the family on sandbox hygiene, deworming pets, and avoiding barefoot play on tropical beaches.[1][3]

Pregnancy and lactation

Uncommon but reported, especially in long-term residents of endemic areas. Ivermectin is generally avoided in pregnancy for lack of safety data; albendazole is conventionally avoided in the first trimester (animal teratogenicity), though recent meta-analyses suggest inadvertent first-trimester exposure does not markedly raise malformation risk. Topical thiabendazole is useful because systemic absorption is minimal. Individualise with obstetric and infectious-disease input, and treat — the itch and sleep loss themselves harm pregnancy.[3]

Elderly and frail

Uncommon because exposure patterns differ, but when it occurs, weigh polypharmacy and hepatic/renal function (albendazole is mildly hepatotoxic). Ivermectin single-dose remains first-line.[3]

Immunocompromised

CLM itself is no worse — but the differential widens to disseminated strongyloidiasis, atypical fungal infection (sporotrichoid, cryptococcosis, histoplasmosis), atypical mycobacteria, and cutaneous leishmaniasis. Biopsy, fungal and mycobacterial cultures, Strongyloides serology, and a careful exposure review are warranted. Ivermectin remains the treatment, but the dose may need repeating and treatment failure watching for.[3][10]

Loa loa co-endemicity

In patients exposed in West or Central Africa (Cameroon, Nigeria, Gabon, both Congos, Angola, Chad, CAR, Equatorial Guinea), consider Loa loa co-infection before giving ivermectin. Heavy Loa loa microfilaraemia (over 30,000 microfilariae/mL) can trigger ivermectin-induced encephalopathy. Screen with a daytime blood film for microfilariae first; if positive, consider albendazole and refer to a tropical-disease specialist.[3]

The evidence and the guideline map

Landmark trials

• Caumes et al. 1993 — the first RCT of ivermectin 200 µg/kg single dose vs albendazole 400 mg daily for 3 days in 43 patients with imported CLM. Ivermectin cured 100%, albendazole 85%, with faster itch relief on ivermectin.[9]
• Caumes 2000 — the comprehensive treatment review that made oral ivermectin the drug of choice on efficacy, single-dose convenience, and tolerability.[4]
• Davies, Sakuls, Keystone 1993 — a 60-case Toronto series that established the presentation, distribution, and natural history of imported CLM in a North American cohort.[8]
• Heukelbach et al. 2008 — a prospective 146-patient Brazilian cohort documenting endemic epidemiology, confirming feet as the commonest site and buttocks second, with a mean tract length of 5–10 cm at presentation.[2]
• Hochedez & Caumes 2007 — the narrative review that set the modern classification of CLM and its place in the larva migrans syndrome.[3]
• Stevens et al. 2015 — the CanTravNet surveillance of dermatoses in returned Canadian travellers, confirming CLM as a top-three travel-acquired skin disease with Caribbean and SE Asia dominant.[11]
• Tian et al. 2023 — a seven-case series and review of larva currens, re-emphasising its speed, recurrence, and the need for two-day ivermectin.[10]
• Hamilton et al. 2018 — a case and review of imported gnathostomiasis mimicking CLM with Löffler-like pulmonary infiltrates, after raw-fish exposure in Asia.[12]

Guidelines

• American Academy of Dermatology and CDC both endorse oral ivermectin 200 µg/kg single dose as first-line for uncomplicated CLM, with oral albendazole second-line.
• British Association of Dermatologists and ECDC concur.
• WHO does not issue a CLM-specific guideline, but its anthelmintic policy backs ivermectin and albendazole for soil-transmitted helminths and flags the Loa loa encephalopathy risk.[1]

Regional practice

• Europe and North America — ivermectin 200 µg/kg single dose is universally first-line; albendazole for contraindications.[3][4][5]
• Brazil and the Caribbean — ivermectin first-line; topical thiabendazole still used for single lesions on cost and access grounds.[2][6]
• India, Sri Lanka, the subcontinent — albendazole often first-line on cost and availability; CLM in returning travellers is a recognised Goa/Kerala presentation.[2]
• West and Central Africa — albendazole preferred where Loa loa co-infection is possible.[3]

The mnemonic, the mantra, and the trap

[1] [1]

The mantra, one last time: centimetres per hour is Strongyloides; millimetres per day is larva migrans — one tablet of ivermectin ends it.[1][10]

Ward-round test — four stems, sixty seconds each

Stem 1 — the woman from Phuket (answer)

A 28-year-old returns from a week in Phuket with an intensely itchy snake-like red track advancing across the dorsum of her foot. She photographed it yesterday and today — it has moved about half a centimetre. Normal blood count, no systemic symptoms. What is the diagnosis, the dose, and the one question you ask before prescribing? Model: This is classic cutaneous larva migrans — beach travel, contact-site serpiginous tract advancing millimetres per day, no eosinophilia. The drug of choice is oral ivermectin 200 µg/kg as a single dose (cure over 95%). Before prescribing, ask about travel to West or Central Africa, because Loa loa co-infection can turn a routine dose of ivermectin into encephalopathy. Mark the leading edge so the patient can confirm it has stopped advancing at one week.[1][9]

Stem 2 — the recurrent perianal track (answer)

A 55-year-old farmer who left Vietnam 20 years ago has a fast-moving urticarial wheal on his buttock that has crossed five centimetres since breakfast. It recurs in the same site every few months. Eosinophil count 0.9 × 10⁹/L. What is the diagnosis, the trap, and the correct regimen? Model: This is larva currens — cutaneous Strongyloides stercoralis — not CLM. The discriminator is the migration rate (centimetres per hour, not millimetres per day), plus recurrence (the autoinfection cycle), perianal/buttock site, and eosinophilia. The trap: treating it as CLM with single-dose ivermectin — Strongyloides needs ivermectin 200 µg/kg daily for two consecutive days, and untreated autoinfection can cause fatal hyperinfection if the patient is ever immunosuppressed. Send Strongyloides serology and stool O&P/agar-plate culture to confirm, and screen anyone sharing the exposure.[10]

Stem 3 — the cryotherapy request (answer)

A junior has just cryotherapy'd the leading edge of a CLM tract on a patient's foot and is puzzled the eruption is still advancing. What went wrong, and what do you do now? Model: The larva sits 1–2 cm ahead of the visible erythema — the tract is an inflammatory wake, not a tunnel. Cryotherapy of the leading edge blisters normal skin and misses the parasite, which is why it is not recommended. Give oral ivermectin 200 µg/kg as a single dose; the itch and progression stop within 24–48 hours and the tract resolves over 1–2 weeks. Reserve cryotherapy for the rare patient in whom oral therapy is contraindicated and the lesion is small and single.[1][4]

Stem 4 — the pregnant traveller (answer)

A pregnant woman at 24 weeks returns from Barbados with a classic CLM tract on her foot and unbearable itch. How do your thresholds and drug choice change? Model: CLM in pregnancy is treated, not watched — the itch and sleep loss themselves harm the pregnancy. Ivermectin is generally avoided for lack of safety data; the preferred option is oral albendazole 400 mg daily for 3–7 days (better safety data than ivermectin for short second- and third-trimester courses, though conventionally avoided in the first trimester). Topical thiabendazole 10–15% is a reasonable alternative for a single localised tract because systemic absorption is minimal. Involve obstetric and infectious-disease colleagues, and add an oral antihistamine for symptom relief.[3]

[1]

References

1. [1]Palaniappan V, et al. Cutaneous larva migrans Clin Exp Dermatol, 2026.PMID 40795202
2. [2]Heukelbach J, et al. Epidemiological and clinical characteristics of hookworm-related cutaneous larva migrans Lancet Infect Dis, 2008.PMID 18471775
3. [3]Hochedez P, Caumes E. Hookworm-related cutaneous larva migrans J Travel Med, 2007.PMID 17883464
4. [4]Caumes E. Treatment of cutaneous larva migrans Clin Infect Dis, 2000.PMID 10816151
5. [5]Kincaid L, et al. Management of imported cutaneous larva migrans: A case series and mini-review Travel Med Infect Dis, 2015.PMID 26243366
6. [6]Feldmeier H, et al. Mini review: Hookworm-related cutaneous larva migrans Eur J Clin Microbiol Infect Dis, 2012.PMID 21922198
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