I came back from Bali with a winding red track on my foot that moves each day. What is it?

This is almost certainly cutaneous larva migrans (CLM), caused by the larvae of dog or cat hookworm (*Ancylostoma braziliense*) penetrating skin from contaminated sand or soil. It is pathognomonic: a serpiginous, intensely itchy erythematous track advancing 2–3 mm per day, usually on the feet or buttocks. It will self-resolve in 4–8 weeks but is very distressing and risks secondary infection from scratching. Treatment is straightforward: a single oral dose of ivermectin at 200 mcg/kg body weight clears approximately 95% of cases. See your GP for a prescription.

What is Buruli ulcer and where does it occur in Australia?

Buruli ulcer is caused by *Mycobacterium ulcerans*, which produces a toxin that destroys skin and soft tissue. In Australia, it is most common on Victoria's Mornington and Bellarine Peninsulas and is emerging in coastal Far North Queensland near the Daintree. The characteristic presentation is a painless nodule that progressively ulcerates with undermined edges — patients often delay seeking care precisely because it doesn't hurt. Early diagnosis with a PCR swab and prompt treatment with rifampicin plus clarithromycin for eight weeks prevents extensive tissue loss. It is a notifiable disease in Victoria.

When should strongyloidiasis be screened for before starting immunosuppression?

Strongyloides stercoralis can persist silently in the gut for decades via an auto-infection cycle. In someone whose immune system is suppressed — by corticosteroids, biologics, chemotherapy, or organ transplantation — the parasite can massively replicate, spreading through the bowel wall to cause sepsis, meningitis, and death with a mortality up to 90%. RACGP and ASID recommend screening with a Strongyloides IgG blood test before any course of immunosuppression in: all people from the Top End, Kimberley, or other remote ATSI communities; all migrants and refugees from endemic regions; and anyone with unexplained eosinophilia after tropical travel.

What does cutaneous leishmaniasis look like and how is it diagnosed?

Cutaneous leishmaniasis begins as a painless papule at a sandfly bite site, slowly expanding over weeks to months into a plaque and then an ulcer with a raised, indurated, rolled border and a central crust — sometimes described as a 'volcano sign'. It does not heal spontaneously in most cases and slowly enlarges. Importantly, species from Central and South America (particularly *Leishmania braziliensis*) can spread to the mucous membranes of the nose and palate years later, causing severe disfigurement. Diagnosis requires a skin biopsy edge-of-lesion for PCR, histology, and Giemsa stain. Refer to infectious diseases — treatment requires specialist-only access medications.

How do I prevent tropical skin diseases when travelling?

The most effective preventive measures are behavioural: wear shoes on beaches and in sandy soil in tropical areas (prevents cutaneous larva migrans and tungiasis); use 20–50% DEET or 20% picaridin repellent against sandflies (leishmaniasis) and mosquitoes; wear permethrin-treated long clothing at dusk and dawn when sandflies feed; avoid wading or swimming in freshwater in sub-Saharan Africa, the Nile, or Southeast Asian rivers (prevents schistosomiasis). Book a travel medicine consultation at least 4–6 weeks before departure for destination-specific vaccines and antimalarial advice. Consult Smartraveller for current destination health advisories.

Tropical dermatology — returned traveller and endemic AU skin disease

Tropical skin diseases: the AU general practice guide

By Dr HB Lo, FACRRM Reviewed 23 October 2026 9 min read

Tropical skin diseases reach AU general practice through returned travellers, migrants, refugees, and residents of north Queensland, the Top End, and coastal Victoria. Pattern recognition drives most diagnoses: a serpiginous itchy track on the foot after beach exposure is cutaneous larva migrans — treat with single-dose ivermectin.

Must-not-miss diagnoses: cutaneous leishmaniasis (indurated ulcer after Middle East or South American travel — refer to infectious diseases), hyperinfection strongyloidiasis (screen before immunosuppression — steroids, biologics, chemotherapy), and Buruli ulcer in coastal Victoria or the Daintree (rifampicin plus clarithromycin for eight weeks).

Tropical skin diseases arrive in Australian general practice along predictable epidemiological pathways: returned travellers from Southeast Asia, Central and South America, the Middle East, and sub-Saharan Africa; migrants and refugees from endemic regions; and residents of Far North Queensland, the Northern Territory Top End, and coastal Victorian localities — particularly the Mornington and Bellarine Peninsulas. The RACGP and eTG complete provide the primary AU guidance on management.

Pattern recognition and a detailed exposure history together drive most diagnoses in this group. Unlike many general practice presentations, the lesion morphology combined with travel history is often sufficient to act on empirically — particularly for the most common condition, cutaneous larva migrans. The key is knowing the patterns, knowing which conditions require urgent specialist referral, and knowing the one pre-treatment safety screen that can prevent a patient’s death: strongyloidiasis serology before any immunosuppression.

A. Core clinical — the AU general-practice framework

History: the diagnosis is usually here

The exact itinerary is diagnostic: countries visited, rural versus urban, whether the patient walked barefoot on beaches, swam in freshwater, had insect bites, or had contact with animals. Key exposures:

Beach or sand contact — cutaneous larva migrans (CLM), tungiasis
Freshwater swimming — schistosomiasis (Africa, Nile, Mekong, Brazil), leptospirosis
Sandfly bites — leishmaniasis (Middle East, Mediterranean, Central and South America)
Blackfly near fast-flowing rivers (sub-Saharan Africa) — onchocerciasis
Walking barefoot — hookworm, strongyloides, tungiasis
Botfly-endemic forest (Central/South America) — myiasis

For migrants and refugees: country and region of origin, refugee camp exposure, duration in Australia.

Associated features that change urgency: fever, lymphadenopathy, weight loss, hepatosplenomegaly, peripheral eosinophilia (strongly supports helminth infection).

Examination: lesion morphology guides the differential

Lesion	Most likely diagnosis
Serpiginous advancing itchy track on foot	CLM, larva currens (strongyloides)
Chronic indurated ulcer, raised rolled border	Cutaneous leishmaniasis, Buruli ulcer
Nodule with central pore + bubbling	Furuncular myiasis
Toe nodule with central black dot	Tungiasis
Painless progressing necrotising ulcer	Buruli ulcer (M. ulcerans)
Diffuse pruritic papular rash post-freshwater	Cercarial dermatitis (schistosomiasis)
Rapidly migrating periumbilical/perianal urticaria	Larva currens (strongyloides)

Investigations

FBC with differential — peripheral eosinophilia strongly suggests helminth infection (strongyloides, schistosoma, hookworm, filaria)
Targeted serology bundle based on exposure: Strongyloides IgG ELISA (high sensitivity), Schistosoma IgG, Leishmania serology, filaria serology as clinically indicated
Stool ova/cysts/parasites × 3 with Baermann technique requested specifically for strongyloides
Skin biopsy and PCR for leishmaniasis, Buruli ulcer, atypical mycobacteria
Blood films and RDT for any febrile returned traveller from a malaria-endemic region

B. The major conditions: CLM, leishmaniasis, and strongyloidiasis

Cutaneous larva migrans

CLM is the most common tropical dermatosis presenting to AU general practice. Ancylostoma braziliense (dog or cat hookworm) filariform larvae penetrate intact skin from animal-faeces-contaminated sand or soil. The track — intensely pruritic, serpiginous, erythematous, advancing 2–3 mm/day — is pathognomonic. Sites of predilection are feet, buttocks, and hands.

Treatment per eTG and AMH:

Ivermectin 200 mcg/kg single dose PO — first-line; cure rate ~95%; may repeat at day 7 if the track persists
Albendazole 400 mg PO daily × 3 days — equally effective alternative
Oral antihistamine and topical corticosteroid for symptomatic relief

Warn patients: the track may continue advancing for several days post-treatment while larvae die. Complete resolution is expected within two weeks.

Cutaneous and mucocutaneous leishmaniasis

Leishmaniasis is transmitted by Phlebotomine sandflies. Old World species (L. major, L. tropica) circulate in the Middle East, Mediterranean, and South/Central Asia; New World species (L. braziliensis, L. mexicana) in Central and South America. The clinically critical distinction: New World L. braziliensis can spread to the nasal and oral mucosa months to years after the initial lesion, causing severe mutilating espundia — an irreversible consequence of untreated cutaneous disease.

Presentation: painless papule → expanding plaque → chronic ulcer with raised, indurated, rolled border and central crust (“volcano sign”); regional lymphadenopathy; no spontaneous resolution in most cases.

All suspected cutaneous leishmaniasis must be referred to infectious diseases. Diagnosis requires skin biopsy for PCR, histology, and Giemsa smear. Treatment in Australia requires specialist-initiated medications:

Oral miltefosine (TGA Special Access Scheme Category B only — limited supply via tropical medicine units)
Liposomal amphotericin B IV for visceral or mucocutaneous involvement (S100 hospital supply)
Single small Old World lesions: possible observation or thermotherapy with specialist input

Always exclude visceral involvement (kala-azar — fever, hepatosplenomegaly, pancytopenia) and mucocutaneous spread (ENT examination) before assuming cutaneous-only disease.

Strongyloidiasis: the immunosuppression emergency

Strongyloides stercoralis is the tropical helminth with the most dangerous general practice implication. An auto-infection cycle allows lifelong persistence; the larva remains dormant in the gut indefinitely in immunocompetent hosts, producing intermittent mild GI symptoms, eosinophilia, and the pathognomonic “larva currens” — a rapidly migrating (5–10 cm/hour) urticarial serpiginous track around the buttocks and perianal area.

The emergency: if a person with undiagnosed strongyloides is commenced on corticosteroids, biologics, chemotherapy, or transplant immunosuppression, massive larval dissemination can follow — hyperinfection syndrome with mortality up to 90% despite treatment. The larvae penetrate the gut wall, dragging Gram-negative bacteria into the bloodstream to cause sepsis, meningitis, and respiratory failure.

Screening recommendations per RACGP, ASID Refugee SIG, and NHMRC Healthy Skin Guideline:

All Aboriginal and Torres Strait Islander patients from the Top End, Kimberley, and remote communities (endemic prevalence 5–60% in some communities)
All migrants and refugees from endemic tropical regions
All returned travellers with eosinophilia or unexplained GI or skin symptoms after tropical exposure
Mandatory pre-immunosuppression in all at-risk patients before corticosteroids, biologics, chemotherapy, or transplantation

Treatment per eTG: ivermectin 200 mcg/kg PO on two doses two weeks apart (or daily × 2 days then repeated after two weeks). Confirm clearance with repeat serology at 6–12 months — titres should decline. Hyperinfection requires daily ivermectin until larvae are cleared from stool.

C. Other important conditions: Buruli ulcer, tungiasis, schistosomiasis

Buruli ulcer (Bairnsdale ulcer)

Mycobacterium ulcerans produces mycolactone toxin causing painless necrosis. In Australia, the condition is most prevalent on Victoria’s Mornington and Bellarine Peninsulas (among the highest incidence globally per capita) and is emerging in the Daintree region of coastal Queensland. Possums and mosquitoes are implicated in transmission.

Presentation: painless papule or subcutaneous nodule progressing to a shallow ulcer with undermined, necrotic edges. Painlessness leads to delayed presentation.

Diagnosis: Victorian Department of Health recommends PCR of a swab or biopsy as first-line — rapid and highly sensitive. Histology shows necrosis and AFB.

Treatment per eTG: rifampicin 10 mg/kg PO daily plus clarithromycin 7.5 mg/kg PO twice daily for 8 weeks. Paradoxical reactions (worsening) occur in approximately 25% and are managed with corticosteroids. Surgery is reserved for large or complex ulcers.

Buruli ulcer is notifiable in Victoria. All suspected cases in VIC should be notified to the local public health unit.

Tungiasis

Tunga penetrans (sand flea) — the gravid female burrows into periungual and interdigital skin, most often on the toes. Presentation: a small white or yellow nodule (5–10 mm) with a central black dot (the flea’s posterior segments), surrounding erythema, intense itching and pain. Endemic to sub-Saharan Africa, the Caribbean, South America, and India.

Treatment: surgical extraction with a sterile needle or curette under local anaesthetic; remove the flea intact to prevent retained-fragment granuloma. Topical antiseptic and tetanus update (Australian Immunisation Handbook). Oral ivermectin 200 mcg/kg is used by some practitioners for multiple lesions.

Schistosomiasis

Schistosoma haematobium (urinary) and S. mansoni / S. japonicum (intestinal/hepatic) cercariae penetrate intact skin during freshwater contact. Not endemic to Australia. High-risk exposures: Lake Malawi, the Nile, Yangtze River tributaries, and sub-Saharan rivers.

Presentations include cercarial dermatitis (acute pruritic papular rash), Katayama fever (acute hypersensitivity syndrome 4–8 weeks post-exposure: fever, urticaria, eosinophilia, hepatosplenomegaly), and chronic sequelae (haematuria, bladder fibrosis, portal hypertension, squamous cell bladder carcinoma in S. haematobium).

Diagnosis: Schistosoma IgG serology post-Katayama period, urine microscopy for ova (S. haematobium — terminal urine sample), stool microscopy.

Treatment per eTG: praziquantel 40 mg/kg PO single dose (60 mg/kg for S. japonicum); repeat at 4–6 weeks if Katayama is present (encysted juvenile worms are not killed by the first dose). Corticosteroids for severe Katayama or neuroschistosomiasis. Refer to infectious diseases for neurological or advanced disease.

D. Australian operations

MBS-funded pathways

Standard consultations 23 / 36 / 44
Refugee health assessment items 701–707 (age-tiered comprehensive assessment within 12 months of arrival) — result in screening obligations including strongyloides serology
ATSI health assessment 715 — annual; strongyloides included in the recommended screening bundle
Skin biopsy — 30071 for ≤10 mm punch or shave biopsy
Pathology: FBC/differential, serology bundles, stool ova/cysts/parasites (specify Baermann technique for strongyloides), wound swab MCS; PCR for Buruli ulcer (specialist-initiated)

PBS-relevant prescribing

Per AMH and PBS:

Ivermectin — PBS listed for strongyloidiasis and crusted/community-outbreak scabies; for CLM typically dispensed as a private script or under the strongyloides PBS listing
Albendazole — PBS general for listed parasitic indications; intermittent supply shortages occur — verify before scripting
Praziquantel — PBS general for schistosomiasis and cestode infections
Rifampicin + clarithromycin — PBS general for ID indications including Buruli ulcer
Miltefosine — NOT PBS listed; TGA Special Access Scheme Category B only; specialist-initiated via tropical medicine units

Referral pathways

Royal Darwin Hospital (Centre for Disease Control NT) — strongyloides, tropical conditions, ATSI infectious disease
Royal Brisbane and Women’s Hospital / Mater — Far North Queensland tropical and refugee health
Westmead Hospital (Centre for Infectious Diseases and Microbiology) — NSW major referral
Royal Melbourne Hospital (Victorian Infectious Diseases Service) — including Buruli ulcer
Dermatology for atypical or refractory presentations requiring biopsy interpretation

Notification

Buruli ulcer is notifiable in Victoria. Malaria, dengue, leishmaniasis, leprosy, and schistosomiasis are variably notifiable across states — check the current state list at the NNDSS.

E. Special populations

Aboriginal and Torres Strait Islander patients from remote or tropical communities. Strongyloides prevalence ranges from 5% to 60% in some Top End and Kimberley communities. Scabies and impetigo are hyperendemic and share transmission routes. The NHMRC Healthy Skin Guideline provides the AU primary reference for community-level skin disease management including strongyloides screening.

Migrants and refugees. Routine post-arrival screens should include strongyloides serology, schistosoma serology (if Sub-Saharan African or Middle Eastern origin), FBC with differential for eosinophilia, stool ova/cysts/parasites, and hepatitis B/C and HIV. Use interpreter services and bilingual health workers; barriers to screening and treatment are significant in this group.

Children. Toxocariasis (Toxocara canis/cati) presents in children with pica or geophagia: eosinophilia with visceral (hepatomegaly, wheeze) or ocular (unilateral granuloma — DDx retinoblastoma) manifestations. Treat with albendazole ± prednisolone; refer to ophthalmology for ocular toxocariasis.

Immunocompromised patients. Strongyloides hyperinfection risk is the critical concern in this group — screen before any immunosuppression. Leishmaniasis behaves more aggressively with visceral dissemination more likely; HIV co-infection alters management significantly.

When to escalate

Refer to infectious diseases urgently when:

Any suspected cutaneous or visceral leishmaniasis — specialist access required for diagnostic biopsy and treatment
Suspected Buruli ulcer — PCR confirmation, specialist wound management, paradoxical-reaction monitoring
Strongyloides hyperinfection — sepsis, pneumonia, meningitis requiring ICU-level support alongside daily ivermectin
Schistosomiasis with neurological features — transverse myelitis, seizures
Any febrile returned traveller from a malaria-endemic region — thick and thin blood films + RDT before disposition; malaria is fatal if untreated
Visceral leishmaniasis (kala-azar) — fever + hepatosplenomegaly + pancytopenia is a medical emergency

Notify local public health unit for Buruli ulcer (VIC), malaria, and other notifiable tropical conditions.

What this article is and is not

This is general health information drawn from current Australian guidelines — eTG complete, AMH, RACGP, NHMRC Healthy Skin Guideline, and ASID — and internationally recognised travel-medicine references. It does not constitute personal medical advice and does not create a doctor–patient relationship. Treatment decisions, particularly for leishmaniasis, Buruli ulcer, and hyperinfection strongyloidiasis, require specialist involvement.

For travel health advice and destination advisories: Smartraveller. For consumer health information: HealthDirect.

Sources cited

Frequently asked questions

I came back from Bali with a winding red track on my foot that moves each day. What is it?

This is almost certainly cutaneous larva migrans (CLM), caused by the larvae of dog or cat hookworm (*Ancylostoma braziliense*) penetrating skin from contaminated sand or soil. It is pathognomonic: a serpiginous, intensely itchy erythematous track advancing 2–3 mm per day, usually on the feet or buttocks. It will self-resolve in 4–8 weeks but is very distressing and risks secondary infection from scratching. Treatment is straightforward: a single oral dose of ivermectin at 200 mcg/kg body weight clears approximately 95% of cases. See your GP for a prescription.
What is Buruli ulcer and where does it occur in Australia?

Buruli ulcer is caused by *Mycobacterium ulcerans*, which produces a toxin that destroys skin and soft tissue. In Australia, it is most common on Victoria's Mornington and Bellarine Peninsulas and is emerging in coastal Far North Queensland near the Daintree. The characteristic presentation is a painless nodule that progressively ulcerates with undermined edges — patients often delay seeking care precisely because it doesn't hurt. Early diagnosis with a PCR swab and prompt treatment with rifampicin plus clarithromycin for eight weeks prevents extensive tissue loss. It is a notifiable disease in Victoria.
When should strongyloidiasis be screened for before starting immunosuppression?

Strongyloides stercoralis can persist silently in the gut for decades via an auto-infection cycle. In someone whose immune system is suppressed — by corticosteroids, biologics, chemotherapy, or organ transplantation — the parasite can massively replicate, spreading through the bowel wall to cause sepsis, meningitis, and death with a mortality up to 90%. RACGP and ASID recommend screening with a Strongyloides IgG blood test before any course of immunosuppression in: all people from the Top End, Kimberley, or other remote ATSI communities; all migrants and refugees from endemic regions; and anyone with unexplained eosinophilia after tropical travel.
What does cutaneous leishmaniasis look like and how is it diagnosed?

Cutaneous leishmaniasis begins as a painless papule at a sandfly bite site, slowly expanding over weeks to months into a plaque and then an ulcer with a raised, indurated, rolled border and a central crust — sometimes described as a 'volcano sign'. It does not heal spontaneously in most cases and slowly enlarges. Importantly, species from Central and South America (particularly *Leishmania braziliensis*) can spread to the mucous membranes of the nose and palate years later, causing severe disfigurement. Diagnosis requires a skin biopsy edge-of-lesion for PCR, histology, and Giemsa stain. Refer to infectious diseases — treatment requires specialist-only access medications.
How do I prevent tropical skin diseases when travelling?

The most effective preventive measures are behavioural: wear shoes on beaches and in sandy soil in tropical areas (prevents cutaneous larva migrans and tungiasis); use 20–50% DEET or 20% picaridin repellent against sandflies (leishmaniasis) and mosquitoes; wear permethrin-treated long clothing at dusk and dawn when sandflies feed; avoid wading or swimming in freshwater in sub-Saharan Africa, the Nile, or Southeast Asian rivers (prevents schistosomiasis). Book a travel medicine consultation at least 4–6 weeks before departure for destination-specific vaccines and antimalarial advice. Consult Smartraveller for current destination health advisories.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.