Cutaneous leishmaniasis

By Dr. Pascal Bafteh · last updated 09/2026

General & Epidemiology

• Third most common vector-borne disease worldwide after malaria + dengue.
• Pathogens are Leishmania protozoa of the family Trypanosomatidae with promastigote/amastigote change.
• Reservoir are rodents/dogs with humans primarily in L. tropica.
• Vector: Sandflies (Phlebotomus in the Old World, Lutzomyia in the New World) — crepuscular/nocturnal.
• Occurrence: Mediterranean region (Portugal, Spain — Mallorca, Southern France, Italy), Africa, Middle East, South and Central America, India.
• Geographical concentration: More than 90 % of all cutaneous leishmaniasis cases occur in only about nine countries — in the Old World Afghanistan, Algeria, Iran, Iraq, Syria and Saudi Arabia, in the New World Brazil, Colombia and Peru.
• Predilection sites: Face and arms (exposed skin areas).

Life Cycle / Pathogenesis Cascade

• Sandfly bites infected host → takes up amastigotes.
• In the sandfly midgut, maturation to promastigotes (flagellated, infectious form).
• Sandfly bites new host → injects promastigotes into the skin.
• Phagocytosis by macrophages + dendritic cells → in the phagolysosome vacuole, transformation to amastigotes (intracellular, without flagellum).
• Replication of amastigotes in macrophages → inflammation + granuloma formation → skin manifestation.
• Repeat sandfly bite → uptake of amastigotes → cycle.

Three Clinical Forms

Cutaneous Leishmaniasis ("Oriental Sore")

• Old World pathogens: L. tropica, L. major, L. infantum.
• New World pathogens: L. mexicana, L. (Viannia) braziliensis, L. amazonensis.
• Clinical presentation shows red nodule → plaque → ulcer with volcano-like rim, often painless, slow development 2–8 weeks after bite.
• Localization: Face, arms, legs — uncovered skin areas.
• Spontaneous healing in 6–18 months for many species; leaves an atrophic sunken scar.

Mucocutaneous Leishmaniasis ("Espundia")

• Main causative agents: L. (Viannia) braziliensis, L. panamensis (South America).
• Clinical presentation: mucosa of nose/oropharynx months–years after cutaneous manifestation with tapir nose/septal perforation.
• Complication: Aspiration pneumonia, stridor, oral dysfunction, cosmetic disfigurement.

Visceral Leishmaniasis ("Kala-Azar", black fever)

• Pathogens are L. donovani/infantum/chagasi with visceral involvement.
• Clinical presentation: Involvement of bone marrow, liver, spleen, lymph nodes — fever episodes, hepatosplenomegaly, pancytopenia, hypergammaglobulinemia, hyperpigmentation ("Kala-Azar" = black fever), cachexia.
• Untreated mortality > 95 %.

Diagnostics

• Specimen collection: with 4–6 mm punch biopsy from active border, divided for culture/histo/Giemsa/PCR.
• Giemsa staining: Detection of intracellular amastigotes ("Leishman-Donovan bodies") in macrophages.
• Leishmania PCR (sensitive, species differentiation possible).
• Culture on NNN medium (Novy-MacNeal-Nicolle) — standard laboratory requirement in tropical medicine.
• For L. donovani / L. infantum with suspected visceral L.: the procedure is exclude visceral manifestation with bone marrow puncture + ultrasound + rK39.

Differential diagnoses

• Sporotrichosis
• Cutaneous myiasis
• Pyogenic granuloma
• Ecthyma
• Secondary syphilis (lues II)
• Atypical fibroxanthoma
• Swimming Pool Granuloma
• Yaws

Sources (selection)

1. World Health Organization. Leishmaniasis — fact sheet. Geneva: WHO.
2. Burza 2018 Lancet — Leishmaniasis
3. AWMF S1 Leishmaniase 2021

More parasitic skin diseases

• Demodicosis
• Filariasis
• Cutaneous larva migrans
• Pediculosis capitis
• Caterpillar dermatitis caused by oak processionary moth (Thaumetopoea processionea)
• Crusted (Norwegian) scabies
• Scabies
• Tungiasis

Note: This page is intended for medical education and does not replace diagnosis or treatment decisions in individual cases. Treatment and follow-up content is available in the app.