In New Zealand, leishmaniasis is managed by tropical medicines. Leishmaniasis is a parasitic disease caused by more than 20 species of Leishmania protozoa transmitted by infected female phlebotomine sandflies. It presents in three main clinical forms with very different consequences: cutaneous leishmaniasis (skin ulcers, around 600,000-1,000,000 new cases each year), mucocutaneous leishmaniasis (destructive ulceration of the nose, mouth, and throat, mainly in Latin America), and visceral leishmaniasis or kala-azar (a systemic disease with fever, hepatosplenomegaly, and pancytopenia that is fatal within months in over 95% of untreated patients).
Leishmaniasis (ICD-10: B55) is a group of parasitic infections caused by obligate intracellular Leishmania protozoa transmitted to humans through bites of infected female phlebotomine sandflies (Phlebotomus species in the Old World; Lutzomyia in the New World). Promastigotes injected during the sandfly blood meal are taken up by macrophages, transform into amastigotes, and replicate inside macrophage phagolysosomes. The clinical syndrome depends on the infecting species, the host immune response, and the geographic setting. Cutaneous leishmaniasis is caused by Leishmania major and Leishmania tropica in the Old World and Leishmania mexicana, Leishmania amazonensis, and Leishmania braziliensis complex in the New World, producing localized, diffuse, or disseminated skin lesions.
The key symptoms of Leishmaniasis are: A painless papule at the site of a sandfly bite (exposed face, arms, or lower legs) that enlarges over weeks into a 1-5 cm ulcer with raised, indurated borders and a clean central crater — the classic cutaneous leishmaniasis lesion., Multiple cutaneous ulcers, satellite nodules along lymphatic drainage, or a single non-healing skin ulcer over six weeks in someone with travel to or residence in an endemic region., Persistent, low-grade fever (often double-quotidian — twice daily) with progressive weight loss over weeks to months — a hallmark of visceral leishmaniasis., Progressive, often massive enlargement of the spleen (commonly palpable below the umbilicus) and moderate hepatomegaly in visceral leishmaniasis., Pallor, fatigue, dyspnoea on exertion, easy bruising, and recurrent infections from pancytopenia (anemia, leukopenia, thrombocytopenia) in advanced visceral leishmaniasis., Skin darkening (kala-azar is Hindi for 'black sickness') on hands, feet, abdomen, and face in chronic visceral leishmaniasis., Hypopigmented macules evolving into papules and nodules, especially on the face, arms, and trunk, appearing months to years after VL treatment — post-kala-azar dermal leishmaniasis..
Diagnosis depends on the clinical form. For cutaneous leishmaniasis, parasitological confirmation by smear, biopsy, or culture from the active edge of the lesion is standard; Giemsa-stained tissue smears show amastigotes inside macrophages, and PCR is more sensitive especially for old lesions. Speciation by PCR or isoenzyme analysis matters because treatment differs between species (Leishmania braziliensis complex requires systemic therapy because of mucocutaneous risk; Leishmania major may resolve spontaneously). For mucocutaneous leishmaniasis, biopsy with histology, smear, and PCR is needed and serology supports the diagnosis. For visceral leishmaniasis, the rK39 immunochromatographic rapid test is the field-standard screening tool: sensitivity over 95% and specificity over 90% on Indian subcontinent samples, slightly lower in East Africa where rK28 or rK39 plus direct agglutination test are used in tandem. Splenic aspirate is the most sensitive parasitological test (sensitivity >95%) but carries bleeding risk and is reserved for treatment-failure or relapse evaluation; bone marrow aspirate (sensitivity 60-85%) is safer and often used at presentation. Liver aspirate and lymph-node aspiration are alternatives. Quantitative PCR on peripheral blood is increasingly used to confirm diagnosis, monitor treatment response, and detect relapse in HIV-VL coinfection. Differential diagnosis for visceral leishmaniasis includes lymphoma, leukemia, miliary tuberculosis, malaria, chronic schistosomiasis, hyper-reactive malarial splenomegaly, and tropical splenomegaly syndrome. For cutaneous lesions, the differential includes squamous cell carcinoma, atypical mycobacterial infection, deep fungal infection, syphilis, leprosy, and pyoderma gangrenosum.
Outcome is determined chiefly by clinical form, immune status, and prompt access to therapy. Cutaneous leishmaniasis usually heals over months to years; effective treatment shortens healing and reduces scarring. Single Old World lesions caused by L. major may resolve without treatment in 6-18 months but with disfiguring scars. Mucocutaneous leishmaniasis carries a more serious prognosis: prolonged systemic therapy is required, mucosal destruction can recur years after apparent cure, and quality-of-life impact is severe. Visceral leishmaniasis is fatal in over 95% of untreated patients within months; with effective treatment, cure rates exceed 95% on the Indian subcontinent and 80-95% in East Africa, depending on drug regimen. HIV-VL coinfection carries much higher mortality (10-25%) and relapse risk (over 60% without secondary prophylaxis), but ART plus secondary prophylaxis dramatically improves outcomes. PKDL responds to extended therapy but treatment failure and chronic course are common, especially in Sudan. Survivors of VL have generally good long-term function but may have residual splenomegaly for months and require nutritional rehabilitation. The 2030 WHO road map targets verification of elimination as a public-health problem of VL on the Indian subcontinent and 85% of countries achieving sustained control.
Tropical medicine and infectious disease specialists confirm species, choose region-appropriate drugs, manage drug toxicities (especially with antimonials), and coordinate HIV testing and treatment. Dermatology referral is essential for cutaneous and mucocutaneous disease, and reconstructive surgery follows treatment for severe mucocutaneous sequelae.
Find specialists →Cutaneous leishmaniasis: lesion healing over 1-6 months with active treatment; scars persist. Mucocutaneous leishmaniasis: mucosal healing over 3-12 months; structural recovery often needs years and reconstructive surgery. Visceral leishmaniasis: fever resolves within 7-14 days of treatment; splenomegaly regresses over 1-3 months; blood counts and hypergammaglobulinemia normalize over 2-6 months. PKDL: lesions improve over 12-24 weeks with extended therapy.
Bed rest during acute febrile phase. Gradual return to activity during convalescence — typically by 4-6 weeks for cutaneous disease and 8-12 weeks for visceral disease. Avoid strenuous exercise during severe pancytopenia and splenomegaly.
Choose a clinician working at or trained by a WHO-collaborating leishmaniasis centre, a national reference laboratory, or a major tropical medicine institute (e.g., Rajendra Memorial Research Institute Patna, Kalaazar Medical Research Center Muzaffarpur, KEMRI Kenya, Médecins Sans Frontières kala-azar programmes). Avoid unverified clinics offering unproven herbal therapies for kala-azar.
Medically reviewed by AIHealz Medical Editorial Board · May 13, 2026
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