# Leishmaniasis > The content on this page is for informational and educational purposes only. It does not constitute medical advice, diagnosis, or treatment recommendations. If you have health concerns, consult a qualified healthcare professional. Medova is not a medical service provider. Source: https://medova.health/en/knowledge/diseases/leishmaniasis · Language: en ## Overview Vector-borne parasitic disease transmitted by sandflies. Three main forms: cutaneous (skin sores), mucocutaneous (destroys mucous membranes), and visceral (kala-azar — affects internal organs, fatal if untreated). ## Medical Information - ICD-10: B55 - ICD-11: 1F54 - Causative Agent: parasite - Severity: Critical - Incubation Period: 14–365 days - Mortality Rate: 5% - Vaccine available: No ## Symptoms - Skin ulcer (85%) - Splenomegaly (95%) - Fatigue (85%) - Fever (95%) - Hepatomegaly (80%) - Nasal congestion (90%) - Weight loss (90%) - Dysphagia (30%) - Hemorrhage (60%) - Loss of appetite (70%) - Malaise (80%) - Night sweats (40%) - Swollen lymph nodes (30%) - Cough (15%) - Diarrhea (20%) - Edema (20%) - Hypotension (5%) - Itching (15%) - Jaundice (10%) - Petechiae (25%) ## Transmission - Sandfly bite (Primary route) - Blood transfusion - Congenital (mother-to-child) - Needle sharing ## Overview Leishmaniasis is a vector-borne parasitic disease caused by protozoa of the genus **Leishmania**, transmitted through the bites of infected female phlebotomine sandflies (genera *Phlebotomus* in the Old World and *Lutzomyia* in the New World). Over 20 *Leishmania* species are pathogenic to humans. The disease manifests in three principal clinical forms: **visceral leishmaniasis** (VL, also known as kala-azar), **cutaneous leishmaniasis** (CL), and **mucocutaneous leishmaniasis** (MCL). Visceral leishmaniasis is the most severe form and is almost always fatal if left untreated. Cutaneous leishmaniasis is the most common form globally, while mucocutaneous disease, primarily caused by *L. braziliensis*, leads to progressive destruction of the nasal and oropharyngeal mucosa. An estimated **700,000 to 1 million new cases** occur annually across 98 endemic countries, with **26,000 to 65,000 deaths** per year. The disease disproportionately affects the poorest populations, and malnutrition, displacement, poor housing, and immunosuppression (particularly HIV co-infection) are major risk factors. Leishmaniasis is classified by the WHO as one of the neglected tropical diseases (NTDs) prioritized for control and elimination. ## Overview Leishmaniasis encompasses a spectrum of diseases caused by obligate intracellular protozoan parasites of the genus *Leishmania*. The parasites are transmitted to humans by the bite of infected female sandflies, which are small (2–3 mm) nocturnal insects that breed in organic-rich soil, rubble, and animal burrows. **Key facts:** - **Causative agents:** Over 20 *Leishmania* species, including *L. donovani*, *L. infantum*, *L. major*, *L. tropica*, *L. braziliensis*, and *L. mexicana* - **Vector:** Phlebotomine sandflies (~70 of 800+ species are proven vectors) - **Reservoir hosts:** Humans (anthroponotic VL caused by *L. donovani*), dogs (zoonotic VL caused by *L. infantum*), and various rodents (zoonotic CL) - **Incubation period:** Visceral: 2–6 months (range: 10 days to years); Cutaneous: 2–8 weeks (range: days to months) - **Global burden:** 700,000–1 million new cases/year; 12 million people currently affected; 350 million at risk The three clinical forms have distinct geographic distributions, causative species, and prognoses. Visceral leishmaniasis accounts for roughly 50,000–90,000 new cases annually, with over 90% occurring in **Brazil, Ethiopia, India, Kenya, Somalia, South Sudan, and Sudan**. Cutaneous leishmaniasis accounts for the largest burden, with hotspots in **Afghanistan, Algeria, Brazil, Colombia, Iran, Iraq, Pakistan, Peru, Saudi Arabia, Syria, and Tunisia**. ## Emergency Signs **Seek immediate medical attention** if you develop any of the following signs or symptoms, particularly if you have traveled to or reside in a leishmaniasis-endemic area: **Visceral leishmaniasis emergencies:** - **High fever persisting for more than 2 weeks** with no identified cause - **Rapidly enlarging abdomen** (hepatosplenomegaly) with abdominal discomfort - **Severe anemia** — extreme pallor, tachycardia, dyspnea on exertion - **Bleeding** — epistaxis, gingival bleeding, petechiae, or ecchymoses indicating thrombocytopenia - **Jaundice** or signs of hepatic dysfunction - **Secondary bacterial infections** — pneumonia, septicemia, or enteritis (leading cause of death in VL) **Cutaneous/mucocutaneous emergencies:** - **Non-healing skin ulcer** persisting beyond 2–3 months, especially after travel to endemic areas - **Nasal obstruction with bloody discharge** following past cutaneous leishmaniasis - **Progressive facial swelling** or destruction of nasal/oral tissue - **Difficulty breathing or swallowing** suggesting laryngeal or pharyngeal involvement **Important:** Visceral leishmaniasis has a **case fatality rate exceeding 95%** if left untreated. Early diagnosis and treatment are critical. Individuals with HIV co-infection have significantly worse outcomes and should be treated as a medical emergency. ## Detailed Symptoms The clinical presentation of leishmaniasis varies considerably depending on the infecting *Leishmania* species and the host immune response. **Visceral leishmaniasis (kala-azar):** - Insidious onset with **prolonged irregular fever** (often double-spiking daily) - Progressive **hepatosplenomegaly** — the spleen can become massively enlarged - **Weight loss** and progressive cachexia - **Pancytopenia** (anemia, leukopenia, thrombocytopenia) due to bone marrow infiltration - Hypergammaglobulinemia and hypoalbuminemia - Darkening of the skin (the Hindi term "kala-azar" means "black fever") - Post-kala-azar dermal leishmaniasis (PKDL) may develop months to years after apparent cure, presenting as macular, papular, or nodular rash **Cutaneous leishmaniasis:** - Begins as a small **papule** at the sandfly bite site, progressing over weeks to a nodule - Central necrosis develops, forming a characteristic **painless ulcer** with raised, indurated borders and a granulating base - Lesions are typically on exposed skin — face, arms, legs - Most CL lesions **self-heal** in 6–12 months but leave disfiguring scars - Diffuse cutaneous leishmaniasis (DCL) produces widespread non-ulcerating nodules resembling lepromatous leprosy **Mucocutaneous leishmaniasis:** - Occurs months to years after an initial cutaneous lesion (primarily *L. braziliensis* in Latin America) - **Nasal mucosal involvement** begins with stuffiness, epistaxis, and crusting - Progressive destruction of the **nasal septum, palate, lips, pharynx, and larynx** - Can lead to severe facial disfigurement ("espundia"), difficulty swallowing, and aspiration pneumonia ## Course of Disease The natural history of leishmaniasis is determined by the infecting species and host immune response, and follows distinct trajectories for each clinical form. **Visceral leishmaniasis:** 1. **Incubation period:** Typically 2–6 months (range: 10 days to several years; reactivation may occur decades after initial infection in immunosuppressed individuals) 2. **Onset:** Insidious, with low-grade fever, malaise, and gradual weight loss 3. **Progressive phase:** Over weeks to months — fever becomes persistent and irregular (often double quotidian), the spleen and liver enlarge progressively, and pancytopenia worsens 4. **Advanced disease:** Severe cachexia, massive splenomegaly, edema, hemorrhagic manifestations, and darkened skin 5. **Terminal phase (untreated):** Death from secondary bacterial infections (pneumonia, tuberculosis, dysentery), severe anemia, or hemorrhage — typically within 1–2 years of symptom onset 6. **Post-treatment:** PKDL may develop 6 months to several years after apparent cure **Cutaneous leishmaniasis:** 1. **Incubation:** 2–8 weeks (range: days to months) 2. **Initial lesion:** Small erythematous papule at the bite site 3. **Progression:** Papule enlarges to a nodule, then develops central necrosis forming an ulcer over 2–6 weeks 4. **Chronic phase:** Ulcer persists for months with a characteristic "volcano-like" morphology 5. **Resolution:** Spontaneous healing in 6–12 months (Old World CL) to 6–18 months (New World CL), leaving an atrophic depressed scar **Mucocutaneous leishmaniasis:** 1. **Latency:** Months to years (even decades) after the initial cutaneous lesion has healed 2. **Mucosal onset:** Nasal congestion, crusting, and epistaxis 3. **Progressive destruction:** Over months to years, erosion of nasal septum, palate, uvula, and pharynx 4. **Complications:** Facial collapse, aspiration pneumonia, and secondary infections ## Diagnosis Definitive diagnosis of leishmaniasis requires demonstration of the parasite or its DNA, combined with clinical and epidemiological assessment. **Visceral leishmaniasis:** - **rK39 rapid diagnostic test (RDT):** Immunochromatographic strip detecting antibodies to the rK39 antigen; sensitivity >95% and specificity >90% in South Asia; lower sensitivity in East Africa (~85%). Recommended as first-line diagnostic in endemic areas - **Splenic aspiration:** Highest sensitivity (~95%) but carries a risk of hemorrhage; requires trained personnel and monitoring facilities - **Bone marrow aspirate:** Sensitivity of 60–85%; safer than splenic aspirate and widely used - **PCR:** Highly sensitive and specific; can be performed on blood, bone marrow, or tissue; increasingly available but costly - **Direct agglutination test (DAT):** High sensitivity and specificity; requires laboratory infrastructure; useful in East Africa where rK39 sensitivity is lower - **Serology limitations:** Antibodies persist after cure, so serology cannot distinguish active from past infection **Cutaneous leishmaniasis:** - **Skin biopsy or scraping** from the ulcer margin with Giemsa staining for amastigotes — sensitivity 50–70% - **PCR from biopsy/scraping** — sensitivity >90%, also allows species identification - **Culture** in NNN (Novy-MacNeal-Nicolle) medium — gold standard for species identification but slow (1–4 weeks) - **Leishmanin skin test (Montenegro test):** Indicates prior exposure; positive in CL, negative in active VL **Mucocutaneous leishmaniasis:** - **Biopsy of affected mucosa** — parasites are often scarce, reducing microscopy sensitivity to 20–30% - **PCR** is the preferred modality for MCL diagnosis (sensitivity >90%) - Serology is usually positive and supports the diagnosis ## Treatment Treatment of leishmaniasis depends on the clinical form, infecting species, geographic region, and patient factors (age, pregnancy, HIV status). **Visceral leishmaniasis:** - **Liposomal amphotericin B** (AmBisome) — WHO-recommended first-line for VL in most settings. Regimen: 3–5 mg/kg total dose over 3–6 days in South Asia; 18–21 mg/kg total in East Africa/Mediterranean - **Miltefosine** — the first oral drug for VL; 2.5 mg/kg/day for 28 days. Effective in South Asia (cure rate ~94%); teratogenic, contraindicated in pregnancy - **Sodium stibogluconate** or **meglumine antimoniate** (pentavalent antimonials) — 20 mg Sb⁵⁺/kg/day for 28–30 days; cardiotoxicity risk; declining use due to resistance in Bihar, India - **Combination therapy:** Single-dose liposomal amphotericin B + miltefosine (or paromomycin) — WHO-recommended in South Asia for shorter, safer treatment - **Paromomycin** — 15 mg/kg/day IM for 21 days; used as monotherapy in East Africa or in combination **Cutaneous leishmaniasis:** - Many CL lesions **self-heal** without treatment, but treatment is recommended for large, multiple, or cosmetically sensitive lesions - **Intralesional sodium stibogluconate** — first-line for localized Old World CL - **Thermotherapy** or **cryotherapy** — non-pharmacological alternatives with ~70% cure rates - **Oral miltefosine** — for New World CL (especially *L. braziliensis*, *L. guyanensis*) - **Systemic pentavalent antimonials** — for multiple lesions or mucocutaneous risk **Mucocutaneous leishmaniasis:** - Always requires **systemic therapy** due to risk of progressive tissue destruction - **Liposomal amphotericin B** or **systemic pentavalent antimonials** for 28 days - Reconstructive surgery may be needed for severe facial deformity ## Prevention Details There is currently **no vaccine** available for human leishmaniasis, although several candidates are in clinical development. Prevention relies on reducing human-sandfly contact and controlling reservoir hosts. **Personal protective measures for travelers:** - **Insecticide-treated bed nets** with fine mesh (sandflies are small enough to pass through standard mosquito nets unless mesh size is <0.6 mm or nets are permethrin-impregnated) - **DEET-based insect repellents** (20–30% concentration) applied to exposed skin during dusk and nighttime hours when sandflies are most active - **Permethrin-treated clothing** — particularly effective as sandflies bite through thin fabric - **Avoiding outdoor activities at night** in endemic areas, especially near rubble, old walls, animal shelters, and forests - **Sleeping in air-conditioned or screened rooms** — sandflies are weak fliers and cannot navigate well in airflow **Public health interventions:** - **Indoor residual spraying (IRS)** with pyrethroids — effective in reducing sandfly density, particularly for VL control in South Asia - **Reservoir control:** Culling or insecticide-collaring of infected domestic dogs (zoonotic VL); rodent control for zoonotic CL - **Environmental management:** Reducing sandfly breeding sites by clearing rubble, waste, and organic matter near homes - **Active case detection and treatment** — reducing the human reservoir (especially VL and PKDL cases) interrupts anthroponotic transmission **Note:** Travelers to endemic areas should be aware that sandfly bites are often painless and may go unnoticed. Any non-healing skin lesion developing weeks to months after travel should prompt evaluation for cutaneous leishmaniasis. ## Travel Advice **Risk assessment for travelers:** Leishmaniasis risk is generally **low** for most short-term tourists staying in urban hotels, but can be **significant** for adventure travelers, researchers, military personnel, and long-term residents in endemic rural areas. The risk is highest during the rainy season when sandfly populations peak. **High-risk destinations:** - **Visceral leishmaniasis:** Indian subcontinent (Bihar state), East Africa (South Sudan, Sudan, Ethiopia, Kenya, Somalia), Brazil (northeast), Mediterranean basin - **Cutaneous leishmaniasis:** Afghanistan, Iran, Iraq, Syria, Saudi Arabia, Algeria, Tunisia, Peru, Colombia, Brazil, Central Asia - **Mucocutaneous leishmaniasis:** Bolivia, Brazil, Peru, and other Amazon basin countries **Pre-travel advice:** - No chemoprophylaxis or vaccine is available - Pack **fine-mesh insecticide-treated bed nets** and DEET-based repellent - Discuss risk with a travel medicine specialist if visiting highly endemic rural areas for extended periods **During travel:** - Avoid outdoor activities between **dusk and dawn** in endemic areas - Sleep under permethrin-treated nets or in screened/air-conditioned rooms - Minimize time near animal shelters, old stone walls, and forest edges - Wear long sleeves and treated clothing in the evenings **Post-travel:** - **Any non-healing skin ulcer** appearing weeks to months after travel to an endemic area should be evaluated for CL — inform your physician of your travel history - **Unexplained prolonged fever** with splenomegaly after travel to VL-endemic areas warrants urgent investigation - Incubation can be prolonged (months to years), so maintain awareness even long after return ## How common is it? Leishmaniasis is endemic in **98 countries** across tropical and subtropical regions, with an estimated **12 million people** currently infected and **350 million** at risk. **Global burden estimates (WHO, 2024):** - **Visceral leishmaniasis:** 50,000–90,000 new cases annually; ~95% of cases reported from Brazil, Ethiopia, India, Kenya, Somalia, South Sudan, and Sudan - **Cutaneous leishmaniasis:** 600,000–1,000,000 new cases annually; ~85% of cases from Afghanistan, Algeria, Brazil, Colombia, Iran, Iraq, Pakistan, Peru, Saudi Arabia, Syria, and Tunisia - **Mucocutaneous leishmaniasis:** ~5,000 cases annually, primarily in Bolivia, Brazil, Ethiopia, and Peru - **Deaths:** 26,000–65,000 per year, predominantly from VL **Regional epidemiology:** - **South Asia:** India (Bihar), Bangladesh, and Nepal historically bore the heaviest VL burden; the Kala-Azar Elimination Programme has reduced cases by >95% since 2005 - **East Africa:** South Sudan and Sudan remain major hotspots; conflict and displacement drive outbreaks - **Americas:** Brazil reports >90% of New World VL and significant CL burden; CL extends from Texas to northern Argentina - **Mediterranean:** *L. infantum* causes sporadic zoonotic VL (dog reservoir); southern Europe, North Africa, and the Middle East - **Central Asia:** CL caused by *L. major* (zoonotic) and *L. tropica* (anthroponotic); conflict zones in Syria, Iraq, and Afghanistan have experienced massive CL outbreaks **Trends:** - Climate change is expanding sandfly habitats to higher altitudes and latitudes (cases now reported in northern Italy, southern Germany) - Urbanization and deforestation are creating new foci - HIV-VL co-infection is an emerging problem in East Africa and southern Europe - The WHO NTD Roadmap 2021–2030 targets elimination of VL as a public health problem (incidence <1/10,000 at district level) ## Risk Factors Multiple host, environmental, and socioeconomic factors influence the risk of acquiring leishmaniasis and the severity of disease. **Environmental and behavioral risk factors:** - **Living in or traveling to endemic areas** — 98 countries have reported cases; risk is highest in rural and peri-urban settings - **Nighttime outdoor exposure** — sandflies are crepuscular and nocturnal feeders - **Proximity to animal reservoirs** — domestic dogs (VL), rodent burrows (CL) - **Poor housing conditions** — mud walls, earth floors, and lack of window screens facilitate sandfly entry - **Sleeping outdoors or on the ground** without bed nets - **Occupational exposure** — agricultural workers, soldiers, forest workers, construction laborers **Host risk factors for severe disease:** - **Malnutrition** — strongly associated with progression from subclinical infection to clinical VL; odds ratio 2–9× depending on severity - **HIV co-infection** — greatly increases risk of VL (10–100× higher in HIV-positive individuals in endemic areas); impairs treatment response and promotes relapse - **Immunosuppression** — organ transplant recipients, patients on TNF-alpha inhibitors, and other immunocompromised states - **Age:** Children under 5 years are at highest risk for VL in endemic areas - **Genetic factors:** Certain HLA alleles and polymorphisms in cytokine genes influence susceptibility **Socioeconomic risk factors:** - **Poverty:** Leishmaniasis is strongly associated with the poorest communities — poor nutrition, inadequate housing, and limited healthcare access - **Displacement and migration** — refugee camps in endemic areas experience outbreaks; non-immune populations entering endemic zones are at high risk - **Deforestation and urbanization** — bring humans into contact with sylvatic transmission cycles ## Complications Details Leishmaniasis can lead to serious and potentially life-threatening complications across all clinical forms. **Visceral leishmaniasis complications:** - **Secondary bacterial infections** — the most common cause of death in VL patients; pneumonia, tuberculosis, and enteritis frequently arise due to profound immunosuppression and neutropenia - **Hemorrhage** — severe thrombocytopenia leads to epistaxis, gastrointestinal bleeding, and petechiae; splenic rupture is a rare but fatal complication - **Severe anemia** — hemoglobin levels can fall below 5 g/dL, requiring transfusion; anemia results from bone marrow suppression, hypersplenism, and hemolysis - **Post-kala-azar dermal leishmaniasis (PKDL)** — macular, papular, or nodular skin lesions developing 6 months to years after VL treatment; more common in East Africa (up to 50%) than South Asia (5–10%); serves as a reservoir for ongoing transmission - **Drug-related toxicity** — pentavalent antimonials cause cardiotoxicity (QT prolongation, fatal arrhythmias), pancreatitis, and hepatotoxicity; amphotericin B can cause nephrotoxicity and infusion reactions **Cutaneous leishmaniasis complications:** - **Disfiguring scarring** — even self-healed lesions leave permanent atrophic scars; facial lesions cause significant psychosocial impact - **Secondary bacterial superinfection** of ulcers - **Leishmaniasis recidivans** — chronic relapsing form with satellite papules around scarred lesions (usually *L. tropica*) - **Progression to mucocutaneous disease** — 5–15% risk with *L. braziliensis* **Mucocutaneous leishmaniasis complications:** - **Nasal septum perforation** and progressive destruction of oropharyngeal structures - **Aspiration pneumonia** from pharyngeal and laryngeal involvement - **Severe psychological and social consequences** — facial disfigurement leads to stigma, isolation, and depression - **Treatment failure and relapse** — common, particularly without prolonged follow-up ## Recovery & Outlook The prognosis of leishmaniasis varies markedly by clinical form and access to treatment. **Visceral leishmaniasis:** - **Untreated:** Case fatality rate (CFR) exceeds **95%** within 1–2 years, typically from secondary infections, hemorrhage, or severe anemia - **Treated:** Cure rates of **90–98%** with liposomal amphotericin B-based regimens; relapse rates of 1–5% in immunocompetent patients - **HIV co-infection:** Dramatically worsened prognosis — relapse rates of 20–60% even after adequate treatment; mortality remains high - **Post-kala-azar dermal leishmaniasis (PKDL):** Develops in 5–10% of VL patients in South Asia and up to 50% in Sudan; usually non-fatal but serves as a parasite reservoir **Cutaneous leishmaniasis:** - **Self-healing** in 6–12 months for most Old World CL (*L. major*, *L. tropica*), but permanent **scarring** is universal - Diffuse cutaneous leishmaniasis (DCL) does **not** self-heal and is extremely difficult to treat - New World CL caused by *L. braziliensis* carries a **5–15% risk** of progressing to mucocutaneous disease **Mucocutaneous leishmaniasis:** - Without treatment, progressive and irreversible destruction of nasopharyngeal tissue - With systemic treatment, cure rates are **70–90%**, though relapse is common - Significant **psychological morbidity** and social stigma associated with facial disfigurement **Overall**, early diagnosis and appropriate treatment yield excellent outcomes for most patients. The greatest determinant of poor prognosis is delayed presentation, particularly for visceral disease. ## Sources & content verification - Data sources: SafeTripVax Medical Team (WHO Fact Sheet 2024, CDC Yellow Book 2024), WHO Disease Factsheets 2024 + CDC Yellow Book 2024 + Heymann CDD 21st ed. - Generated by: AI + Human review - Review status: Awaiting medical review - Last updated: 2026-03-29 - [www.who.int](https://www.who.int/news-room/fact-sheets) --- The content on this page is for informational and educational purposes only. It does not constitute medical advice, diagnosis, or treatment recommendations. If you have health concerns, consult a qualified healthcare professional. Medova is not a medical service provider. [Full terms of use](https://medova.health/en/terms)