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Transmitted by sandfly bites, mainly at dusk/night. Use insect repellent and bed nets in endemic areas (Middle East, South Asia, East Africa, Latin America). Cutaneous form is more common in travelers. Seek evaluation for non-healing skin ulcers after travel.
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).
Symptoms | Frequency | Severity | Onset |
|---|---|---|---|
| Fatigue | 85% | Mild | Early |
| Fever | 95% | Moderate | Early |
| Nasal congestion | 90% | Moderate | Early |
| Loss of appetite | 70% | Mild | Early |
| Malaise | 80% | Mild | Early |
| Swollen lymph nodes | 30% | Mild | Early |
| Edema | 20% | Mild | Early |
| Skin ulcer | 85% | Moderate | Peak |
| Splenomegaly | 95% | Severe | Peak |
| Hepatomegaly | 80% | Moderate | Peak |
| Weight loss | 90% | Moderate | Peak |
| Dysphagia | 30% | Moderate | Peak |
| Hemorrhage | 60% | Moderate | Peak |
| Night sweats | 40% | Mild | Peak |
| Cough | 15% | Mild | Peak |
| Diarrhea | 20% | Mild | Peak |
| Itching | 15% | Mild | Peak |
| Petechiae | 25% | Moderate | Peak |
| Hypotension | 5% | Moderate | Late |
| Jaundice | 10% | Moderate | Late |
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.
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.
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.
Most common signs and 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
Knowing the symptoms is the first step to a quick response.
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:
Cutaneous leishmaniasis:
Mucocutaneous leishmaniasis:
How this disease is identified
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
Available treatment methods
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
Most cases are effectively treated with early diagnosis.
How to protect yourself
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.
Preparation is the best protection.
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
Statistics and geographic data
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)
Who is most at risk
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
Potential complications
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
Expected outcomes and recovery
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.
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.
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