Leishmaniasis in United States: Symptoms, Causes & Treatment | aihealz
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Leishmaniasis.Care & specialists in United States
In United States, 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.
key facts
Prevalence
Cutaneous leishmaniasis: approximately 600,000-1,000,000 new cases per year; visceral leishmaniasis: 50,000-90,000 new cases per year (WHO 2024)
Demographics
Endemic in 90+ countries on five continents; over 1 billion people live in endemic areas. Visceral leishmaniasis concentrated in Brazil, East Africa, and Indian subcontinent
Avg. age
Visceral leishmaniasis peaks under age 15 in endemic regions; cutaneous leishmaniasis any age
Global cases
Estimated 12 million people currently infected globally; visceral leishmaniasis carries 95%+ mortality if untreated
Specialist
Tropical Medicine
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How you might notice it
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..
01A 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.
02Multiple 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.
03Persistent, low-grade fever (often double-quotidian — twice daily) with progressive weight loss over weeks to months — a hallmark of visceral leishmaniasis.
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How it’s diagnosed
diagnosis
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.
Key tests
01
rK39 rapid immunochromatographic test (VL)Rapid bedside screening for visceral leishmaniasis with very high sensitivity in the Indian subcontinent
02
Bone marrow aspirate with Giemsa stain and cultureParasitological confirmation of visceral leishmaniasis with moderate sensitivity (60-85%) and excellent specificity
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Treatment & cost
medical treatments
✓Liposomal amphotericin B 10 mg/kg single intravenous dose (Indian subcontinent VL)
✓Miltefosine 50-100 mg orally daily for 28 days
✓Pentavalent antimonials (sodium stibogluconate / meglumine antimoniate) 20 mg Sb⁵⁺/kg/day for 20-28 days
✓Paromomycin (aminosidine) 15 mg/kg/day intramuscular for 21 days
surgical options
SplenectomyResolution of hypersplenism and pancytopenia in most operated patients; reserved for treatment-failure cases
Reconstructive surgery for mucocutaneous sequelaeVariable; staged reconstruction often required over 1-3 years
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Causes & risk factors
known causes
Infection by Leishmania donovani complex causing visceral disease
Leishmania donovani drives anthroponotic VL in the Indian subcontinent (India, Nepal, Bangladesh) and East Africa (Sudan, South Sudan, Ethiopia). Leishmania infantum (synonym L. chagasi) drives zoonotic VL around the Mediterranean basin and in Latin America, with domestic dogs as the principal reservoir. The parasite is transmitted by Phlebotomus argentipes in India, P. orientalis in East Africa, and P. perniciosus in the Mediterranean.
Infection by Old World cutaneous Leishmania species
Leishmania major causes zoonotic CL in rural Middle East, North Africa, and Central Asia with rodent reservoirs and Phlebotomus papatasi vectors. Leishmania tropica causes anthroponotic CL in urban Middle Eastern, Mediterranean, and Asian foci with Phlebotomus sergenti vectors. Leishmania aethiopica causes CL and diffuse CL in Ethiopian highlands.
Infection by New World cutaneous and mucocutaneous Leishmania species
Leishmania mexicana complex causes CL in Mexico, Central America, and parts of South America. Leishmania braziliensis complex (L. braziliensis, L. panamensis, L. guyanensis) cause CL that can progress to mucocutaneous disease in Bolivia, Peru, Ecuador, and Brazil. Lutzomyia species are vectors. Forest mammals are reservoirs.
Phlebotomine sandfly bite
Female sandflies smaller than 3 mm bite at dusk and dawn and through the night. They breed in cracks in dwellings, animal sheds, rodent burrows, and forest leaf litter. A single infected sandfly bite can transmit the parasite; bites are often unnoticed because of the small mouthparts.
Person-to-person transmission via blood and shared injecting equipment
Anthroponotic VL caused by L. donovani persists through human-to-sandfly-to-human transmission; PKDL patients are an under-recognized reservoir. Transmission via blood transfusion, organ transplantation, congenital infection, and shared needles in injecting drug users has been documented.
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Living with it
01Sleep under a long-lasting insecticidal net (treated with deltamethrin or permethrin) in endemic regions, particularly in Bihar, Nepal, and East Africa.
02Use indoor residual spraying programmes targeting sandflies — a cornerstone of the Kala-Azar Elimination Programme.
03Apply DEET-, picaridin-, or IR3535-based repellent during dusk and dawn outdoor activity in endemic areas.
04Wear long sleeves and trousers during dusk and dawn; sandflies are crepuscular and small enough to pass through normal mesh.
05Treat domestic dogs with insecticidal collars or topical preparations in zoonotic L. infantum foci (Mediterranean, Latin America).
06Engage with active case detection campaigns; treat PKDL promptly to break the human-to-sandfly transmission cycle.
07Vaccinate dogs against canine leishmaniasis where licensed canine vaccines are available (CaniLeish, Letifend).
recommended foods
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When to seek help
why see a tropical medicine
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.
Cutaneous leishmaniasis (CL)Most common form, with around 600,000-1,000,000 new cases per year. Causes one or more skin ulcers at the site of sandfly bites — exposed face, arms, and lower legs — beginning as a papule that enlarges into a painless 1-5 cm ulcer with raised borders. Heals over months to years leaving a depressed scar.
Mucocutaneous leishmaniasis (MCL, espundia)Destructive ulceration of the mucous membranes of the nose, mouth, palate, and pharynx that appears months to years after an apparently healed cutaneous lesion. Mainly caused by Leishmania braziliensis in Bolivia, Peru, and Brazil. Can cause severe disfigurement and airway compromise.
Visceral leishmaniasis (VL, kala-azar)Systemic infection of reticuloendothelial organs (spleen, liver, bone marrow). Fever, weight loss, massive hepatosplenomegaly, pancytopenia, and hypergammaglobulinemia. Fatal in over 95% of untreated patients within 2 years of symptom onset.
Post-kala-azar dermal leishmaniasis (PKDL)Hypopigmented macules and papules that evolve into nodules, especially on the face, arms, and trunk, appearing months to years after VL treatment. Occurs in roughly 5-10% of Indian and up to 50% of Sudanese VL patients. PKDL patients are a key reservoir for ongoing transmission.
Diffuse cutaneous leishmaniasis (DCL)Rare anergic form resembling lepromatous leprosy: multiple non-ulcerating papules and nodules covering large areas of the body in patients with poor cell-mediated immunity. Difficult to treat and often relapses.
HIV-VL coinfectionVisceral leishmaniasis in HIV-infected individuals presents atypically, responds less well to standard therapy, and relapses frequently. Co-endemic in Ethiopia, Brazil, and the Mediterranean basin.
Living with Leishmaniasis
Timeline
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.
Lifestyle
01Complete the full course of treatment as prescribed; partial treatment promotes drug resistance and PKDL.
02Attend monthly follow-up after VL treatment for the first 6 months and at 12 months to detect relapse.
03Report any new hypopigmented patches or papules after kala-azar treatment promptly.
04Avoid sleeping outdoors in endemic regions during peak sandfly activity.
05Maintain adequate nutrition during recovery — malnutrition predicts poor outcomes.
06Disclose travel history to endemic regions to all clinicians during any future febrile illness, even years later.
Daily management
01Take oral medications (miltefosine) on a full stomach and at consistent times.
02
Complementary approaches
Topical paromomycin ointment (15% paromomycin/methylbenzethonium chloride or paromomycin/gentamicin)Effective topical therapy for Old World cutaneous leishmaniasis. Applied twice daily for 20 days. Suited to single small lesions in low-risk species.
Oral fluconazole / ketoconazole for selected Old World cutaneous leishmaniasisFluconazole 200 mg orally daily for 6 weeks improves cure rates for Leishmania major in Saudi Arabia and Iran in randomized trials; ketoconazole has activity against Leishmania mexicana.
Choosing a doctor
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.
Leishmaniasis is a parasitic disease caused by Leishmania protozoa transmitted by sandfly bites. It has three main forms: cutaneous (skin ulcers), mucocutaneous (destructive nose and mouth lesions), and visceral (kala-azar — fatal systemic disease). Endemic across 90+ countries, mainly in tropical and subtropical regions.
What is kala-azar?▾▴
Kala-azar is the Hindi term ('black sickness') for visceral leishmaniasis, the systemic form caused by Leishmania donovani in India and Africa and Leishmania infantum in the Mediterranean and Latin America. It causes fever, weight loss, hepatosplenomegaly, and pancytopenia. Untreated, mortality exceeds 95% within two years.
How is leishmaniasis spread?▾▴
Leishmaniasis is transmitted by bites of infected female phlebotomine sandflies, mostly at dusk and dawn. Sandflies pick up parasites from infected humans (anthroponotic transmission) or animal reservoirs such as dogs, rodents, or forest mammals (zoonotic transmission). Person-to-person spread by blood, organ transplant, congenital, and shared needles has also been documented.
What are the first symptoms of leishmaniasis?▾▴
Cutaneous leishmaniasis starts as a painless papule at a bite site that enlarges into an ulcer over weeks. Visceral leishmaniasis begins with low-grade fever, weight loss, and progressive abdominal swelling from splenomegaly over 2-8 weeks. Mucocutaneous disease can appear months to years after an apparently healed skin lesion as nasal congestion and ulceration.
Is leishmaniasis curable?▾▴
Yes, with appropriate treatment. Single-dose liposomal amphotericin B cures over 95% of visceral leishmaniasis in the Indian subcontinent. Cutaneous disease typically responds to topical, intralesional, or systemic therapy. Mucocutaneous and HIV-coinfected disease require prolonged and combination therapy. Untreated visceral disease is almost always fatal.
What is the treatment for kala-azar?▾▴
In the Indian subcontinent, WHO recommends single-dose intravenous liposomal amphotericin B 10 mg/kg, with cure rates above 95%. Where liposomal amphotericin B is unavailable, multidose regimens, oral miltefosine for 28 days, or combination therapy are used. In East Africa, sodium stibogluconate plus paromomycin for 17 days remains standard.
What is the rK39 test?▾▴
The rK39 immunochromatographic rapid test is a finger-prick antibody test for visceral leishmaniasis. Sensitivity exceeds 95% in the Indian subcontinent and is around 80% in East Africa. Results in 10-20 minutes. Antibody persists after cure, so a positive test in someone previously treated does not by itself prove active disease.
What is post-kala-azar dermal leishmaniasis?▾▴
Post-kala-azar dermal leishmaniasis (PKDL) is a hypopigmented, papular, or nodular skin eruption that appears months to years after apparent cure of visceral leishmaniasis. It affects 5-10% of treated Indian patients and up to 50% of Sudanese patients. PKDL is highly infectious to sandflies and is a key reservoir for transmission; prompt treatment is essential.
Can leishmaniasis come back after treatment?▾▴
Relapse after treatment is uncommon in immunocompetent patients with effective initial therapy (under 5% in Indian VL). Relapse rates are much higher in HIV-VL coinfection (over 60% without secondary prophylaxis). Mucocutaneous leishmaniasis can recur years after apparent cure and requires long follow-up.
How is cutaneous leishmaniasis treated?▾▴
Treatment depends on species, lesion size and number, and risk of mucocutaneous progression. Options include topical paromomycin, intralesional pentavalent antimony, cryotherapy, thermotherapy, oral miltefosine or fluconazole, or systemic pentavalent antimony or liposomal amphotericin B. Species at risk of mucocutaneous progression (L. braziliensis complex) require systemic therapy.
Is leishmaniasis common in India?▾▴
Yes — historically India bore the largest VL burden globally, concentrated in Bihar. The Kala-Azar Elimination Programme has cut incidence by more than 95% since 2007, and most endemic blocks now meet the WHO elimination threshold of under 1 case per 10,000 people. Cutaneous leishmaniasis is rare in India.
Can leishmaniasis be prevented?▾▴
Yes, through a combination of insecticide-treated bed nets, indoor residual spraying, insect repellents, long clothing at dusk and dawn, and treatment of human and (where applicable) canine reservoirs. The Indian Kala-Azar Elimination Programme combines surveillance, prompt diagnosis, drug treatment, and vector control.
How long is the incubation period of leishmaniasis?▾▴
Cutaneous lesions usually appear 2 weeks to 3 months after the sandfly bite. Visceral leishmaniasis has a longer and more variable incubation period of 2-6 months, sometimes years. Mucocutaneous disease can appear months to many years after an initial cutaneous lesion.
Can leishmaniasis affect HIV-positive people more severely?▾▴
Yes. HIV-VL coinfection produces atypical presentations, blunted antibody response (lower rK39 sensitivity), poorer treatment response, and high relapse rates above 60% without secondary prophylaxis. WHO recommends combination antiparasitic therapy plus antiretroviral therapy and ongoing secondary prophylaxis until sustained CD4 recovery.
Is there a vaccine for leishmaniasis?▾▴
No licensed human vaccine is currently available, although several candidates are in clinical trials. Canine vaccines (CaniLeish, Letifend) are licensed in Europe and Brazil and reduce risk of zoonotic transmission. Live-attenuated leishmanization (deliberate inoculation with L. major to prevent disfiguring lesions) was historically used in the Middle East.
Why does kala-azar darken the skin?▾▴
Chronic visceral leishmaniasis is associated with hyperpigmentation of the skin of the hands, feet, abdomen, and face — hence the Hindi name kala-azar ('black sickness'). The mechanism involves immune-driven melanocyte activation; pigmentation usually fades over months to years after successful treatment.
What is miltefosine and is it safe?▾▴
Miltefosine is the first oral drug for leishmaniasis, taken at 50-100 mg daily for 28 days. It is effective for VL, CL, MCL, and PKDL. Common side-effects are gastrointestinal upset and transient elevations in transaminases and creatinine. Miltefosine is teratogenic and requires effective contraception during and for 4 months after therapy in women of reproductive age.
Can sandflies transmit other diseases?▾▴
Yes. Phlebotomine sandflies can also transmit sandfly fever viruses (including Sicilian, Naples, and Toscana viruses), bartonellosis (Carrión's disease), and Vesiculovirus species. Vector-control measures for leishmaniasis incidentally reduce risk of these other infections.
Is leishmaniasis contagious between people?▾▴
Leishmaniasis is not typically contagious by casual contact. Anthroponotic VL caused by L. donovani requires the sandfly intermediate vector. However, transmission by blood transfusion, organ transplant, shared needles, and rarely from mother to child has been documented; sexual transmission has been reported anecdotally.
What follow-up is needed after kala-azar treatment?▾▴
Patients are reviewed at 1, 3, 6, and 12 months after treatment. Clinical assessment of spleen size, weight, and energy is combined with full blood count. Active surveillance for PKDL skin lesions continues for at least 12 months. Patients with HIV coinfection require ongoing secondary prophylaxis until sustained CD4 recovery above 200 cells/µL for 6 months.
Can children get kala-azar?▾▴
Yes — children under 15 bear the heaviest VL burden in endemic regions. Pediatric VL responds to weight-based dosing of liposomal amphotericin B. Nutritional rehabilitation, anemia treatment, and treatment of coexistent infections (especially malaria and pneumonia) are essential.
Progressive, often massive enlargement of the spleen (commonly palpable below the umbilicus) and moderate hepatomegaly in visceral leishmaniasis.
05Pallor, fatigue, dyspnoea on exertion, easy bruising, and recurrent infections from pancytopenia (anemia, leukopenia, thrombocytopenia) in advanced visceral leishmaniasis.
06Skin darkening (kala-azar is Hindi for 'black sickness') on hands, feet, abdomen, and face in chronic visceral leishmaniasis.
07Hypopigmented 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.
08Progressive nasal congestion, epistaxis, ulceration of the nasal septum, and palatal perforation in mucocutaneous leishmaniasis.
09Hoarseness, dysphagia, and progressive disfigurement when mucocutaneous disease involves the pharynx and larynx.
10Bleeding gums, recurrent fevers, and opportunistic infections in HIV-VL coinfection.
early warning signs
•A non-healing painless skin ulcer or papule for more than 4-6 weeks at a site previously exposed to insect bites in an endemic region
•Persistent low-grade fever with palpable spleen in a child or young adult from rural Bihar, eastern Sudan, or rural Brazil
•Unexplained progressive splenomegaly in a person with no obvious haematological or hepatic explanation
•Recurrent epistaxis, nasal crusting, or ulceration in a person who travelled to or lived in the Amazon basin years earlier
•Hypopigmented macules and papules on the face of a person treated for kala-azar within the past 1-2 years
● emergency signs
•Severe pancytopenia with bleeding or systemic infection in visceral leishmaniasis — requires admission for transfusion, broad-spectrum antibiotics, and urgent leishmaniasis treatment
•Hemodynamic instability or splenic rupture from massive splenomegaly
•Airway compromise from mucocutaneous leishmaniasis affecting larynx or pharynx
•Severe drug reactions to pentavalent antimonials — QT prolongation, arrhythmia, pancreatitis, hepatitis — particularly in older or HIV-coinfected patients
•VL relapse in HIV coinfection with severe sepsis or multi-organ failure
03
Splenic aspirateHighest sensitivity parasitological test for VL (>95%); reserved for treatment-failure or relapse where bone marrow and rK39 are non-diagnostic
04
Skin lesion smear or punch biopsy with Giemsa stain, culture, and PCR (CL/MCL)Confirms cutaneous or mucocutaneous leishmaniasis and identifies species
05
Leishmania PCR (qPCR or kinetoplast DNA assays)Sensitive confirmation in tissue, blood, and bone marrow; quantitates parasite load for treatment monitoring; identifies species
06
Full blood count, biochemistry, and protein electrophoresisDetects pancytopenia, hypergammaglobulinemia, and impaired hepatic and renal function characteristic of VL
07
HIV testingIdentifies coinfection that affects treatment choice, prognosis, and follow-up duration
Outlook
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.
HIV coinfection, solid-organ transplantation, and TNF-alpha inhibitor therapy can reactivate latent leishmaniasis and produce severe, relapsing disease. HIV-VL coinfection accounts for a substantial proportion of VL cases in Ethiopia and is rising in Brazil.
risk factors
Residence or travel in an endemic regionenvironmental
Endemic in 90+ countries. Bihar (India), Terai (Nepal), eastern Sudan, South Sudan, Ethiopia, north-east Brazil, Mediterranean basin, and rural Iran, Iraq, Afghanistan, Syria are major foci. Sandflies are most active at dusk and dawn and feed indoors and outdoors.
Outdoor or rural residenceenvironmental
Living in mud or thatch-walled houses, sleeping outdoors, or working in agriculture, forestry, or military operations in endemic areas increases exposure to sandfly bites.
Poverty and crowdingmodifiable
Visceral leishmaniasis is strongly associated with poverty, malnutrition, and poor housing. Income gradient is steep in Bihar and East Africa.
Malnutritionmodifiable
Children with protein-calorie malnutrition are at higher risk of progressing from asymptomatic infection to symptomatic VL. Vitamin A and zinc deficiency further increase risk.
HIV coinfection or immunosuppressionmodifiable
HIV-VL coinfection produces atypical presentations, poorer treatment response, and higher relapse rates. Solid-organ transplant recipients and patients on TNF inhibitors can reactivate latent infection.
Domestic dog ownership in zoonotic transmission zonesenvironmental
In Mediterranean and Latin American VL foci, domestic dogs are the principal reservoir for Leishmania infantum. Canine vaccines and insecticidal collars reduce human risk.
Recent prior cutaneous leishmaniasis caused by Leishmania braziliensis complexnon-modifiable
Roughly 1-10% of L. braziliensis cutaneous infections progress to mucocutaneous disease months to years later; risk persists for decades.
High-protein diet (1.2-1.5 g/kg/day) during recovery to address weight loss
•Iron-, folate-, and B12-rich foods to support hematologic recovery
•Vitamin A- and zinc-rich foods (carrots, leafy greens, oysters) to strengthen mucosal and cellular immunity
•Calorie-dense small frequent meals during convalescence
foods to avoid
•Alcohol during and shortly after antimonial therapy because of hepatotoxicity
•Excess salt during fluid retention with amphotericin therapy
•Raw or undercooked meat in immunocompromised patients during treatment
•Unverified herbal remedies that may delay effective therapy
Frequent VL relapse in HIV coinfection without sustained immune reconstitution.
08Secondary bacterial infections during severe pancytopenia.
choosing the right hospital
01Access to rK39 rapid testing and PCR for VL
02Pharmacy stocking liposomal amphotericin B and miltefosine
03Capacity for bone marrow and (where indicated) splenic aspirate
04Cardiology and biochemistry monitoring for patients on antimonials
05HIV testing and antiretroviral therapy services
Essential facilities
WHO-collaborating leishmaniasis centresRajendra Memorial Research Institute, PatnaKEMRI / KAMRC East African leishmaniasis sitesMédecins Sans Frontières kala-azar programmesTertiary tropical medicine and infectious disease units
Monitor for nausea, vomiting, or rash and report promptly to prescriber.
03Use barrier contraception during and for 4 months after miltefosine therapy in women of reproductive age.
04Apply broad-spectrum sunscreen to healing cutaneous lesions to reduce hyperpigmentation.
05Attend follow-up at 1, 3, 6, and 12 months after VL treatment.
06Use insecticide-treated nets at home to prevent re-infection.
Exercise
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.