Leishmaniasis (Complete Notes)

Leishmaniasis — MD Pediatrics Note (Based on Nelson Textbook of Pediatrics)

Introduction

• Leishmaniasis is a spectrum of protozoal diseases caused by Leishmania species, transmitted by the bite of infected female phlebotomine sandflies.

  cutaneous leishmaniasis

• Disease manifestations depend on the species involved and the host immune response.

• Major clinical forms:

  1. Visceral leishmaniasis (VL / kala-azar)

  2. Cutaneous leishmaniasis (CL)

  3. Mucocutaneous leishmaniasis (MCL)

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Etiology and Classification

Form	Causative Species	Geographic Distribution
Visceral	L. donovani, L. infantum (chagasi)	South Asia, East Africa, Latin America
Cutaneous	L. tropica, L. major, L. mexicana, L. braziliensis	Middle East, Africa, Americas
Mucocutaneous	L. braziliensis complex	Central & South America

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Epidemiology

• Endemic in >80 countries; affects poor, rural populations.

• Vectors: Phlebotomus (Old World), Lutzomyia (New World).

• Reservoirs: Humans (L. donovani), dogs, rodents.

• Transmission: Sandfly bite, rarely congenital or via transfusion.

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Pathogenesis

• Inoculation of promastigotes → engulfed by macrophages → transform into amastigotes → intracellular multiplication → spread to RES (liver, spleen, bone marrow).

• Disease severity depends on cell-mediated immunity (CMI).

• Strong CMI → localized CL.

• Poor CMI → disseminated VL.

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Clinical Features

A. Visceral Leishmaniasis (Kala-azar)

• Incubation: 2 weeks–18 months.

  Visceral Leishmaniasis (Kala-azar)

• Onset: Insidious.

• Major triad:

  1. Fever: Remittent, double-quotidian, or irregular.

  2. Hepatosplenomegaly: Marked splenomegaly, moderate hepatomegaly.

  3. Pancytopenia: due to hypersplenism and marrow infiltration.

• Other features:

  • Weight loss, wasting, darkening of skin (“kala-azar” = black fever)

  • Lymphadenopathy (esp. African form)

  • Anemia, bleeding, infections (esp. bacterial superinfection)

  • Growth retardation and cachexia in chronic disease.

Post-kala-azar dermal leishmaniasis (PKDL):

• Occurs months–years after VL cure.

• Hypopigmented macules, papules, nodules (face, arms, trunk).

• Serves as a reservoir in endemic areas (notably India).

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B. Cutaneous Leishmaniasis

• Lesion: Painless papule → ulcer with indurated margin (“oriental sore”).

• Usually heals spontaneously in 3–6 months but leaves scar.

• Chronic forms may resemble lupus vulgaris.

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C. Mucocutaneous Leishmaniasis

• Extension from cutaneous lesion (nasal/oral mucosa).

• Causes destructive ulcerations → severe disfigurement.

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Laboratory Diagnosis

1. Direct demonstration

• Amastigotes (Leishman–Donovan bodies) in:

  • Splenic aspirate (most sensitive, but risky)

  • Bone marrow aspirate (safe, moderately sensitive)

  • Lymph node or buffy coat smear

• Giemsa-stained smears show:

  • Oval amastigotes (2–5 μm) with nucleus and kinetoplast inside macrophages.

2. Culture

• Novy–MacNeal–Nicolle (NNN) medium → promastigote growth.

3. Serologic tests

• rK39 dipstick test: Highly sensitive & specific for VL (field use).

• Direct agglutination test (DAT), IFA, ELISA also available.

4. Molecular tests

• PCR: Highly sensitive, species-specific; used in reference labs.

5. Hematology

• Pancytopenia, hypergammaglobulinemia, elevated ESR.

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Treatment

First-line (Visceral Leishmaniasis)

• Liposomal Amphotericin B (preferred):

  • Total dose 10–21 mg/kg (varies by region/protocol)

  • Short-course regimens effective.

• Alternative:

  • Amphotericin B deoxycholate: 1 mg/kg/day × 15–20 doses (toxic, nephrotoxic)

  • Miltefosine: 2.5 mg/kg/day (max 150 mg/day) × 28 days (oral)

  • Paromomycin (IM): 11 mg/kg/day × 21 days

  • Combination regimens (to prevent resistance):

    • Single-dose liposomal amphotericin B + short-course miltefosine or paromomycin.

Cutaneous Leishmaniasis

• Local therapy (cryotherapy, intralesional antimony) for small lesions.

• Systemic therapy for multiple, mucosal, or immunocompromised cases:

  • Miltefosine, liposomal amphotericin B, or pentavalent antimonials.

Mucocutaneous Leishmaniasis

• Liposomal amphotericin B or pentavalent antimonials for ≥28 days.

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Prevention and Control

• Vector control: Insecticide spraying, bed nets.

• Reservoir control: Treat dogs, cull infected reservoirs.

• Personal protection: Repellents, protective clothing.

• Early diagnosis and treatment reduce transmission.

• Vaccine: None yet in routine use; trials ongoing.

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Complications

• Secondary bacterial infections

• Severe anemia, hemorrhage

• Disseminated infection in HIV patients

• PKDL (in endemic regions like India/Nepal)

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Prognosis

• Excellent with prompt diagnosis and treatment.

• Mortality >90% if untreated (mainly from secondary infections, cachexia).

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Key Points from Nelson

• Visceral leishmaniasis should be suspected in any febrile child with splenomegaly and pancytopenia in an endemic area.

• rK39 test is the diagnostic test of choice in field settings.

• Liposomal amphotericin B is the preferred therapy in both immunocompetent and immunocompromised children.

• PKDL represents an important reservoir for ongoing transmission.

• HIV co-infection complicates disease course and increases relapse risk.