Leishmaniasis

On this page

Leishmaniasis: Intro & Life Cycle - Sandfly's Sinister Secret

  • Protozoal disease caused by genus Leishmania; transmitted by sandflies.
  • Key Species & Manifestations:
    • L. donovani: Visceral Leishmaniasis (Kala-azar)
    • L. tropica: Cutaneous Leishmaniasis (Oriental Sore)
    • L. braziliensis: Mucocutaneous Leishmaniasis (Espundia)
  • Vector (India): Phlebotomus argentipes.
  • Life Cycle Forms:
    • Promastigote: Motile, flagellated; in sandfly (infective stage).
    • Amastigote (Leishman-Donovan/LD body): Non-motile, intracellular; in vertebrate macrophages (diagnostic stage). 📌 Mnemonic: Promastigote in Phlebotomus (sandfly); Amastigote in Animal/human. Leishmania life cycle: sandfly and human stages
  • Transmission Cycle:
    • Sandfly injects promastigotes into skin.
    • Macrophages phagocytose promastigotes → transform to amastigotes → multiply.
    • Sandfly ingests macrophages with amastigotes during blood meal.
    • Amastigotes → promastigotes in sandfly gut, migrate to proboscis.

⭐ Amastigote form (LD body) is found intracellularly in macrophages of the vertebrate host.

Leishmaniasis: Clinical Spectrums - Viscera, Skin & Scars

FeatureVisceral (VL) / Kala-azarCutaneous (CL)Mucocutaneous (MCL)Post-Kala-azar Dermal (PKDL)
AKAKala-azar, Dumdum feverOriental sore, Chiclero ulcerEspundiaDermal leishmanoid
Key SitesSpleen, Liver, Bone marrowSkinNaso-oro-pharyngeal mucosaSkin
ManifestationsProlonged fever (biphasic), massive Splenomegaly & Hepatomegaly, Pancytopenia, ↑Hypergammaglobulinemia, CachexiaChronic, painless papule → ulcer (raised border, central depression). Cutaneous Leishmaniasis ulcerDestructive mucosal lesions (nasal, oral, pharyngeal); epistaxis, septal perforation.Hypopigmented/erythematous macules, papules, nodules (face). PKDL lesions, parasite load, and histology
Outcome/NotesFatal if untreated.Self-heals (scar); can be chronic.Progressive, disfiguring; risk of secondary infection.Appears post-VL cure (months-years); reservoir.

Leishmaniasis: Diagnosis Decoded - Finding Hidden Foes

  • Microscopy: Gold standard for definitive diagnosis.
    • Giemsa stain: Visualizes Leishman-Donovan (LD) bodies (amastigotes within macrophages).
    • Specimens:
      • VL: Spleen (highest yield), bone marrow, lymph node aspirates.
      • CL: Skin biopsy from lesion edge / slit-skin smear. Leishmania donovani in macrophage, Giemsa stain
  • Culture:
    • NNN medium: Cultivates promastigotes; slow (takes 1-4 weeks).
  • Serology (Mainly for VL):
    • rK39 strip test: Rapid, field-friendly immunochromatographic test.
    • DAT (Direct Agglutination Test), ELISA: Detect antibodies.
  • Montenegro Skin Test (Leishmanin Test):
    • Assesses cell-mediated immunity (CMI); positive in CL & PKDL.
    • Typically negative during active VL.
  • Molecular Methods:
    • PCR: Highest sensitivity & specificity; allows species identification.

⭐ rK39 antigen-based immunochromatographic test is highly sensitive and specific for Visceral Leishmaniasis diagnosis in field settings.

Leishmaniasis: Treatment & Control - Eradicating Endemics

Management aims to cure the patient, prevent relapse, reduce transmission, and prevent drug resistance. Treatment varies by species, clinical form, and region.

Key Drugs for Leishmaniasis:

DrugMOA (Simplified)Key Doses/RegimensMajor Side EffectsPregnancy
Sodium Stibogluconate (SSG)Inhibits glycolysis & nucleic acid synth.20 mg/kg/day IV/IM x 28d (VL/PKDL)Cardiotoxicity (QT), pancreatitisContraindicated
Amphotericin B (Deoxycholate)Binds ergosterol, forms pores0.75-1 mg/kg/day IV x 15-20 dosesNephrotoxicity, hypokalemia, rigorsUse if benefit > risk
Liposomal Amphotericin BErgosterol binding, targeted deliveryVL: Single dose 10 mg/kg IV; PKDL: 5 mg/kg x 6 doses (alternate days)Infusion reactions, less nephrotoxicPreferred
MiltefosineAffects cell signaling, apoptosis50-100 mg/day PO x 28d (VL)GI upset, teratogenicityContraindicated
ParomomycinAminoglycoside (protein synth. inhib.)11 mg/kg/day IM x 21d (VL); Topical for CLOtotoxicity, nephrotoxicity, injection painAvoid (limited data)
  • Drug Resistance: Growing concern, especially with antimonials. Requires monitoring and combination therapy considerations.
  • Control (NVBDCP, India):
    • Early case detection & complete treatment.
    • Integrated vector management (IRS with DDT).
    • Kala-azar elimination targets (reducing annual incidence <1/10,000 population at block level).

High‑Yield Points - ⚡ Biggest Takeaways

  • Transmitted by female Phlebotomine sandflies; L. donovani causes Kala-azar (Visceral Leishmaniasis).
  • Infective form: Promastigote (sandfly); Diagnostic form: Amastigote (LD bodies) in macrophages.
  • Kala-azar: Features prolonged fever, massive splenomegaly, pancytopenia, hypergammaglobulinemia.
  • PKDL: Post-Kala-azar Dermal Leishmaniasis involves skin lesions post-VL treatment.
  • Diagnosis: LD bodies in splenic/bone marrow aspirates; rk39 antigen test for VL.
  • Treatment: Liposomal Amphotericin B (drug of choice for VL); Miltefosine (oral).

Practice Questions: Leishmaniasis

Test your understanding with these related questions

All of the following helps in the diagnosis of leishmaniasis except:

1 of 5

Flashcards: Leishmaniasis

1/10

_____ medium is used for the culture of Trypanosoma and Leishmania

TAP TO REVEAL ANSWER

_____ medium is used for the culture of Trypanosoma and Leishmania

NNN (Novy, McNeal, and Nicolle)

browseSpaceflip

Enjoying this lesson?

Get full access to all lessons, practice questions, and more.

Start Your Free Trial