Life cycle of Leishmania donovani

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Leishmania donovani life cycle stages sandfly host

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Life Cycle of Leishmania donovani

L. donovani is the causative agent of visceral leishmaniasis (kala-azar), the most severe form of leishmaniasis. It is a digenetic parasite - completing its life cycle in two different hosts.

Hosts

Host Type	Species
Definitive/Primary host	Humans and other mammals (dogs, rodents, jackals)
Intermediate host / Vector	Female phlebotomine sandfly (Phlebotomus argentipes in India)
Reservoir hosts	Dogs, jackals, gerbils, squirrels

Two Morphological Stages

1. Amastigote (Leishmanial / LD Body) - occurs in humans

Microscopic, rounded or oval: 2-4 µm in length
No free flagellum - it is reduced to a fibril-like structure embedded in cytoplasm
Nucleus: central or eccentric
Kinetoplast: rod-shaped, lying at a right angle to the nucleus
Axoneme: delicate filament from kinetoplast to body margin
Stains well with Giemsa or Wright stain - these are the classic Leishman-Donovan (LD) bodies
Lives intracellularly inside macrophages/reticuloendothelial cells

2. Promastigote (Leptomonad) - occurs in sandfly

Elongated, slender, spindle-shaped: 15-20 µm long, 1-2 µm wide
Has a long free flagellum (15-28 µm), arising from a basal body near the anterior end
No undulating membrane (flagellum does not curve around the body)
Nucleus: centrally placed; kinetoplast near the anterior end
Multiplies by binary fission at 27°C (sandfly body temperature)

Life Cycle in Detail

Stage I: In the Human Host

Step 1 - Inoculation (Infective Stage) An infected female sandfly takes a blood meal and injects promastigotes into the human skin along with salivary peptides that can inactivate host macrophages.

Step 2 - Phagocytosis by Macrophages Promastigotes in the skin activate complement (by the classic pathway in L. donovani), becoming opsonized with C3. This mediates attachment to CR1 and CR3 complement receptors on macrophages, which then phagocytose the parasites.

Step 3 - Transformation to Amastigotes Inside the phagolysosome of the macrophage, promastigotes lose their flagella and transform into rounded amastigotes. The parasite survives intracellularly through:

A surface lipophosphoglycan coating
Membrane-bound acid phosphatase - this inhibits the macrophage's oxidative burst and inactivates lysosomal enzymes

Step 4 - Multiplication and Spread Amastigotes multiply by binary fission inside the macrophage. When their number reaches 50-200 (or more), the host cell ruptures, releasing daughter cells. These:

Invade neighboring mononuclear phagocytic cells (macrophages)
Disseminate via the bloodstream to visceral organs - spleen, liver, bone marrow, lymph nodes (this is unique to L. donovani compared to cutaneous species, aided by its relative resistance to normal serum microbicidal activity and ability to survive at 37°C)

L. donovani's dissemination is associated with a dramatic inhibition of the TH1 immune response, preventing effective IFN-γ-mediated macrophage activation and nitric oxide killing.

Stage II: In the Sandfly Host

Step 5 - Ingestion A sandfly takes a blood meal from an infected host, ingesting macrophages packed with amastigotes.

Step 6 - Transformation in the Gut In the sandfly's midgut (at ~27°C), amastigotes transform back into flagellated promastigotes.

Step 7 - Multiplication Promastigotes undergo rapid binary fission in the midgut, multiplying extensively.

Step 8 - Migration to Proboscis The promastigotes migrate anteriorly from the midgut to the proboscis (the biting mouthparts), ready to be injected into the next host during a blood meal.

Summary Flowchart

Sandfly injects promastigotes into skin
         ↓
Promastigotes opsonized by C3 → phagocytosed by macrophages
         ↓
Transform into amastigotes inside phagolysosome (LD bodies)
         ↓
Multiply by binary fission → rupture macrophage
         ↓
Spread to spleen / liver / bone marrow / lymph nodes
         ↓
Sandfly ingests amastigote-filled macrophages
         ↓
Amastigotes → promastigotes in sandfly midgut
         ↓
Promastigotes multiply → migrate to proboscis
         ↓
Injected into new host (cycle repeats)

Key Points for Exams

Feature	Detail
Vector	Phlebotomus argentipes (India), P. orientalis (Africa)
Infective stage (to humans)	Promastigote
Diagnostic stage (in humans)	Amastigote (LD body)
Site in human	Reticuloendothelial cells (spleen, liver, bone marrow, lymph nodes)
Intracellular location	Phagolysosome of macrophages
Survival mechanism	Lipophosphoglycan + acid phosphatase inhibit oxidative killing
Disease caused	Kala-azar (visceral leishmaniasis)
Immune evasion	Inhibits TH1 response, blocks IFN-γ-mediated macrophage activation

Sources: Sherris & Ryan's Medical Microbiology, 8th Ed. (pp. 1794-1796); CDC DPDx Leishmaniasis; MicrobeNotes.

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