Leishmania Overview and Life Cycle

Leishmania Overview

• Phylum: Kinetoplastida
• Four morphological forms: amastigote, promastigote, epimastigote, trypomastigote
• Amastigote: ovoid, vertebrate host, single nucleus, short flagellum
• Promastigote: elongate, insect vector, longer flagellum than amastigote
• Epimastigote: kinetoplast posterior to nucleus, undulating membrane present
• Trypomastigote: various forms, longer body, undulating membrane, kinetoplast anterior to nucleus

Leishmania Life Cycle

• Endemic to tropical and subtropical regions
• Two genera of sand fly vectors:
  • Phlebotomus (Eastern hemisphere)
  • Lutzomyia (Western hemisphere)
• Sand flies feed on blood and lymph.
• Difficult to distinguish Leishmania species morphologically.
• Causes leishmaniasis.
• Amastigote transforms into promastigote in the fly gut, multiplying asexually, then becoming metacyclic promastigotes.
• Recent evidence suggests sexual reproduction in fly gut.
• Leishmania-infected sand flies have midgut valve dysfunction, causing regurgitation of blood containing promastigotes onto the host wound.
• Leishmania relies on host cell phagocytic activity, particularly of the phagolysosome for survival.
• Suppresses generation of reactive oxygen species (ROS).

Leishmaniasis Types and Manifestations

• Three clinically distinguishable types:

  • Cutaneous Leishmaniasis (CL):

    • Self-healing, dry skin lesions (papules, nodules, ulcers).
    • New World (e.g., L. mexicana, L. braziliensis), Old World (e.g., L. tropica, L. major).
    • Old World anthroponotic, New World sylvatic.
    • May lead to co-infections.
    • Treated with pentavalent antimony if disseminated cutaneous leishmaniasis (DCL)
    • Recidivans (recurrent CL) most parasites eliminated, but infection not cured.

  • Mucocutaneous Leishmaniasis (MCL):

    • Caused by L. braziliensis and L. tropica.
    • Often develops from CL.
    • Two forms: ulcerative (rapid mutilation of mucous membranes) and non-ulcerative (edema and hypertrophy).
    • Treated with amphotericin B or antimony drugs.

  • Visceral Leishmaniasis (kala-azar):

    • Most serious form, potentially asymptomatic.
    • 90% fatality if untreated, infects reticuloendothelial system.
    • Symptoms include fever, weight loss, hepatosplenomegaly, anemia, enlarged lymph nodes.
    • Complications: Post kala-azar dermal leishmaniasis (PKDL).
      • PKDL mainly self-healing in Africa, but not in India

Lipophosphoglycan (LPG)

• Protects Leishmania from digestive activities in the fly's gut.
• Elongates during development in the fly.
• Protects against macrophage enzymes, host immune responses, and natural killer T (NKT) cell recognition.
• Binds to host macrophage receptors for phagocytosis.
• Inhibits ROS.

Host Immune Response

• Strong Th1 response: resistant, localized infections.
• Th1 cells release INF-γ, enhances macrophage killing, promoting healing and activating cytotoxic T cells.
• Strong Th2 response: susceptible to DCL or VL.
• Th1 is intracellular, Th2 is extracellular; Th1 is cell-mediated, Th2 is humoral (body fluids).

Diagnosis of Leishmaniasis

• Cutaneous Leishmaniasis: Specimen collected from lesion edge; biopsy, incision; in vivo culture (1 week), hamster culture (2-3 months)
• Visceral Leishmaniasis: Aspirates from bone marrow, lymph nodes, spleen (higher parasitemia).
• Serological tests: Detect antibodies (e.g., DAT - detection of antibodies to Leishmania); K39 test uses serum.
• Leishmanin skin test (LST): Measures delayed-type hypersensitivity (DTH) response to Leishmania.

Explore the fascinating world of Leishmania, a genus of protozoa known for causing leishmaniasis. In this quiz, you will learn about its morphological forms, life cycle, and the role of sand fly vectors in its transmission. Test your knowledge of this important topic in parasitology and infectious diseases.