Leishmania — Notes OmpathStudy

LEISHMANIA 1. INTRODUCTION & BASIC FACTS What is Leishmania? Flagellate protozoan parasite Causes leishmaniasis (including Kala-azar) Obligate intracellular parasite Requires TWO hosts to complete life cycle Key Classifications: Definitive hosts: Humans, dogs, other mammals Vector: Female sandfly (Phlebotomus & Lutzomyia species) Infective form: Metacyclic promastigote 2. GLOBAL DISTRIBUTION & EPIDEMIOLOGY Geographic Distribution: Tropical and subtropical regions worldwide Central & South America, North America (parts) Central & Southeast Asia, India, China Mediterranean region, Africa Risk Factors: Low socioeconomic status Overcrowding and poor ventilation Accumulation of organic material in houses Poor sanitation 3. CLINICAL TYPES OF LEISHMANIASIS A. VISCERAL LEISHMANIASIS (Kala-azar) Causative agent: L. donovani complex Organs affected: Liver, spleen, bone marrow Most severe form B. CUTANEOUS LEISHMANIASIS Causative agents: L. tropica, L. major, L. aethiopica, L. mexicana complex Affects: Skin only Forms ulcerative lesions C. MUCOCUTANEOUS LEISHMANIASIS Causative agent: L. braziliensis complex Affects: Skin and mucous membranes Can cause facial disfigurement 4. MORPHOLOGY - TWO FORMS A. AMASTIGOTE FORM (LD Body) Location: Inside human/mammalian cells Shape: Oval, small (2-4 μm) Features: No external flagellum Nucleus and kinetoplast visible Found in macrophages Also called Leishman-Donovan (LD) body B. PROMASTIGOTE FORM Location: In sandfly and culture Shape: Elongated (15-25 μm) Features: Long anterior flagellum Motile Infective metacyclic form 5. LIFE CYCLE - STEP BY STEP STAGE 1: INFECTION OF HUMAN Transmission: Infected female sandfly bites human Inoculation: Promastigotes injected into skin wound Phagocytosis: Promastigotes engulfed by macrophages Transformation: Promastigotes → Amastigotes inside cells Multiplication: Amastigotes multiply by binary fission Cell rupture: Infected macrophages burst, releasing amastigotes Spread: Released amastigotes infect new macrophages STAGE 2: INFECTION OF SANDFLY Blood meal: Sandfly feeds on infected human Ingestion: Amastigotes enter sandfly's midgut Transformation: Amastigotes → Promastigotes in midgut Multiplication: Promastigotes multiply rapidly Migration: Parasites migrate to pharynx and proboscis Blockage: Parasites block sandfly's feeding apparatus Transmission: Next bite releases infective promastigotes Extrinsic incubation period: 10 days in sandfly 6. VISCERAL LEISHMANIASIS (KALA-AZAR) - DETAILED A. PATHOGENESIS Primary process: Reticuloendothelial system (RES) blockade Mechanism: Massive multiplication in fixed macrophages Result: RES dysfunction and organ damage B. ORGAN INVOLVEMENT LIVER Enlargement: Hepatomegaly Cells affected: Küpffer cells, vascular endothelial cells Hepatocytes: NOT affected Appearance: "Nutmeg" cut surface Function: Mostly preserved (slight ↓ prothrombin) SPLEEN Most affected organ Massive enlargement: Splenomegaly Consistency: Soft and friable Color: Red/chocolate on cut section Microscopy: Reticulum cells loaded with LD bodies BONE MARROW Heavy infiltration with parasitized macrophages Result: Crowding of hematopoietic tissue Consequence: Severe anemia (Hb 5-10 g/dL) C. CLINICAL FEATURES Onset: Insidious Fever: Continuous, remittent, or irregular Splenomegaly: Early, progressive, massive Hepatomegaly: Present but less prominent Skin changes: Dry, rough, darkly pigmented Hair changes: Thin and brittle General: Cachexia, anemia, weight loss Bleeding: Epistaxis, gum bleeding Prognosis: Death in ~2 years if untreated D. INCUBATION PERIOD Usual: 2-6 months Range: 10 days to 2 years 7. POST KALA-AZAR DERMAL LEISHMANIASIS (PKDL) A. BASIC FACTS Occurrence: 3-10% of visceral leishmaniasis patients Timing: 1-2 years after recovery Geographic: Mainly India and East Africa Nature: Non-ulcerative skin lesions B. LESION TYPES Depigmented macules: Trunk/extremities, resemble leprosy Erythematous patches: Face, butterfly distribution Nodular lesions: Painless, yellowish-pink, granulomatous 8. CUTANEOUS LEISHMANIASIS A. OLD WORLD CUTANEOUS LEISHMANIASIS Type 1: Anthroponotic Urban Type (L. tropica) Vector: P. sargenti Lesions: Painless, dry, ulcerating Names: Oriental sore, Delhi boil Healing: Spontaneous in ~1 year Scars: Disfiguring Type 2: Zoonotic Rural Type (L. major) Vector: P. papatasi Lesions: Moist, inflamed, often multiple Reservoirs: Gerbils, rats, rodents Healing: Faster than L. tropica Type 3: Diffuse Cutaneous (L. aethiopica) Vector: P. longipes Location: Ethiopia, Kenya highlands Lesions: Non-ulcerative, diffuse, nodular Immunity: Low humoral and cell-mediated Duration: Years to lifetime Treatment: Difficult B. LEISHMANIASIS RECIDIVANS Immunity: High cell-mediated immunity Pattern: Chronic, alternating activity/healing Appearance: Central scar with peripheral activity Parasites: Very scanty Leishmanin test: Strongly positive C. NEW WORLD LEISHMANIASIS Agents: L. braziliensis & L. mexicana complexes Vector: Lutzomyia species Re