Explore haemoflagellates like Trypanosoma and Leishmania. Learn about African Sleeping Sickness, Chagas disease, their transmission, symptoms, diagnosis, and tr
Introduction Haemoflagellates belong to the family Trypanosomatidae and include two pathogenic genera: Trypanosoma (causes African Sleeping Sickness and Chagas disease) and Leishmania (causes Leishmaniasis). They are blood and tissue parasites requiring an insect vector as an intermediate host. Morphological Stages 1. Amastigote: Oval, intracellular, lacks flagellum. 2. Promastigote: Elongated, flagellum present, kinetoplast anterior. 3. Epimastigote: Kinetoplast closer to nucleus, undulating membrane present. 4. Trypomastigote: Fully developed undulating membrane, kinetoplast posterior. General Characteristics - Possess a single nucleus, kinetoplast, and flagellum. - Kinetoplast contains a parabasal body and blepharoplast connected by thin fibrils. - Flagellum originates from the blepharoplast and runs along the parasite as an undulating membrane. - Staining: Giemsa, Wright, or Leishman stains (cytoplasm: blue; nucleus/flagellum: pink; kinetoplast: deep red). Hematoxylin & eosin (H&E) is used for tissue sections. Trypanosomes Life Cycle and Development Trypanosomes require two hosts (vertebrate and insect vector). Development in the insect vector occurs via: - Salivaria (Anterior station): Development in the salivary glands (e.g., T. brucei). - Stercoraria (Posterior station): Development in the hindgut; transmission via feces (e.g., T. cruzi). African Trypanosomiasis (Sleeping Sickness) Caused by Trypanosoma brucei gambiense (West African) and T. brucei rhodesiense (East African). Transmission - Vector: Tsetse fly (Glossina species). - Mode: Bite of infected fly or congenital transmission. - Reservoirs: Humans (T. b. gambiense); Wild animals/cattle (T. b. rhodesiense). Pathogenesis and Clinical Features - Stage 1 (Hemolymphatic): Trypanosomal chancre at bite site, intermittent fever, and Winterbottom’s sign (posterior cervical lymphadenopathy). - Stage 2 (Neurological): Invasion of the CNS. Symptoms include daytime somnolence, tremors, confusion, and coma. - Histopathology: Meningoencephalitis with Morula cells (IgA-containing plasma cells) and perivascular cuffing. Diagnosis - Microscopy: Trypomastigotes in blood, lymph node aspirates, or CSF (Giemsa stain). - Serology: Card Agglutination Test for Trypanosomiasis (CATT) for T. b. gambiense. - CSF Analysis: Elevated protein, IgM, and pleocytosis. Treatment - Stage 1: Pentamidine (T. b. gambiense) or Suramin (T. b. rhodesiense). - Stage 2: Eflornithine (T. b. gambiense) or Melarsoprol (T. b. rhodesiense). Note: Melarsoprol is highly toxic and can cause reactive encephalopathy. American Trypanosomiasis (Chagas Disease) Caused by Trypanosoma cruzi. Transmission - Vector: Reduviid bug (Triatomine/Kissing bug). - Mode: Bug defecates while feeding; parasites enter via the bite wound or mucous membranes. Clinical Features - Acute Phase: Chagoma (swelling at bite site) and Romana’s sign (unilateral periorbital edema). - Chronic Phase: Occurs years later; includes dilated cardiomyopathy, megaesophagus, and megacolon due to autonomic nerve destruction. Diagnosis and Treatment - Diagnosis: Microscopy (blood smear), PCR, or Xenodiagnosis. - Treatment: Nifurtimox or Benznidazole (effective primarily in the acute phase). Key Summary - Antigenic Variation: Trypanosomes use Variant Surface Glycoproteins (VSGs) to evade the host immune system. - Myocarditis: Common in both T. b. rhodesiense and T. cruzi infections. - Vectors: Tsetse fly for African types; Reduviid bug for American types.