Haemoflagellates: Trypanosoma, Leishmania, and Pathogenic Diseases

## 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.