Q. What is Trypanosoma cruzi?
- Protozoan parasite, flagellated, causes Chagas disease (American trypanosomiasis)
- Transmitted mainly by triatomine (kissing) bug; also congenital, blood transfusion, organ transplant, oral ingestion of contaminated food
Q. Morphology of Trypanosoma cruzi
- Length 15‑30 µm, width 1‑3 µm, slender, spindle‑shaped
- Undulating membrane running along body
- Free anterior flagellum (≈ 10 µm) attached to flagellar pocket
- Prominent kinetoplast (DNA‑containing mitochondrion) near nucleus
- Nucleus centrally placed, round to oval
Q. Life cycle (step‑wise, arrows show flow)
- Triatomine bug takes a blood meal from an infected person → parasites (trypomastigotes) enter bug gut
- Parasites multiply as epimastigotes in the mid‑gut → differentiate into infective metacyclic trypomastigotes in the hind‑gut
- Bug defecates on the skin while feeding → metacyclic trypomastigotes in feces contaminate bite wound or mucous membranes → enter host
- In the human, metacyclic trypomastigotes invade cells (especially muscle, heart, macrophages) → transform into intracellular amastigotes
- Amastigotes multiply by binary fission → fill cytoplasm, cause cell rupture
- Amastigotes differentiate back into bloodstream trypomastigotes → released into circulation → can infect new cells or be taken up by another bug
Memory trick: “Bug Bites, Feces Meet, Cells Eat, Blood Beats”
Q. Pathogenesis (step‑wise)
- Parasite entry through skin/mucosa → reaches bloodstream
- Invasion of nucleated cells → intracellular amastigote replication
- Cell lysis releases parasites → local tissue necrosis
- Host immune response → chronic inflammation, cytokine release
- Fibrosis and scar formation in myocardium, esophagus, colon → functional loss
Memory rhyme: “In‑Cell, Kill‑Cell, Inflamm‑Cell, Fibro‑Cell”
Q. Clinical features – acute phase (usually mild)
- Often asymptomatic; if present: fever, malaise, headache, myalgia
- Local swelling at entry site (chagoma) or conjunctival congestion (Romaña’s sign)
- Generalized lymphadenopathy, hepatosplenomegaly, mild myocarditis
Q. Clinical features – chronic phase (years to decades)
- Cardiac: arrhythmias, conduction block, dilated cardiomyopathy, heart failure, apical aneurysm, sudden death
- Gastro‑intestinal: megaesophagus (dysphagia, regurgitation), megacolon (constipation, abdominal distension)
- Neurological: peripheral neuropathy, meningoencephalitis (rare)
Q. Major complications
- Chronic chagasic cardiomyopathy (leading cause of death)
- Gastro‑intestinal megasyndromes (esophageal, colonic)
- Thromboembolism from ventricular aneurysm
- Pregnancy complications (vertical transmission)
Q. Laboratory diagnosis
- Direct microscopy: wet mount or Giemsa stain of fresh blood (trypomastigotes) – best in acute phase
- Concentration methods (microhematocrit, buffy‑coat) for low parasitemia
- Serology (ELISA, indirect immunofluorescence, hemagglutination) – detects IgG, used in chronic phase
- PCR: detects parasite DNA, high sensitivity, useful for treatment monitoring
- Xenodiagnosis: allowing uninfected bug to feed, then examining bug feces – rarely used now
Mnemonic for labs: “MSP – Microscopy, Serology, PCR”
Q. Management (exam‑relevant points)
- Antiparasitic therapy: benznidazole (5‑7 mg/kg/day for 60 days) or nifurtimox (10‑15 mg/kg/day for 60 days); most effective in acute phase and early chronic infection in children
- Cardiac care: anti‑arrhythmic drugs, ACE inhibitors, beta‑blockers, pacemaker/ICD for conduction defects, heart transplantation in end‑stage disease
- Gastro‑intestinal: esophageal dilation, surgical myotomy for megaesophagus; colonic resection for severe megacolon
- Preventive measures: vector control (insecticide spraying, housing improvement), screening of blood donors, prenatal screening, education on food safety
All points are drawn from Robbins, Harsh Mohan, Ananthanarayan & Paniker, Chatterjee, and essential NCH/ MUHS syllabus.