Trypanosomiasis

Not in India

Neither form endemic to Indian subcontinent (vector-geography restricted). Taught alongside kala-azar (same family, Trypanosomatidae).

African Trypanosomiasis (Sleeping Sickness)

T. b. gambiense (West/Central Africa, CHRONIC, months-years) vs T. b. rhodesiense (East Africa, ACUTE, weeks, more rapidly fatal). Vector: tsetse fly (Glossina). T. b. rhodesiense: cattle/game = animal reservoir (zoonotic dimension).

Pathogenesis: EXTRACELLULAR throughout (unlike Leishmania/T. cruzi — no intracellular phase). Multiplies in blood+lymph.

Stages:

1. Hemolymphatic: fever, headache, joint pain, LAD (posterior cervical = “Winterbottom’s sign,” historical slave-trade screening sign). ± painless chancre at bite site.
2. Meningoencephalitic: BBB crossed → sleep-wake disturbance (day somnolence, night insomnia) + personality change + confusion → coma/death untreated.

Diagnosis: trypomastigotes (blood/LN aspirate/CSF microscopy). CSF ESSENTIAL for staging (determines Rx — different drugs by CNS penetration). CATT serology = field screening (mainly gambiense).

Treatment (stage-dependent, CNS drugs more toxic/stage2-only):

• Stage 1: Pentamidine, Suramin. Fexinidazole (oral, preferred, gambiense both stages where available)
• Stage 2 (gambiense): NECT (nifurtimox-eflornithine combo, gentler) OR Melarsoprol (OLD, HIGHLY TOXIC, fatal reactive encephalopathy risk)

American Trypanosomiasis (Chagas Disease)

T. cruzi. Vector: triatomine/“kissing”/“assassin” bug — bites face during sleep, DEFECATES near bite → trypomastigotes enter via bite wound or rubbed into eye/mouth (NOT direct bite inoculation). Latin America.

UNLIKE African trypanosomes: T. cruzi DOES have intracellular phase — amastigotes in cardiac/smooth muscle + glial cells → back to trypomastigote → bloodstream.

Acute: mild/asymptomatic. Chagoma (localized nodule, inoculation site) or Romaña’s sign (unilateral painless periorbital swelling, if eye = entry point).

Chronic (years-decades later, substantial minority): REAL DISEASE BURDEN.

• Chagas cardiomyopathy — LEADING cause of non-ischemic HF + sudden cardiac death in endemic Latin America
• GI megasyndromes — megaesophagus, megacolon (autonomic/myenteric ganglia destruction) → dysphagia/constipation

Diagnosis: Acute = trypomastigotes DIRECT blood microscopy (high parasitemia). Chronic = serology (need 2 DIFFERENT positive tests, no single assay fully reliable) or PCR.

Treatment: benznidazole/nifurtimox. MOST effective early acute/early chronic (young patients). Established chronic disease (cardiomyopathy/megasyndrome) — LOWER efficacy (drugs act on parasite, can’t reverse fibrotic damage already done).

Not Endemic to India

Neither form of human trypanosomiasis occurs naturally on the Indian subcontinent — both are geographically confined to the regions their insect vectors inhabit. The disease is covered here because it is conventionally taught alongside kala-azar as the other major blood/tissue-dwelling flagellate disease, sharing the same broad parasite family (Trypanosomatidae) and diagnostic approach.

African Trypanosomiasis (Sleeping Sickness)

Caused by two subspecies of Trypanosoma brucei, each with a distinct clinical tempo and geography: T. b. gambiense (West and Central Africa, causing a chronic, slowly progressive disease that can smoulder for months to years) and T. b. rhodesiense (East Africa, causing a much more acute, rapidly fatal illness over weeks). Both are transmitted by the bite of the tsetse fly (Glossina species), with cattle and wild game serving as an animal reservoir for T. b. rhodesiense specifically — a genuine zoonotic dimension that complicates control efforts for that form.

Pathogenesis and clinical stages: the tsetse bite introduces trypomastigotes that multiply extracellularly in blood and lymph — unlike Leishmania and Trypanosoma cruzi, African trypanosomes never enter an intracellular phase, remaining fully extracellular throughout the human infection. Disease unfolds in two stages:

• Stage 1 (haemolymphatic stage): fever, headache, joint pain, and lymphadenopathy — classically posterior cervical lymphadenopathy, known as Winterbottom’s sign, historically used by slave traders as a crude screening sign. A painless chancre can appear at the bite site.
• Stage 2 (meningoencephalitic stage): occurs once trypanosomes cross the blood-brain barrier, producing the disease’s namesake feature — a progressive disturbance of the sleep-wake cycle (daytime somnolence, nighttime insomnia), alongside personality change, confusion, and, untreated, progression to coma and death.

Diagnosis: demonstration of trypomastigotes by microscopy of blood, lymph node aspirate (from an enlarged node, particularly useful early), or CSF (essential for staging — CSF examination determines whether stage 1 or stage 2 treatment is required, since the two need very different drug regimens based on CNS penetration). Serology (CATT — card agglutination test for trypanosomiasis) is used for field screening, particularly for T. b. gambiense.

Treatment is strictly stage-dependent, since CNS-penetrating drugs are more toxic and are reserved for stage 2: fexinidazole (now the preferred oral option for T. b. gambiense, both stages, where available), pentamidine or suramin for stage 1 disease; melarsoprol (older, highly toxic — historically associated with fatal reactive encephalopathy in a meaningful minority of patients) or the gentler nifurtimox-eflornithine combination therapy (NECT) for stage 2 T. b. gambiense disease specifically.

American Trypanosomiasis (Chagas Disease)

Caused by Trypanosoma cruzi, transmitted by the bite — or more precisely, by faecal contamination of the bite wound or mucous membranes — of the triatomine (“kissing” or “assassin”) bug, which characteristically bites around the face while a person sleeps and defecates near the bite site, with the infective trypomastigotes entering through the bite wound or via rubbing the faeces into the eye or mouth. Endemic across Latin America. Unlike African trypanosomes, T. cruzi does enter an intracellular phase, multiplying as amastigotes within host cells (especially cardiac and smooth muscle, and glial cells) before converting back to trypomastigotes and re-entering the bloodstream.

Acute Chagas disease is often mild or entirely asymptomatic, sometimes marked by a localized inflammatory nodule (chagoma) at the inoculation site, or, when the entry point is the eye, the classically described Romaña’s sign (unilateral, painless periorbital swelling).

Chronic Chagas disease is where the real disease burden lies, developing years to decades after the initial infection in a substantial minority of those infected, driven by ongoing tissue damage to the organs where amastigotes preferentially persist:

• Chagas cardiomyopathy — a leading cause of non-ischaemic heart failure and sudden cardiac death in endemic Latin American regions, from progressive myocardial damage and conduction system involvement.
• GI megasyndromes — megaesophagus and megacolon, from destruction of the autonomic (myenteric) ganglia controlling motility in these organs, producing severe dysphagia or constipation respectively.

Diagnosis: acute infection — trypomastigotes visible directly in blood by microscopy (parasitaemia is high enough in the acute phase for reliable direct detection). Chronic infection — parasitaemia is too low for reliable microscopy, so diagnosis relies on serology (requiring two different positive serological tests, given no single assay is fully reliable alone) or PCR.

Treatment: benznidazole or nifurtimox, both most effective when given early in acute infection or in early chronic infection in younger patients; efficacy in established chronic disease (especially once cardiomyopathy or megasyndrome has developed) is considerably lower, since these drugs act on the parasite but cannot reverse fibrotic organ damage already done.