🦟 Human African Trypanosomiasis (HAT), or sleeping sickness, is a vector-borne parasitic disease of sub-Saharan Africa. It is caused by protozoan parasites of the genus Trypanosoma. Accurate recognition is crucial as untreated disease is almost always fatal.

📍 Aetiology

Transmitted via bites of the tsetse fly (Glossina spp.) 🪰, which acquire infection from humans or animals.
Restricted to certain rural regions of sub-Saharan Africa 🌍 — high exposure in farming, fishing, herding, or hunting communities.
Transmission intensity varies widely, from small foci (one village) to entire endemic regions.

🧬 Forms of the Disease

Trypanosoma brucei gambiense (West & Central Africa):
- ~97% of cases.
- Chronic infection 🕒 — may remain asymptomatic for years.
- Eventually invades the CNS → neurological disease.
Trypanosoma brucei rhodesiense (East & Southern Africa):
- <3% of cases.
- Acute infection ⚡ — symptoms appear within weeks to months.
- Rapid CNS involvement and faster progression.
🚨 Not to confuse: Chagas disease (American trypanosomiasis) is caused by T. cruzi, with a different vector (reduviid “kissing bug”) and seen in Latin America.

🩺 Clinical Features

Stage 1 – Haemo-lymphatic:
- Parasites multiply in blood, lymph, and subcutaneous tissue.
- Fever 🌡️, headache 🤕, arthralgia, pruritus.
- Winterbottom’s sign: painless cervical lymphadenopathy.
Stage 2 – Neurological:
- Parasites cross the blood-brain barrier 🧠.
- Behavioural changes, confusion, sensory loss, poor coordination.
- Disturbed sleep cycles 😴 → reversed day/night rhythm.
- Movement disorders: tremor, chorea, fasciculations, ataxia.
- Fatal if untreated (though asymptomatic carriers exist).

🔬 Investigations

Serological screening (available for T.b. gambiense only).
Direct parasite identification in blood, lymph aspirates, or CSF.
Lumbar puncture + CSF analysis:
- ↑ Protein and mononuclear cells.
- ↑ Intracranial pressure.

💊 Management

First stage: drugs act outside CNS, less toxic.
- Pentamidine: for T.b. gambiense, well-tolerated.
- Suramin: for T.b. rhodesiense; can cause allergic/renal side effects.
Second stage: must cross blood-brain barrier.
- Melarsoprol: effective vs both forms, but arsenic-based ⚠️ (reactive encephalopathy risk, up to 10% fatal).
- Eflornithine: less toxic, but only for T.b. gambiense; requires intensive IV therapy.
- NECT (Nifurtimox–Eflornithine Combination): 💡 Since 2009, recommended by WHO for T.b. gambiense. Safer, shorter regimen.
Follow-up: up to 24 months with repeat CSF analysis to detect relapse.

🛡️ Prevention

Personal protection: insecticide-treated clothing/nets, avoid tsetse habitats.
Vector control: clearing vegetation, insecticide spraying, sterile insect techniques.
Screening of at-risk populations and treatment of asymptomatic carriers.

📌 Key Points

Think HAT in any patient from endemic Africa with fever + neuropsychiatric symptoms.
T.b. gambiense = chronic, insidious → CNS signs late. T.b. rhodesiense = acute, aggressive → CNS early.
Untreated disease is almost always fatal.

📚 References

💡 Exam Tip: High reticulocyte count + anaemia = haemolysis. But in HAT, anaemia is due to both haemolysis and marrow suppression — so reticulocyte response may be blunted. Always integrate lab with clinical context!

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African Trypanosomiasis (Sleeping sickness)