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Questions and Answers
What is the main reservoir of infection for T.b. gambiense?
What is the main reservoir of infection for T.b. gambiense?
How does T.b. rhodesiense typically infect humans?
How does T.b. rhodesiense typically infect humans?
What is the first clinical manifestation of a trypanosomal infection after a tsetse fly bite?
What is the first clinical manifestation of a trypanosomal infection after a tsetse fly bite?
Which immune response is primarily generated against trypanosomal infection?
Which immune response is primarily generated against trypanosomal infection?
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What symptom is characteristic of Stage 2 of the illness caused by T.b. gambiense?
What symptom is characteristic of Stage 2 of the illness caused by T.b. gambiense?
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What is an early symptom of Stage 1 of T.b. gambiense infection?
What is an early symptom of Stage 1 of T.b. gambiense infection?
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What can cause the fluctuations in parasitaemia during trypanosomal infections?
What can cause the fluctuations in parasitaemia during trypanosomal infections?
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Which of the following is NOT a symptom of Stage 2 of the illness?
Which of the following is NOT a symptom of Stage 2 of the illness?
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What species of Trypanosoma causes Human African Trypanosomiasis?
What species of Trypanosoma causes Human African Trypanosomiasis?
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Which of the following is a major reservoir for T.brucei rhodesiense?
Which of the following is a major reservoir for T.brucei rhodesiense?
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What insect is responsible for the transmission of Human African Trypanosomiasis?
What insect is responsible for the transmission of Human African Trypanosomiasis?
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Which stage of infection occurs 5-12 days after the tsetse fly bite?
Which stage of infection occurs 5-12 days after the tsetse fly bite?
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What is the initial local effect at the site of the tsetse fly bite?
What is the initial local effect at the site of the tsetse fly bite?
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What is the primary route of administration for Suramin?
What is the primary route of administration for Suramin?
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Which of these changes occurs in the tsetse fly's salivary glands during the life cycle of Trypanosoma brucei?
Which of these changes occurs in the tsetse fly's salivary glands during the life cycle of Trypanosoma brucei?
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Which side effect is associated with Pentamidine?
Which side effect is associated with Pentamidine?
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What happens to the size of the trypanosomal chancre after it forms?
What happens to the size of the trypanosomal chancre after it forms?
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Which geographical area is primarily affected by T.brucei gambiense?
Which geographical area is primarily affected by T.brucei gambiense?
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Why are corticosteroids given during melarsoprol treatment?
Why are corticosteroids given during melarsoprol treatment?
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What is the dose regimen for Eflornithine?
What is the dose regimen for Eflornithine?
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What major risk is associated with the use of Melarsoprol?
What major risk is associated with the use of Melarsoprol?
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Which statement about monitoring treatment success is correct?
Which statement about monitoring treatment success is correct?
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What is a notable effect of delaying treatment in patients with CNS involvement?
What is a notable effect of delaying treatment in patients with CNS involvement?
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What is a potential consequence of abnormal parameters post-treatment?
What is a potential consequence of abnormal parameters post-treatment?
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Which sign may occur in convulsions related to T.b.rhodesiense infection?
Which sign may occur in convulsions related to T.b.rhodesiense infection?
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What is a common clinical feature of T.b.rhodesiense infection?
What is a common clinical feature of T.b.rhodesiense infection?
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In advanced cases of T.b.rhodesiense, how are the tendon reflexes typically affected?
In advanced cases of T.b.rhodesiense, how are the tendon reflexes typically affected?
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Which diagnostic method is NOT useful in identifying T.b.rhodesiense?
Which diagnostic method is NOT useful in identifying T.b.rhodesiense?
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What type of complications can occur due to cardiac manifestations in T.b.rhodesiense infection?
What type of complications can occur due to cardiac manifestations in T.b.rhodesiense infection?
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What kind of findings are expected in CSF examination of late-stage T.b.rhodesiense?
What kind of findings are expected in CSF examination of late-stage T.b.rhodesiense?
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What characterizes the prognosis of untreated T.b.rhodesiense infection?
What characterizes the prognosis of untreated T.b.rhodesiense infection?
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Which feature distinguishes T.b.rhodesiense from T.b.gambiense?
Which feature distinguishes T.b.rhodesiense from T.b.gambiense?
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Study Notes
Human African Trypanosomiasis (Sleeping Sickness)
- Human African Trypanosomiasis (HAT), also known as sleeping sickness, is a parasitic disease caused by Trypanosoma brucei.
- There are two main types of HAT:
- Trypanosoma brucei gambiense: Found in West and Central Africa. Humans are the primary reservoir.
- Trypanosoma brucei rhodesiense: Found in East and Southern Africa. Infected wild animals (reservoir).
- Transmission occurs through the bite of tsetse flies (genus Glossina), found only in Africa.
- Infected areas generally lie south of the Sahara and north of the Zambezi River.
Trypanosome Morphology
- Trypanosomes are flattened, fusiform parasites with a kinetoplast and flagellum.
- They have undulating membranes.
- They exhibit active motility.
- Two key forms exist— Trypanosoma brucei rhodesiense and Trypanosoma brucei gambiense.
- They feature variable surface glycoprotein coats, enabling antigenic variation to evade the immune response.
Life Cycle
- Tsetse flies ingest trypomastigotes (parasites) during a blood meal from an infected host.
- Inside the fly's midgut, trypomastigotes multiply by simple fission.
- They migrate to the salivary glands, undergoing morphological changes.
- The kinetoplast moves anterior (in front of) the nucleus, and they transition to epimastigotes (crithidia).
- Epimastigotes transform into metacyclic trypomastigotes in the salivary glands.
- Metacyclic trypomastigotes are present in the fly's saliva up to 20 days after an initial blood meal.
- The fly remains infectious throughout its life (several months).
Pathogenesis (Local Effects)
- At the site of the tsetse fly bite, metacyclic trypanosomes cause an acute inflammatory lesion.
- Lesion is known as a trypanosomal chancre.
- This lesion then multiplies parasites, causing inflammation, edema, and local tissue destruction.
- Parasites spread to local lymph nodes and then bloodstream.
Pathogenesis (Systemic Effects-"Stage 1")
- Trypanosome multiplication in the lymphatic system leads to parasitaemia (presence of parasites in the blood) roughly 5-12 days post-bite.
- Characterized by widespread lymphadenopathy and histiocytic infiltration, later progressing to fibrosis.
Pathogenesis (Systemic Effects– Meningo-encephalitic Stage-"Stage 2")
- Parasites enter the central nervous system (CNS) through choroid plexus or transcytosis across endothelial cells.
Clinical Features: T. brucei gambiense
- Stage 1: Chancre develops (1-2 weeks post-bite).
- Early symptoms: fever, headache, joint pain, sometimes cutaneous oedema and lymphadenopathy.
- Stage 1 Chancre (often resolves within weeks).
T. brucei gambiense (Stage 2)
- Insidious onset of neurologic symptoms: headache, somnolence, listless gaze, extrapyramidal signs (tremors, spasticity).
- Behavioral changes, psychiatric manifestations, CSF abnormalities.
- Sleep patterns change with gradually longer sleep periods.
- Speech and motor functions are severely affected; convulsions are rare.
- Keárandel's sign (delayed hyperaesthesia).
- Reflexes often over-exaggerated; plantar responses are extensor.
- Death usually within months; CNS involvement may delay until up to a year post-infection.
Clinical Features: T. brucei rhodesiense
- Illness more acute, onset of symptoms a few days after insect bite.
- Common features: intermittent fever, rash.
- Pleural and pericardial, and myocarditis (heart muscle inflammation) are common.
- Lymphadenopathy is less prominent in the East African disease type compared to the West African type.
- Hepatocellular jaundice and anemia are common.
Diagnosis
- Direct parasite demonstration: Blood film (wet prep and Giemsa stain) is most likely positive in the haemolymphatic stage. It's even more positive in East African trypanosomiasis. Concentration techniques (e.g., buffy coat) improve sensitivity.
- Aspirate from chancre or lymph node in acute infections (wet smear and Giemsa stain).
- Bone marrow biopsy is also useful if other methods are negative.
- CSF examination: increased cell count (> 5/mm³), increased CSF pressure, and increased IgM and total protein.
Treatment
- Treatment depends on species, drug resistance pattern, and disease stage.
Treatment: T. b. gambiense
- Stage 1: Pentamidine or Suramin.
- Stage 2: Eflornithine or Melarsoprol and prednisolone (steroid used to reduce encephalopathy risk).
Treatment: T. b. rhodesiense
- Suramin.
- Melarsoprol in cases of relapse and second courses.
Prevention
- Vector control (tsetse flies).
- Early treatment of identified cases (humans are only reservoir in T.b. gambiense).
- No vaccine.
Monitoring Treatment
- Patient symptoms should resolve.
- CSF cell counts fall below 5/mL and normal protein concentrations (potentially taking 6 months or more).
Relapse
- In T. b. gambiense cases, relapse following treatment with different drugs can be treated with different drugs like Melarsoprol; Eflornithine can be used.
- In T. b. rhodensiense, relapse is usually treated with a second course of Melarsoprol.
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Description
Test your knowledge on Human African Trypanosomiasis, specifically focusing on the infections caused by Trypanosoma brucei gambiense and rhodesiense. This quiz covers modes of transmission, clinical manifestations, and immune responses associated with the disease. Challenge yourself with questions on the symptoms and stages of infection.