1. Trypanosomiasis Jane Ngai – Simon Zappia

2. Protista  Kinetoplastida  Trypanosoma

3. African Trypanosomiasis – 400,000 affected causing 50,000 to 70,000 deaths/year.
American Trypanosomiasis – 11 million people affected causing 50,000 deaths/year.

4. Trypomastigote
Epimastigote
Promastigote
Amastigote
FORM

5. African Trypanosomiasis
Sleeping Sickness
Trypanosoma brucei brucei (cattle)
Trypanosoma brucei gambiense
Trypanosoma brucei rhodesiense
American Trypanosomiasis
Chagas Disease
 Trypanosoma cruzi

6. AFRICAN TRYPANOSOMIASIS
Fly belt distribution

7. Transmission Via vector – bite from the tse tse fly
Mother to child infection (perinatal death)
Blood transfusion
Sexual contact

8. Lifecycle
Parasite reproduces asexually in the fly’s gut (epimastigotes), migrates to the fly’s salivary glands (metacyclic trypomastigote)
Fly injects metacyclic trypomastigotes when it feeds on blood.
Fly ingests trypomastigotes when it feeds on blood of infected individual.
Trypomastigotes reproduce asexually in the bloodstream

9. Pathogenesis (2 stages)
Stage 1: Haemolymphatic stage (ACUTE)
Most patients do not notice this stage of infection.
Small papule from bite may develop exciting local inflammation.
When trypomastigotes enter the haemo-lymphatic system to multiply,clinical symptoms include:
Fever, headache and joint pain
Winterbottom’s sign: swelling of lymph nodes at the posterior neck region.

10. Stage 2: Meningoencephaltic stage (CHRONIC)
Sleeping sickness stage because trypanosomes have crossed the blood-brain barrier
Personality changes, headaches and withdrawal from the environment.
Simple tasks become harder to accomplish as individual experience nocturnal insomnia and daytime lethargy, apathy and ultimately succumb to secondary infections such as pneumonia.

11. Treatment
Stage I
Pentamidine: 7-10 injections for T. b. gambiense infection. Side effects include: Painful injections with risk of hypotension and shock, pancreatic, renal or hepatic dysfunction; bone marrow suppression and polyneuropathy
Suramin – multiple doses on varying days for T.b. rhodesiense infection. Side effect include: renal impairment, peripheral neuropathy and bone marrow suppression.

12. Treatment
Stage II
Melarsoprol (arsenical compound) – slow IV injection. Side effects include: encephalopathy
Eflornithine – infusion for 2 weeks every 6 hours. Drug is expensive and more effective against T. b. gambiense.

13. Cyclical waves of infection

14. Prevention Control in the reservoirs like livestock and wildebeest
Remove scrub (where tse tse flies reproduce)
DDT
Education
Public awareness

16. Only specific species of genus Glossina transmit the parasite resulting in a spotty distribution through the fly belt.
T. b. rhodesiense
(Acute)
T. b. gambiense
(Chronic)

17. AMERICAN TRYPANOSOMIASIS

18. Transmission
Mediated via vector of genus Triatoma, Rhodnius and Panstrongylus also known as “kissing bugs”
Ingestion of food contaminated with parasites
Blood transfusion
Fetal transmission (13% stillborn deaths/year in Brazil)

19. Lifecycle

20. Pathogenesis (Acute) Acute phase Starts 1 week after infection
Fever, lymph node enlargement, unilateral swelling of the eyelids (Romana’s sign), acute myocarditis, damaged muscle cells and edema.

21. Pathogenesis (Chronic)
Chronic Phases:
Starts 2 months after initial infection.
Indeterminate form: 60-70% of people with Chagas. Completely free of cardiac, gastrointestinal and neurological symptoms but 2-5% of patients convert to cardiac or digestive forms each year (reason not clear).

22. Cardiac manifestation
Cardiac form:
30-40% of people with Chagas. Induces arrhythmia, cardiac failure, thromboembolism, atrioventricular fibrillation, ventricular hypertrophy

23. Gastrointestinal manifestation
Digestive form:
10% of people. Megaoesophagus 3%, megacolon and may be associated with cardiac form. Difficulty in swallowing, regurgitation, aspiration may cause pneumonia and death. Chronic constipation, fecal compacting causes perforation of the colon.

24. Treatment
Treatment exists for symptoms but there are no cures for the disease.
All available pharmaceuticals are expensive and are of inefficient efficacy. No medications are given to patients with the chronic phase.

25. Prevention
Elimination of “kissing bug” environment with building structures that discourage the bug’s habitation.
Avoid pets in the home environment to limit attraction.
Avoid building homes with palm roofs and cracks.
Use of insecticides.
Mechanical elimination of the vector (ie. squish it).
Education.

27. New developments
Clinical manifestations of the cardiac and gastrointestinal forms are unknown.
Heart problems may be linked to autoimmune responses triggered by parasites being engulfed in the macrophage and not completely destroyed.
Others think heart problems may be linked to the parasites themselves.
Inconclusive data.

28. Questions
Consider the nature of both diseases; their vector, distribution and impact on local populations. Which disease, in your opinion, deserves more attention and funding? Why? How would you invest the money?