1. The Vector Glossina “Host” seeking behavior: –Visual sense used to search for animal or human to feed on. –Spend most of their time resting on vegetation waiting in ambush for their prey to come into range.

2. Stimulate feeding by uric acid, leucine, valine and lactic acid (Human Sweat).

3. The Vector Glossina The genus is divided into 23 species (three species groups).

4. The Vector Glossina The genus is divided into 23 species (three species groups). Most of these can transmit Trypanosomes.

5. The Vector Glossina The genus is divided into 23 species (three species groups). Most of these can transmit Trypanosomes. However two species are important in the transmission to people, Glossina palpalis (T. b. gambiense) and Glossina morsitans (T. b. rhodesiense).

6. Glossina spp. have different “host” preference!

7. The G. morsitans group tends to feed on suids (mainly warthogs), and bovids (buffalo), less so on people.

8. The G. palpalis group tends to feed on reptiles, and loves to feed on people.

9. G. morsitans is a savanna species. G. palpalis is associated with rivers and lakes.

10. Life Cycle Only 2 stages in life cycle – Epimastigote and Trypomastigote.

11. Trypanosoma brucei life cycle 1. Uninfected tsetse fly (Glossina) bites an infected vertebrate host and ingests trypomastigote circulating in the bloodstream.

12. Trypanosoma brucei life cycle 1. Uninfected tsetse fly (Glossina) bites an infected vertebrate host and ingests trypomastigote circulating in the bloodstream. 2. Trypomastigotes multiply by longitudinal binary fission in fly gut.

13. Trypanosoma brucei life cycle 3. Trypomastigotes migrate to the salivary glands and transform into epimastigotes and multiply for several generation.

14. Trypanosoma brucei life cycle 3. Trypomastigotes migrate to the salivary glands and transform into epimastigotes and multiply for several generation. 4. Epimastigotes transform back into Metacyclic Trypomastigotes (short stumpy forms) in the salivary glands. These form the infective stage.

15. Trypanosoma brucei life cycle 3. Trypomastigotes migrate to the salivary glands and transform into epimastigotes and multiply for several generation. 4. Epimastigotes transform back into Metacyclic Trypomastigotes (short stumpy forms) in the salivary glands. These form the infective stage. 5. Tsetse fly bites a human or ruminant host and inoculates metacyclic trypomastigotes into bloodstream.

16. Trypanosoma brucei life cycle 3. Trypomastigotes migrate to the salivary glands and transform into epimastigotes and multiply for several generation. 4. Epimastigotes transform back into Metacyclic Trypomastigotes (short stumpy forms) in the salivary glands. These form the infective stage. 5. Tsetse fly bites a human or ruminant host and inoculates metacyclic trypomastigotes into bloodstream. 6. Trypomastigotes live and multiply in the blood and lymph. In some cases, trypomastigotes migrate to the central nervous system.

17. Trypanosoma brucei life cycle For our purposes we will consider only two life cycle stages trypomastigotes in vertebrate host and epimastigote in Glossina which will be transmitted anterior station or salivarian transmission to the vertebrate host.

18. African Trypanosomiasis Course of Infection There are four phases. The first two phases of trypanosomiasis only show up in people of non-African decent (Europeans).

19. African Trypanosomiasis Course of Infection Phase I: Incubation Period. –Trypomastigote in skin. –Red lesion and chancre at site of bite, painful. –Itching and inflammation of skin. –Duration one to two weeks.

20. African Trypanosomiasis Course of Infection Phase II: Trypomastigotes enter circulation. –Fever –Headache –Skin rash –Duration is variable

21. African Trypanosomiasis Course of Infection Phase III: Trypomastigotes collect in lymph nodes and channels. –Cells not invaded but there is proliferation of endothelial cells –Infiltration of leukocytes –Enlargement of lymph nodes

22. Phase III Enlargement of lymph nodes in cervical triangle (on back of neck) Winterbottom’s Sign one of the cardinal signs of African Trypanosomiasis.

23. African Trypanosomiasis Course of Infection Phase III: Trypomastigotes collect in lymph nodes and channels. –Fever, headache, and delayed sensation to pain –General weakness –Duration many years with T. b. gambiense; less than 1 year and usually less than 4 mo for T. b. rhodesiense

24. African Trypanosomiasis Course of Infection Phase IV: Invasion of Central Nervous System- African Sleeping Sickness.

25. African Trypanosomiasis Course of Infection Phase IV: Invasion of Central Nervous System-African Sleeping Sickness. –Headaches are severe –Emaciation –Mental dullness –Apathy; disinclination to work –Drowsiness and coma –Death from asthenia, heart failure, meningitis, severe fall, etc.

26. African Trypanosomiasis Course of Infection Phase IV: Invasion of Central Nervous System-African Sleeping Sickness. –Duration variable with T. b. gambiense; usually does not occur with T. b. rhodesiense.

27. Pathology 1) Parasites themselves are toxic. -Their byproducts are toxic and end up circulating in the blood steam.

28. Pathology 1) Parasites themselves are toxic. -Their byproducts are toxic and end up circulating in the blood steam. 2) Hyper stimulated immune system. -Parasite has variable antigenic types (VATs) which are constantly changing. -This compromises our immune system, and those infected can be susceptible to other bacteria and virus infections.

29. Pathology 3) Host lyses its own erythrocytes (RBCs). -This is why anemia is a symptom of this disease. So why does this happen?

30. Diagnosis Can find Trypanosomes in plasma. Concentrated in lymph nodes. –Treatment differs if there has been invasion of CNS If questionable do a lumbar puncture.

31. Treatment Drug of choice  Suramin (Bayer 205) –Not affected against CNS forms!

32. Treatment Drug of choice  Suramin (Bayer 205) –Not affected against CNS forms! Melarsoprol (and arsenical; toxic) is used with Bayer 205 to treat CNS forms. –Vomiting, and kidney damage. –10% of patients will die from treatment.

33. Treatment Drug of choice  Suramin (Bayer 205) –Not affected against CNS forms! Melarsoprol (and arsenical; toxic) is used with Bayer 205 to treat CNS forms. –Vomiting, and kidney damage. –10% of patients will die from treatment. Ornidyl (DFMO)  Current drug of choice. –Tolerated well; effective against CNS, but 2 week treatment is $150!

34. Distribution T. b. rhodesiense  occurs in E. Africa.

35. Distribution T. b. rhodesiense  occurs in E. Africa. T. b. gambiense  occurs in costal W. Africa and in drainages of Congo and Niger Rivers.

36. So What is the Big Deal! No Leishmaniasis in the US! No African Trypanosomiasis in the US!

37. The Big 3 Tropical Fevers To Be Feared! (3) Kala-azar (2) African Trypanosomiasis (1) Malaria

38. Negative Effects of African Trypanosomiasis (1) Depopulation: –Uganda 1901-1905. 30,000  100,000 due to T. b. rhodesiense epidemic. –Equality of life –Lack of productivity in society –Social stability

39. Negative Effects of African Trypanosomiasis (2) Agriculture

40. African Land