Trypanosomiasis Dr Nzau Muange, MBCHB,MMeD2021.ppt

The presentation and treatment of Trypanosomiasis in humans

2. Trypanosomiasis
Dr Nzau Muange

3. Definition
•Several diseases in vertebrates caused by
protozoa of genus Trypanosoma
•In humans, two diseases are identified,
namely; African Trypanosomiasis (African
Sleeping Sickness) and American
Trypanosomiasis (Chaga’s disease)

4. Types
•There are two types of trypanosomiasis that affect
humans, they are divided according to their
geographical location :
African trypanosomiasis, or sleeping sickness, is
caused byTrypanosoma bruceiparasites in Africa
and is transmitted by thetsetse fly.
•American trypanosomiasis, or Chagas disease, is
caused byTrypanosoma cruziparasites in Latin
America and is transmitted by the Triatomine
(Kissing) bug.

5. Tsetse fly
intermediate host

6. Reduviid (Triatomine) bug

7. African Trypanospmiasis

8. 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.

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

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

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

12. 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).

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

14. Distribution of T. brucei
•T. b. rhodesienseoccurs in E. Africa
•T. b. gambienseoccurs in coastal W.
Africa and in drainages of Congo and
Niger Rivers

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

16. Morphology

17. Trypanosoma brucei life cycle
For our purposes we will consider only two
life cycle stages trypomastigotes in
vertebrate host and epimastigote in
Glossinawhich will be transmitted to the
vertebrate host

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

19. 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.

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

21. 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.

22. 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.

23. 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.

24. Trypanosomelife cycle
•The trypanosome parasite is first introduced into the mammalian
host as trypomastigoteswhen a tsetse fly takes a blood meal and
secretes parasite-filled saliva into the host’s skin.
•Once in the bloodstream the trypomastigotesmultiply in the
blood,lymphorspinal fluid
.

25. Trypanosomiases

26. 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).

27. 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.

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

29. 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

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

31. 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

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

33. 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.

34. 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.

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

36. 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.

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

38. 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.

39. Treatment
•Drug of choice: IV Suramin 100mg Test
Dose then 1g on days 1, 3,7,14 and 21
•Not effective against CNS forms!

40. Treatment ctd
Melarsoprolis used with Suraminto treat
CNS forms.
–Vomiting, and kidney damage.
–10% of patients will die from treatment.

41. Treatment
Ornidyl(DFMO)Current drug of choice.
–Tolerated well; effective against CNS phase, but
Expensive (2 week treatment is Ksh15,000!)