Clinical Parasitology trypansomaiasis.ppt

Clinical parasitology, presentation about trypanosomaiasis, description pathogenicity, clinical features, treatment.

1. It is caused by Trypanosoma species

2. Trypanosomiasis
There are two types of Trypanosomiasis :
1. African trypanosomiasis (sleeping sickness).
2. American trypanosomiasis (Chagas’ disease).

3. African trypanosomiasis (sleeping
sickness).
The disease is restricted between the 14
th
latitude
North and the 29
th
latitude South on the African
continent.

4. African trypanosomiasis (sleeping
sickness).
It is caused by two species of Trypanosoma:
1. Trypanosoma rhodesiense
2. Trypanosoma gambiense

5. Tsetse fly (Glossina)
The vector is the tsetse fly of the genus Glossina
(both females and males).
Tsetse fly dependant on blood sucking to derive
nutrients.
The vectors are found near lakes and rivers.

6. Tsetse fly (Glossina)

7. Environment of T. gambiense

8. African trypanosomiasis (sleeping
sickness).
Trypanosoma rhodesiense is transmitted by the bite of
other Glossina sp.
These vectors are found in savannah areas.

9. Environment of T. rhodesiense

10. Life Cycle
•T. gambienseis found only in West Africa and is
transmitted solely from person-to-personvia the
tsetse fly vector causing non-zoonotic disease.
•T. rhodesiense, which is found in Eastern and Southern
Africa and is primarily transmitted from person-to-
animal and then back to personvia the vector causing
a zoonotic disease.

11. Life Cycle
•1)Infection of a human host occurs when a tsetse fly
bites a human and transmits from its salivary glands
the metacylic stage (the infective state) of the
tryponosome.
•2)This metacylic stage quickly gives way to a blood-
borne stage that begins a series of binary fission
divisions at the site of inoculation.
•This process leads to formation of a primary chancre.

12. Life Cycle
3)The trypanosomes enter the bloodstream via the
lymphaticsand continue to multiply. They also enter
the CNSfrom here.
4)A subsequent tsetse fly becomes infected by
ingesting a blood meal that contains the trypanosomes
from the infected host.

13. Life Cycle
•5) In the gut of the fly, the trypanosomes transform
into trypmastigotesthat divide for about 10 days.
•6)The organisms then migrate to the salivary glands
and transform into epimastigotes, which later
transform into metacyclic trypanosomes that can
infect a new host.

14. Pathology
AfricanTrypanosoma have a specialized mechanism to
overcome the obstacles of the mammalian immune
system.
Days after infection, host antibodies recognize
surface glycoproteins that coat the protozoa
and kill the organisms.

15. Pathology
few protozoa escape destruction via changing their
glycoprotein composition.
Days later the immune system recognizes this change
and attack the new glycoprotein.

16. Pathology
This cycle is repeated with a pattern of high parasite
load followed by a period of low parasite load.
For this reason, patients exhibit an irregular pattern of
high-grade fevers followed by an afebrile period
throughout the course of a systemic infection.
For this reason, vaccine development has failed.

17. Clinical Presentation
•Incubation Period:
The first clinical manifestation of African
trypanosomiasis occurs a few days after infection as a
chancreat the site of tsetse fly inoculation
The incubation period for the Gambian species may
last several weeks to months.

18. Clinical Presentation
Dissemination:
By the end of the incubation period, the organisms
have already disseminated into the bloodstream,
leading to the emergence of a characteristic
intermittentfeverpattern.

19. Clinical Presentation
Invasion of the Central Nervous System:
Invasion of the central nervous system (CNS) occurs
within several weeks in the Rhodesian species and
months to even years in the Gambian species of
trypanosomiasis.
Lymphadenopathyespecially in the posterior cervical
nodes is characteristic sign of African sleeping
sickness.

20. Clinical Presentation
Symptoms include headache, stiff neck, sleep
disturbance, and depression, followed by progressive
mental deterioration.
This progresses to coma and the ultimate deathof the
patient often secondary to pneumonia or sepsis.

21. Diagnosis
A historyof travel within an endemic regionand
especially a memory of a bitefrom a tsetse fly are both
key to a clinician’s ability to consider African sleeping
sickness when encountering a patient outside an
endemic region.

22. Diagnosis
•Detection of the parasite in:
•Blood .
•Lymph node aspirate.
•Bone marrow aspirate.
•Cerebrospinal fluid.

23. Trypanosomes in blood
Smears are made and stained by Giemsa stain or
Leishman stain.

24. Diagnosis
Serology:
ELISA is used to identify antigens
Card Agglutination Test for Trypanosomiasis (CATT)

25. Treatment
Unless treated, African trypanosomiasis is a fatal.
The most effective treatment intervention for this
disease must begin before the organism migrates into
the CNS because the most effective drug does not
cross the blood-brain barrier.

26. Treatment
This drug,Suramin, is administered intravenously and
most often results in the full recovery of the patient.
Side effects include nausea, vomiting, itching, uricaria
, photophobia and peripheral neuropathy.

27. Treatment
Most of these symptoms are not dangerous and
disappear after a few days of treatment.
Pentamidineis an alternative therapeutic agent, but
also has many side effects.
Melarsoprol is the drug of choice should the disease
have progressed sufficiently to affect the central
nervous system.
More recently, Difluormethylornithine (DFMO) more
safely and efficacious

28. Prevention and Control
Early detection and treatment of infected individuals
is the key to prevention and control.

29. Tsetse fly traps to aid in the
avoidance of fly-human contact

30. American Trypanosomiasis
(Chagas’ disease)
It found in South America.
It is caused by Trypanosoma cruzi.
Transmission occurs when the bugdeposits faeces on
the skin surface and subsequently bites;
The human host then scratchesthe bite area which
facilitates penetration of the infected faeces.

31. American Trypanosomiasis
(Chagas’ disease)
•The parasite has two forms, a trypomastigotefound in
human blood and an amastigotefound in tissues.
•The acute form of the disease usually goes unnoticed
and may present as a localized swelling at the site of
entry.
•The chronic form may develop 10 to 20 years after
infection. This form affects internal organs (e.g. the
heart, eosophagus, colon and the peripheral nervous
system).

32. American Trypanosomiasis
American trypanosomiasis, or Chagas disease, is a
potentially fatal disease of humans.

33. Life cycle
Trypanosoma cruzilife cycle starts in an animal
reservoir, usually mammals, wild or domestic, and
include humans.
A triatomine bug serves as the vector.
While taking a blood meal, it sucks up the T. cruzi.
In the bug, they go into the epimastigote stage.

34. Life cycle
After reproducing through mitosis, the epimastigotes
move onto the rectalcell wall. There, they become
infectious. Infectious T. cruziare called
trypomastigotes.Then, while the triatomine bug is
taking a blood meal from a human, it defecates. The
trypomastigotes are in the faeces.

35. Life cycle
The trypomastigotes enter the human host through
the bite wound or by crossing mucous membranes.
When they enter a human cell, they become
amastigotes.This is another reproductive stage.
After reproducing through mitosis until a large
amount of amastigotes are in a cell, pseudocysts are
formed in infected cells.

36. Life cycle
The amastigotes then turn back into trypomastigotes,
and the cell bursts. The trypomastigotes swim along to
either infect other cells or get sucked up by other
triatomine bugs.

37. Triatomine bug

38. Diagnosis
Specimens:
Blood, Bone marrow, biopsy.
Stain the smear with Giemsa or Leishman stain.

39. Diagnosis
Culture in NNN medium.
Animal inoculation(mouse).
Xenodiagonsis:
The method of choice for T. cruzi. By feeding lab. bugs
on the suspected blood the after few day examine the
faeces of the bug.

40. Trypanosoma cruzi

41. Treatment
There is no effective drug treatment.

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