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Trypanosomes
It is the etiologic agent of trypanosomiasis.
These species may have amastigote,
promastigote and trypomastigote stages in their
life cycle.
Clinical Importance
Trypanosoma brucei complex – African
trypanosomiasis (sleeping sickness)
Trypanosoma cruzi – American
trypanosomiasis (Chagas’ disease)
1.African trypanosomiasis;
Trypanosoma gambiense & Trypanosoma
rhodesiene are causative agents of the African
typanosomiasis, transmitted by insect bites.
Pathogenesis
The trypomastigotes spread from the
skin through the blood to the lymph node
and the brain.
The typical somnolence (sleeping
sickness) usually progresses to coma.
In acute form, cyclical fever spike
(approximately every 2 weeks) occurs
Epidemiology
T.burcei gambiense is limited to tropical
west and central Africa, correlating with
the range of the tsetse fly vector.
The tsetse flies transmitting T.b.
gambiense prefer shaded stream banks
for reproduction and proximity to human
dwellings.
People who work in such areas are at
greatest risk of disease.
An animal reservoir has not been proved
for this parasite.
Cont…
T.burcei rhodeseinse is found primarily
in East Africa, especially the cattle-
raising countries, where tsetse flies
breed in the brush.
T.b. rhodeseines also differs from T.b.
gambiense in that domestic animal
hosts (cattle and sheep) and wild
animals act as reservoir hosts.
This makes the organism more difficult
to control than T.b. gambiense.
Clinical features
Although both species cause sleeping
sickness, the progress of the diseases are
different. T.gambiense disease runs a low-
grade chronic course over a few years.
One of the earliest signs of disease is an
occasional ulcer at the site of the fly bite.
As reproduction of organisms continues,
the lymph nodes are invaded, and fever,
myalgia, arthralgia, and lymph node
enlargement results. Chronic disease
progresses to CN involvement with
lethargy, tremors, mental retardation, and
general deterioration.
Cont…
In the final stages,
 convulsions,
 hemiplegia,
 and incontinence occur,
eventually progressing to a comatose
state.
Then death can come which is the result
of CNS damage.
In T.rhodesiense, the disease is a more
rapidly progressive that is usually fatal.
This virulent organism also develops in
greater numbers in the blood.
Cont…
CNS invasion occurs, resulting in
lethargy, anorexia, and mental
disturbance.
The chronic stages for T.gambiense are
not often seen, but in addition to above
stated symptoms, the organism causes
kidney damage & myocarditis, leading to
death.
Cont…
 Immunity
Both the humoral and cellular immunity
involve in these parasites.
The immune responses to the presence
of these parasites, however, is faced
with antigenic variation, in which
organisms that have changed their
antigenic identity can escape the
immune response and initiate another
disease process with increased level of
parasitemia
Prevention
 Control of breeding sites of tsetse flies
and use of insecticides.
Treatment of human cases to reduce
transmission to flies.
 Avoiding insect bite by wearing
protective clothing & use of bed netting
and insect repellants
Laboratory
 Examination of thin and thick films.
 Aspiration from lymph nodes.
 concentrating parasites in blood
including centrifugation.
Microscopic attempts to visualize the
organism.

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Pp3

  • 1. Trypanosomes It is the etiologic agent of trypanosomiasis. These species may have amastigote, promastigote and trypomastigote stages in their life cycle. Clinical Importance Trypanosoma brucei complex – African trypanosomiasis (sleeping sickness) Trypanosoma cruzi – American trypanosomiasis (Chagas’ disease) 1.African trypanosomiasis; Trypanosoma gambiense & Trypanosoma rhodesiene are causative agents of the African typanosomiasis, transmitted by insect bites.
  • 2. Pathogenesis The trypomastigotes spread from the skin through the blood to the lymph node and the brain. The typical somnolence (sleeping sickness) usually progresses to coma. In acute form, cyclical fever spike (approximately every 2 weeks) occurs
  • 3. Epidemiology T.burcei gambiense is limited to tropical west and central Africa, correlating with the range of the tsetse fly vector. The tsetse flies transmitting T.b. gambiense prefer shaded stream banks for reproduction and proximity to human dwellings. People who work in such areas are at greatest risk of disease. An animal reservoir has not been proved for this parasite.
  • 4. Cont… T.burcei rhodeseinse is found primarily in East Africa, especially the cattle- raising countries, where tsetse flies breed in the brush. T.b. rhodeseines also differs from T.b. gambiense in that domestic animal hosts (cattle and sheep) and wild animals act as reservoir hosts. This makes the organism more difficult to control than T.b. gambiense.
  • 5. Clinical features Although both species cause sleeping sickness, the progress of the diseases are different. T.gambiense disease runs a low- grade chronic course over a few years. One of the earliest signs of disease is an occasional ulcer at the site of the fly bite. As reproduction of organisms continues, the lymph nodes are invaded, and fever, myalgia, arthralgia, and lymph node enlargement results. Chronic disease progresses to CN involvement with lethargy, tremors, mental retardation, and general deterioration.
  • 6. Cont… In the final stages,  convulsions,  hemiplegia,  and incontinence occur, eventually progressing to a comatose state. Then death can come which is the result of CNS damage. In T.rhodesiense, the disease is a more rapidly progressive that is usually fatal. This virulent organism also develops in greater numbers in the blood.
  • 7. Cont… CNS invasion occurs, resulting in lethargy, anorexia, and mental disturbance. The chronic stages for T.gambiense are not often seen, but in addition to above stated symptoms, the organism causes kidney damage & myocarditis, leading to death.
  • 8. Cont…  Immunity Both the humoral and cellular immunity involve in these parasites. The immune responses to the presence of these parasites, however, is faced with antigenic variation, in which organisms that have changed their antigenic identity can escape the immune response and initiate another disease process with increased level of parasitemia
  • 9. Prevention  Control of breeding sites of tsetse flies and use of insecticides. Treatment of human cases to reduce transmission to flies.  Avoiding insect bite by wearing protective clothing & use of bed netting and insect repellants
  • 10. Laboratory  Examination of thin and thick films.  Aspiration from lymph nodes.  concentrating parasites in blood including centrifugation. Microscopic attempts to visualize the organism.