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AMERICAN TRYPANOSOMIASIS
TRYPANOSOMA CRUZI
Causal Agent
• The protozoan parasite, Trypanosoma cruzi,
causes Chagas disease, a zoonotic disease that
can be transmitted to humans by blood-
sucking triatomine bugs.
A triatomine bug
Life cycle
An infected triatomine insect vector (or “kissing” bug) takes a blood
meal and releases trypomastigotes in its feces near the site of the bite
wound (stercorarian mode of transmission). Trypomastigotes enter the
host through the wound or through intact mucosal membranes, such
as the conjunctiva. Common triatomine vector species for
trypanosomiasis belong to the genera Triatoma, Rhodnius, and
Panstrongylus. Inside the host, the trypomastigotes invade cells near
the site of inoculation, where they differentiate into intracellular
amastigotes. The amastigotes multiply by binary fission and
differentiate into trypomastigotes, and then are released into the
circulation as bloodstream trypomastigotes. Trypomastigotes infect
cells from a variety of tissues and transform into intracellular
amastigotes in new infection sites.
Life-cycle
• Clinical manifestations can result from this infective
cycle. The bloodstream trypomastigotes do not replicate
(different from the African trypanosomes). Replication
resumes only when the parasites enter another cell or are
ingested by another vector. The “kissing” bug becomes
infected by feeding on human or animal blood that contains
circulating parasites. The ingested trypomastigotes
transform into epimastigotes in the vector’s midgut. The
parasites multiply and differentiate in the midgut and
differentiate into infective metacyclic trypomastigotes in
the hindgut.
Trypanosoma cruzi can also be transmitted through blood
transfusions, organ transplantation, transplacentally, and in
laboratory accidents.
LIFE CYCLE
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.
Chronic Phases:
– Starts 2 months after initial infection.
– 60-70% of people with Chagas may be completely free of cardiac,
gastrointestinal and neurological symptoms, but 2-5% of patients
convert to cardiac or digestive forms each year (reason not clear).
In 30-40% of people Chagas induces
arrhythmia, cardiac failure,
thromboembolism, atrioventricular
fibrillation, ventricular hypertrophy
• Digestive form:
–10% of people may have
Megaoesophagus and 3% with
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.
Gastrointestinal manifestation
Megacolon
Megacolon
Chagoma (Romana’s sign) and Chancre
Geographic Distribution:
The Americas from the southern United States
to southern Argentina. Mostly in poor, rural
areas of Mexico, Central America, and South
America. Chronic Chagas disease is a major
health problem in many Latin American
countries.
Laboratory Diagnosis
• Demonstration of the causal agent is the diagnostic procedure in acute
Chagas disease. It almost always yields positive results, and can be
achieved by:
• Microscopic examination: a) of fresh anticoagulated blood, or its buffy
coat, for motile parasites; and b) of thin and thick blood smears stained
with Giemsa, for visualization of parasites.
• Isolation of the agent: a) inoculation in culture with specialized media (e.g.
NNN, LIT); b) inoculation into mice; and c) xenodiagnosis, where
uninfected triatomine bugs are fed on the patient's blood, and their gut
contents examined for parasites 4 weeks later.
• Note: In certain circumstances, investigational molecular diagnostic tools,
such as PCR, may be useful.
• Diagnostic Findings
• Microscopy
• Antibody detection
Immunity, treatment and Prevention
• Immunity
Unlike African trypanosomiasis, the antigenic variation is less common
in T. cruzi infection. Therefore, the humoral and cellular immune
responses function in the immune system.
• Treatment
The drug of choice is nifurtimox. Alternative agents include allopurinol
& benzimidazole.
• Prevention
Bug control, eradication of nests
Treating infected person & exclusion of donors by screening blood.
Development of vaccine.
Treatment
• Medication for Chagas disease is usually
effective when given during the acute phase
of infection and may be indicated for patients
in the chronic phase as well. The drugs of
choice are benzinidazole (5mg/kg body wt
daily for 60 days orally) or nifurtimox (8 to 10
mg/kg body wt 3 times daily for 60 to 120
days, orally).

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AMERICAN TRYPANOSOMIASIS.pptx

  • 2. Causal Agent • The protozoan parasite, Trypanosoma cruzi, causes Chagas disease, a zoonotic disease that can be transmitted to humans by blood- sucking triatomine bugs.
  • 4. Life cycle An infected triatomine insect vector (or “kissing” bug) takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound (stercorarian mode of transmission). Trypomastigotes enter the host through the wound or through intact mucosal membranes, such as the conjunctiva. Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodnius, and Panstrongylus. Inside the host, the trypomastigotes invade cells near the site of inoculation, where they differentiate into intracellular amastigotes. The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes. Trypomastigotes infect cells from a variety of tissues and transform into intracellular amastigotes in new infection sites.
  • 5. Life-cycle • Clinical manifestations can result from this infective cycle. The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The “kissing” bug becomes infected by feeding on human or animal blood that contains circulating parasites. The ingested trypomastigotes transform into epimastigotes in the vector’s midgut. The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut. Trypanosoma cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents.
  • 7. 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. Chronic Phases: – Starts 2 months after initial infection. – 60-70% of people with Chagas may be completely free of cardiac, gastrointestinal and neurological symptoms, but 2-5% of patients convert to cardiac or digestive forms each year (reason not clear).
  • 8. In 30-40% of people Chagas induces arrhythmia, cardiac failure, thromboembolism, atrioventricular fibrillation, ventricular hypertrophy
  • 9. • Digestive form: –10% of people may have Megaoesophagus and 3% with 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.
  • 12. Geographic Distribution: The Americas from the southern United States to southern Argentina. Mostly in poor, rural areas of Mexico, Central America, and South America. Chronic Chagas disease is a major health problem in many Latin American countries.
  • 13. Laboratory Diagnosis • Demonstration of the causal agent is the diagnostic procedure in acute Chagas disease. It almost always yields positive results, and can be achieved by: • Microscopic examination: a) of fresh anticoagulated blood, or its buffy coat, for motile parasites; and b) of thin and thick blood smears stained with Giemsa, for visualization of parasites. • Isolation of the agent: a) inoculation in culture with specialized media (e.g. NNN, LIT); b) inoculation into mice; and c) xenodiagnosis, where uninfected triatomine bugs are fed on the patient's blood, and their gut contents examined for parasites 4 weeks later. • Note: In certain circumstances, investigational molecular diagnostic tools, such as PCR, may be useful. • Diagnostic Findings • Microscopy • Antibody detection
  • 14. Immunity, treatment and Prevention • Immunity Unlike African trypanosomiasis, the antigenic variation is less common in T. cruzi infection. Therefore, the humoral and cellular immune responses function in the immune system. • Treatment The drug of choice is nifurtimox. Alternative agents include allopurinol & benzimidazole. • Prevention Bug control, eradication of nests Treating infected person & exclusion of donors by screening blood. Development of vaccine.
  • 15. Treatment • Medication for Chagas disease is usually effective when given during the acute phase of infection and may be indicated for patients in the chronic phase as well. The drugs of choice are benzinidazole (5mg/kg body wt daily for 60 days orally) or nifurtimox (8 to 10 mg/kg body wt 3 times daily for 60 to 120 days, orally).