parasite, Trypanosoma cruzi, causes Chagas disease, a zoonotic
disease that can be transmitted to humans by blood-sucking triatomine
triatomine insect vector (or “kissing” bug) takes a blood meal and
releases trypomastigotes in its feces near the site of the bite wound.
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, Rhodinius, and Panstrongylus.
Inside the host, the trypomastigotes invade cells, where they
differentiate into intracellular amastigotes
The amastigotes multiply by binary fission
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. 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
The ingested trypomastigotes transform into epimastigotes in the
The parasites multiply and differentiate in the midgut
differentiate into infective metacyclic trypomastigotes in the hindgut
Trypanosoma cruzi can also be transmitted through blood
transfusions, organ transplantation, transplacentally, and in laboratory
The Americas from
the southern United States to southern Argentina. Mostly in poor, rural
areas of Central and South America. Chronic Chagas disease is a major
health problem in many Latin American countries. With increased
population movements, the possibility of transmission by blood
transfusion has become more substantial in the United States.
A local lesion (chagoma,
palpebral edema) can appear at the site of inoculation. The acute phase
is usually asymptomatic, but can present with manifestations that
include fever, anorexia, lymphadenopathy, mild hepatosplenomegaly, and
myocarditis. Most acute cases resolve over a period of 2 to 3 months
into an asymptomatic chronic stage. The symptomatic chronic stage may
not occur for years or even decades after initial infection. Its
manifestations include cardiomyopathy (the most serious manifestation);
pathologies of the digestive tract such as megaesophagus and megacolon;
and weight loss. Chronic Chagas disease and its complications can be
the causal agent is the diagnostic procedure in acute Chagas disease.
It almost always yields positive results, and can be achieved by:
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.
the agent by: a) inoculation into mice; b) culture in specialized
media (e.g. NNN, LIT); and c) xenodiagnosis, where uninfected
reduviid bugs are fed on the patient's blood, and their gut contents
examined for parasites 4 weeks later.
In certain circumstances, investigational molecular diagnostic tools,
such as PCR, may be useful.
Chagas disease is usually effective when given during the acute stage of
infection. The drugs of choice are benznidazole or nifurtimox (under an
Investigational New Drug protocol from the CDC Drug Service). In the
chronic stage, treatment involves managing the clinical manifestations
of the disease, e.g., pacemaker for heart block; the decision about
whether to use antiparasitic therapy should be individualized in
consultation with an expert.