Chagas’ disease is named after the Brazilian physician Carlos Chagas who first discovered the parasite responsible for the signs and symptoms of the disease. The causative agent is the hemoflagellate protozoan Trypanosoma cruzi. This proto-zoan parasite is transmitted to the blood-sucking reduviid bug vector when the reduviids take a blood meal from animals or humans who are infected with circulat-ing T. cruzi. When the infected bug takes a subsequent blood meal, it usually def-ecates on the skin of the next victim and deposits T. cruzi as well. The individual then becomes infected either by the feces deposited at the site of the puncture or inadvertent contamination of a mucous membrane of the human secondary to hand contamination with organisms. The distribution of the arthropod vectors is limited to the Western Hemisphere and is widely distributed in the southern United States, Mexico, and Central America. The reduviid vectors are common in most South American countries, especially Brazil, Argentina, Bolivia, and Chile. Chagas’ is a disease primarily of the poor largely because the reduviid bugs favor living in adobe mud or enter poor housing through cracks or holes in the walls and thatched roofs.
An estimated 20 million people are cur-rently infected with T. cruzi, and approxi-mately 100 million people are at risk of infection. The endemic area of Chagas’ disease is huge, stretching from Mexico to southern Argentina, but is limited to the Western Hemisphere. The incidence, prev-alence, and severity of Chagas’ disease and T. cruzi infection seem to be higher in South America than Central America; this may be due to differences in vector behavior or strain variation of T. cruzi or differences in disease recognition and reporting.
T. cruzi is transmitted by blood-feed-ing reduviid insect vectors, vertically from mother to child, or by blood transfusions. Vector transmission is responsible for most of T. cruzi infections, and most of this transmission is secondary to the deposit of infected feces and urine by the reduviid bug at the time of the blood meal. As an alternative, humans have been reported to
be infected by accidental oral ingestion of reduviid bugs, which presumably release metacyclic trypomastigotes to invade the oral mucosal cells. Parasites persist in the blood of seropositive asymptomatic indi-viduals, and blood from these individuals can transmit infection in approximately 12 percent to 25 percent of transfusions. Blood transfusion transmission has become less frequent as blood banks in endemic areas screen blood with serologic tests to deter-mine whether the blood is likely to be con-taminated with T. cruzi. However, some areas do not routinely screen donors for T. cruzi infection. Congenital transmission occurs in approximately 1 percent of preg-nancies of infected women, but the inci-dence is higher if the woman is infected during pregnancy. Infection of the fetus probably occurs transplacentally in months 5 to 9 of pregnancy.
The reduviid vectors that transmit T. cruzi are members of the order Hemiptera, family Reduviidae, and sub-family Triatominae. Although there are more than 100 species of triatomines, few are epidemiologically significant as vectors of T. cruzi to humans. Species that colonize housing (domiciliary app.) are important in transmission to humans in the south-ern part of South America. Triatoma infes-tans is the principal vector responsible for the most transmissions in these “southern cone” countries of South America.
Many reduviid species live in wild habitats and do not invade housing; thus, they do not come in contact with humans and are not important in transmission to humans, although they are important in the propagation of T. cruzi in nature. Some sylvatic species (e.g., Triatoma dimidiata andRhodnius prozlixus) can inhabit both wild habitants and housing, and these sylvatic species are important in human transmission in the northern part of South America and in Central America.