Academic journal article International Public Health Journal

Chagas Disease

Academic journal article International Public Health Journal

Chagas Disease

Article excerpt


Although Carlos Chagas first described the disease that carries his name in 1909, there is still no cure. Recently there has been an increased interest in the condition because globalization has made it an emergent health problem in non endemic areas (1-4). Although the common disabling symptom complexes occur in adults, primary infection usually occurs in children. Without solving childhood infection, adult morbidity and mortality will never be resolved.


Chagas disease is caused by the protozoan parasite Trypanosoma cruzi., whose genome parasite was described in 2005. The life cycle of T cruzi is complex. A triatomine bug takes blood from an infected source (a human with chronic Chagas disease, for example) and ingests trypomastigotes, which transform into epigmastigoes and replicate by binary fission in the insect's midgut. The epimastigotes migrate to the hindgut as well as rectum and differentiate into metacylic trypomastigotes; they are then released by defecation onto the skin of a mammalian host. The metacyclic trypomastigotes enter the host through the host's rubbing or scratching the bite wound or by contamining mucosal or conjunctival tissues. Trypomastigotes are recruited and fused with lysosomes to penetrate local cells and differentiate into amastigotes, which replicate by binary fission and then transform into trypomastigotes. [1-4].


Chagas disease is transmitted to humans by large blood sucking reduviid bugs of the subfamily Triatominae. The most important T cruzi vectors in the transmission to man are Triatoma infestans, Rhodnius prolixus, and Triatoma dimidiata. (1). Other documented forms of transmission are blood transfusion, vertically transmission from mother to infant (5), and organ or bone marrow transplantation (6-8).

The risk of acquiring Chagas disease by blood transfusion from an infected donor depends on the concentration of parasites in the blood product, the blood component transfused, and the parasite strain. Blood transfusions carry a transmission risk of approximately 10 to 20% depending on the parasite load. The risk appears to be higher with transfusion of platelets (2).

Vertical transmission from chronically infected women studied in endemic areas of South America occurs in 5% of pregnancies (1,2). Several investigators describe the prevalence of mother to child transmission in endemic areas to be the same as in non-endemic areas where the child has no environmental risk (2,5,9).

According to Buekens, in 2008, there were 944,993 Hispanic live births per year to an estimated 3,780 seropositive mothers in the United States; assuming a 0.4% seropositivity, there is thus an estimated 189 newborns who were infected, based on a 5% mother to child transmission rate (5). Verani estimated that there are 300 congenital infections annually in the United States (10).


Chagas disease is caused by the parasite and by the host immune-inflammatory response. Rodriguez describes several determinant factors of disease such as the quantity of parasites in the initial infection, infective forms in the initial inoculation, lineage of inoculated T cruzi (Tcl-TcVI), re-infection, quality of the strains and clones, specific clonal histotropic receptors of the host, and the patient's initial immune response (11). The detailed biological interactions between T cruzi and its host have been extensively described in recent articles but go beyond the scope of this discussion (1,12).

The parasites deposited in the skin of the host create a local inflammatory reaction, specifically a lymphoreticular response. Clinically this is described as the Romana's sign or inoculation Chagoma (1). Trypomastigotes are taken up by macrophages and circulate to the liver, spleen, ganglia, and muscles, where they form pseudocysts of amastigotes. The parasite creates an immune response led by T-helper 1 and both CD4 and CD8 cells. …

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