The Organism T. cruzi has three developmental stages: epimastigotes in the vector, trypomastigotes (in the bloodstream), and a rounded intracellular stage, the amastigote. The blood forms of T. cruzi are present during the early acute stage and at intervals thereafter in smaller numbers. They are typical trypomastigotes with a large, rounded terminal kinetoplast in stained preparations, but they are difficult to morphologically distinguish from African trypanosomes. The tissue forms, which are most common in heart muscle, liver, and brain, develop as amastigotes that multiply to form an intracellular colony after invasion of the host cell or phagocytosis of the parasite (Figure 1).
Fig1. T. cruzi amastigote colonies (arrows) in heart muscle. Amastigotes are 1–3 μm in diameter in tissue sections. (Used with permission from Sullivan J: A Color Atlas of Parasitology, 8th ed. 2009.) Diagram of an amastigote with the characteristic “dot” (nucleus) and “dash” (kinetoplast).
Pathology and Pathogenesis
Infective forms of T. cruzi do not pass to humans by triatomine bug bites (which is the mode of entry of the nonpathogenic Trypanosoma rangeli); rather, they are introduced when infected bug feces are rubbed into the conjunctiva, the bite site, or a break in the skin. At the site of T. cruzi entry, there may be a subcutaneous inflammatory nodule or chagoma. Unilateral swelling of the eyelids (Romaña’s sign) is characteristic at onset, especially in children. The primary lesion is accompanied by fever, acute regional lymphadenitis, and dis semination to blood and tissues. Acute Chagas disease can also be asymptomatic.
In the chronic stage, the most serious complication is chagasic cardiomyopathy associated with fibrosis in response to the presence of intracellular parasites in heart tissue. When fibrosis occurs in the conduction system of the heart, arrhythmias can develop that can lead to sudden death. Invasion or toxic destruction of nerve plexuses in the alimentary tract walls leads to megaesophagus and mega colon, especially in Brazilian Chagas disease. Megaesophagus and megacolon are absent in Colombian, Venezuelan, and Central American Chagas disease. T. rangeli of South and Central America infects humans without causing dis ease and must therefore be carefully distinguished from the pathogenic species.
Epidemiology
American trypanosomiasis (Chagas disease) is especially important in Central and South America, although infection of animals extends much more widely—for example, to Maryland and southern California. Autochthonous trans mission of human Chagas disease has now been well documented in Texas and possibly elsewhere in the southwestern United States (Garcia et al, 2015). Drug treatment with benznidazole or nifurtimox is effective at the acute stages of the illness, or early in the chronic phase, but does not improve the clinical outcome once the progression of heart disease begins. Since treatment options are limited it is particularly important to control the vectors with residual insecticides and habitat modification, such as replacement of mud-brick (adobe) houses with thatched roofs where the insects live, and to avoid contact with animal reservoirs. Chagas dis ease occurs largely among people in poor economic circumstances. An estimated 7–8 million people harbor the parasite, and many of these individuals sustain heart damage, with the result that their ability to work and their life expectancy are sharply reduced.
