Trypanosoma cruzi belongs to the subkingdom Protozoa. They are flagellar organisms that have one nucleus and an organelle, the kinetoplast, that gives rise to one mitochondrion and mitochondrial DNA. T. cruzi reproduce asexually by binary fission. Like all other trypanosomes, T. cruzi live one stage of their lives in the blood and/or tissues of vertebrate hosts and during other stages they live in the digestive tracts of invertebrate vectors (temporary hosts). T. cruzi's vectors, Triatoma infectans (vinchucas) are triatomine insects, with over 100 species that carry the parasite. (For other endemic and dangerous species see Kiss of Death: Chagas Disease in the Americas, pages 186 through 193.)

The subspecies Stercorian

T. cruzi belong to the subspecies A. stercoria, because the parasite develops its infectious stage in the insect's digestive tract. When the vector defecates, the parasite travels in the feces. The parasite enters the bite wound or through abrasions on the skin caused by the victim scratching the sore bite. As one prevention, not scratching the bite and morning washing of the wound may help to decrease chagas. The vector's effectiveness in spreading the infectious T. cruzi is related to infestation of houses by T. infectans, and the proximity and short time between blood feeding and defecation, and a lack of personal hygiene.

T. cruzi changes forms in its life cycle as it travels from insects to humans. The general forms are trypomastigote (tryps), amastigote, sluggish trypomastigote, and epimastigote. Because it undergoes different forms, it easily adapts to different/hostile environments and renders itself a difficult and evasive target for attack by the immune system and immunization because it changes its surface area. Metacyclic trypomastigotes are effective forms of T. cruzi that pass from the insect's hindgut in the fecal matter and burrow into the skin, either through the bite site or skin abrasions. Metacyclic tryps have a nuclei near the posterior of their bodies. They have a free flagellum (tail) attached to an undulating membrane on the body. The flagella whip them along in the person's blood and attaches to the insect's intestinal wall. Infinitesimally small, these tryps are 20 microns (0.20 mm) long and 3 microns wide. (More than a million can fit in a pixel, so Bill Gates beware!) After metacyclic tryps pass through the skin, they briefly travel in the blood stream (and area of quick attack from the immune system) and then colonize muscle and neuron tissue, areas less vulnerable to attack, where they encyst and form amastigotes

After they have entered muscle tissue, metacyclic form amastigotes. Amastigotes are intracellular, round and oval in shape, and without flagella. They are 1.5 to 5 microns long. Amastigotes cluster into cysts - bundles of evolving forms that erupt amastigotes into the bloodstream where they move on to other tissue cells. This provides for rapid proliferation. Amastigote also provide stumpy trypomastigotes that are ingested by vinchucas during bloodfeeding. This sustains the parasite's life cycle.

When vinchucas blood feed upon an infected animal or human, they ingest stumpy trypomastigotes from chagas victims. The vinchucas become carriers of T. cruzi for life, as the parasite reproduces and transforms. These trypomastigotes travel to the insect's midgut and transform into epimastigotes, which are more adaptable to survive the insect's intestines. Epimastigotes have flagellum attached near the center of the body, which differ from tryps whose flagellum starts near the rear end of the body. Epimastigotes have a central nucleus and kinetoplast. They multiply by binary fission. Epimastigotes are 10 to 20 microns long at first, but grow another 10 microns as they travel to the insect's hindgut, where they transform into metacyclic trypomastigotes. The insect stage of T. cruzi takes from six to sixteen days, and the parasite apparently does no damage to the vinchucas.

This complicated and delicate relationship between T. cruzi and triatomines is the result of millions of years of selective pressure, natural selection, and adaptive strategies that provide T. cruzi with excellent defenses against human and animal immune systems. T.cruzi employ an adaptive strategy common to many parasites in maintaining their population levels within hosts. It is not to their advantage to destroy the host organism too quickly because this would destroy their home. This leads to relatively low levels of parasitemia for those already with acute phase chagas. After the acute phase, sufferers from chagas rarely suffer another acute phase of the disease because this is adverse to the survival of T.cruzi.