Chagas' Disease: Parasite

In stained blood preparations the parasites are C- or S-shaped with a prominent kinetoplast towards the rear (trypomastigotes). The nucleus is elongated and the undulating membrane is usually not clearly visible. After infection, multiplication of the parasite in the human is solely intracellular. They form microscopic pseudocysts in the tissues (similar to toxoplasmosis and sarcocytosis). This occurs mainly in the heart, muscle cells, some nerve cells and the lymphatic system. In the cell the parasite is small and rounded, with no flagellum (amastigote). When the infected cell ruptures, the parasites are released into the blood circulation where they become elongated and develop a flagellum. These forms can then infect other cells or be ingested by a bug.

An important protease for the parasite is lysosomal cruzipain (cruzain), a substance related to papain. This is being investigated as a possible therapeutic target. An unusual parasite-derived proline racemase was identified as a B-cell mitogen, resulting in polyclonal B-cell activation. The surface of the parasite is covered by mucin-type glycoproteins that attach to the membrane by glycosylphosphatidylinositol (GPI) anchors, similar to those of the variant surface glycoproteins in African trypanosomes. Mucins are recipients of the sialic acid transferred by surface trans-sialidase. T. cruzi has several hundreds of such mucin genes. The exposed N-terminal moiety of the molecules is hypervariable. It is postulated that this might play a role in immune evasion.

Category: Medicine Notes