The trypanosomes comprise a large number of species of pathogenic protozoa of animals and plants. Some present a simple life cycle in the insect; others, however, present a complex life cycle involving vertebrate and invertebrate hosts, with the participation of different developmental stages, some of which are localised within cells of the vertebrate host. These organisms present some characteristic features such as the presence of the kinetoplast, a highly specialised organisation of mitochondrial DNA, compartmentalisation of the glycolytic pathway in glycosomes, the presence of a network of filaments forming the paraflagellar rod connected to the flagelar axonme.

Key Concepts

  • Ideally the identification and classification of protozoa shall combine the use of classical taxonomic parameters with phylogenetic analysis.

  • Despite significant advances in biomedical sciences diseases caused by protozoa still constitute important health problem throughout the world.

  • Cell transformation in response to environmental factors is fundamental for parasitic protozoa survival both in the vertebrate and invertebrate hosts.

  • Intracellular parasites developed the ability to attach to host cell surface and to trigger various mechanism leading to their internalisation into the cells.

  • Endocytosis in protozoa of the Trypanosomatidae family is a highly polarised taking place only in the flagellar pocket and the cytostome.

  • In some protozoa the glycolytic pathway does not take place in the cytosol but is compartmentalised in an organelle known as glycosome, which is part of the family of organelles designated as peroxisome.

  • Protozoa of the Trypanosomatidae family may contain up to 30% of the total DNA concentrated in a special region of its unique mitochondrion, localised close to the origin of the flagellum, and known as the kinetoplast.

Keywords: Trypanosoma; Leishmania; Phytomonas; kinetoplast; glycosome

Figure 1.

The various developmental stages presented by trypanosomatids. These stages are defined on the basis of the general form of the cell, the position of the kinetoplast in relation to the nucleus and the region where the flagellum emerges from the flagellar pocket. (a) Amastigote; (b) epimastigote; (c) trypomastigote; (d) spheromastigote; (e) promastigote; (f) paramastigote; (g) ophistomastigote; and (h) choanomastigote.

Figure 2.

Photomicrographs of Giemsa‐stained preparations showing the various developmental stages. In the case of amastigotes, the parasites are found within a host cell. (a) Trypomastigote; (b) promastigote; (c) amastigote; (d) paramastigote; (e) epimastigote; (f) ophistomastigote; (g) ophistomorph; (h) intermediate form; (i) choanomastigote. All ×1500. Note. Although Figure shows drawings displaying the shape and relative position of the various developmental stages, Figure shows photographs of Giemsa‐stained samples. Since there is no available good light micrograph of the spheromastigote stage only its drawing is shown in Figure . On the other hand, Figure shows a photograph of a form designated as ophistomorph which does not appear in Figure since still there is no consensus about it real existence.

Figure 3.

Stages in the life cycle of Trypanosoma cruzi in the gut of the invertebrate host. (1) Bloodstream trypomastigotes, ingested during a bloodmeal, once in the stomach transform into (2) spheromastigotes. In the intestine, these transform (3) into (a) short or (b) long epimastigotes, which divide in the gut and attach to the intestinal epithelial surface. In the distal intestine, some of the epimastigotes transform into trypomastigotes, known as (4) metacyclics, which are released together with the faeces or the urine of the insect. These forms are highly infective.

Figure 4.

Stages in the life cycle of Trypanosoma cruzi in the vertebrate host. Initially the trypomastigote (or the amastigote, which is infective) attaches to the host cell surface (a) and triggers either a phagocytic process, with formation of surface projections (b) or a depression in the cell surface (c). In both cases a parasitophorous vacuole (d) forms. Host cell lysosomes fuse with the vacuole (d). The trypomastigote gradually changes its shape with the concomitant disruption of the membrane of the parasitophorous vacuole (e), transforming into a rounded amastigote (f), which is now in direct contact with the host cell cytoplasm. The amastigote divides several times, forming a large number of parasites that occupy most of the cytoplasm (g). At a certain point, these forms change their shape (h), transforming into trypomastigotes (i), which are highly motile. The host cell membrane is disrupted and releases trypomastigotes into the intercellular space (j).

Figure 5.

Ultrastructure of the trypomastigote of Trypanosoma cruzi. The most important structures and organelles are indicated.



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Further Reading

De Souza W (1995) Structural organization of the cell surface of pathogenic protozoa. Micron 26: 405–430.

Smith DF and Parsons M (eds) (1996) Molecular Biology of Parasitic Protozoa. New York: IRL Press.

Tapia FJ, Cáceres‐Dittmar G and Sánchez MA (1996) Molecular and Immune Mechanisms in the Pathogenesis of Cutaneous Leishmaniasis. New York: Springer.

Tropical Disease Research (1995) Progress 1975–94. Geneva: World Health Organization.

Vickerman K and Preston TM (1976) Comparative cell biology of the kinetoplastid flagellates. In: Lumsden WHR and Evans DA (eds) Biology of Kinetoplastida, pp. 66–102. New York: Academic Press.

Wyler DJ (1990) Modern Parasite Biology. New York: Freeman.

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de Souza, Wanderley(Sep 2011) Trypanosoma. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1002/9780470015902.a0001974.pub2]