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. 2012 Aug;6(8):e1749.
doi: 10.1371/journal.pntd.0001749. Epub 2012 Aug 28.

Interactive multimedia to teach the life cycle of Trypanosoma cruzi, the causative agent of Chagas disease

Dirceu E Teixeira  1 , Marlene Benchimol, Paulo Henrique Crepaldi, Wanderley de Souza
Affiliations

Interactive multimedia to teach the life cycle of Trypanosoma cruzi, the causative agent of Chagas disease

Dirceu E Teixeira et al. PLoS Negl Trop Dis. 2012 Aug.
No abstract available

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. The life cycle of T. cruzi.
1. The insect vector (female or male) bites a mammalian host and ingests trypomastigotes located in the blood. 2. Metacyclic trypomastigotes. 3. Trypomastigotes transform into epimastigotes and some spheromastigotes. 4. Epimastigotes multiply in the midgut. 5. Epimastigotes transform into metacyclic trypomastigotes in the hindgut. 6. The insect vector passes the metacyclic trypomastigotes in feces near a bite site after feeding on a mammalian host. 7. Metacyclic trypomastigotes form. 8. Metacyclic trypomastigote infects macrophages. 9. Metacyclic trypomastigote transforms into amastigote. 10. Amastigote is released from the parasitophorous vacuole. 11. Amastigotes multiply in the cytoplasm. 12. Amastigotes transform into trypomastigotes. 13. Trypomastigotes burst out of the cell. 14. Amastigotes and trypomastigotes form. 15. (a) Trypomastigotes and (b) amastigotes infect macrophages. In the central portion of the figure, we added the most important animal reservoirs involved in the maintenance of the parasite in the domestic and peridomestic environment.
Figure 2
Figure 2. Schematic representations of T. cruzi amastigote organelles.
(A) 2D and (B) 3D models. These images were made based on micrographs of light microscopy as well as scanning and transmission electron microscopy.
Figure 3
Figure 3. Schematic representations of T. cruzi epimastigote organelles.
(A) 2D and (B) 3D models. These images were made based on micrographs of light microscopy as well as scanning and transmission electron microscopy.
Figure 4
Figure 4. Schematic representations of T. cruzi trypomastigote organelles.
(A) 2D and (B) 3D models. These images were made based on micrographs of light microscopy as well as scanning and transmission electron microscopy.
Figure 5
Figure 5. General view depicting the stages of amastigote division by binary fission.
(A) In the preliminary phase of cell division, the nucleus displays condensed chromatin and a single nucleolus. (B) The early phase of the division process begins with the decondensation of chromatin and the disappearance of the nucleolus. (C) In the equatorial stage, there is early lateral growth of the kinetoplast and the appearance of a new basal body. This change is followed by the appearance of an arranged set of ten dense plaques in the equatorial region of the nucleus. These plaques are associated with an intranuclear spindle formed by microtubules. (D) The early elongational phase begins with the splitting of dense plaques, which migrate toward the nucleus poles. The nucleus elongates, and the spindle microtubules modify their distribution. The new flagellum emerges from the flagellar pocket. (E) In the final phase of elongation, the split dense plaques begin to migrate toward the nucleus poles, which exhibit an hourglass shape. This form represents the last stage of nucleus constriction. (F) In the reorganizative phase, the microtubules fade out in a stepwise fashion, the nucleolus begins to reconstitute, and the chromatin begins to condense. In this phase, the nuclei and kinetoplasts are already individualized. (G) At the stage of constriction, cytokinesis occurs and culminates with the formation of two independent amastigotes (H). These images were made based on micrographs of transmission electron microscopy.
Figure 6
Figure 6. The endocytic pathway in the epimastigote form of
(A) Endocytosis occurs in two sites of macromolecular ingestion: the cytostome-cytopharinx complex and the flagellar pocket. (B) In cytostome-cytopharinx complex the macromolecules migrate through the cytopharynx and are internalized via small vesicles, which are formed in the final portion of the cytopharynx. (C) Subsequently, the macromolecules cross through the early tubular endosomal network and are delivered to a reservosome (D). (E) The macromolecules are also internalized via vesicles that form in the flagellar pocket. (F) The endocytic pathway continues through a network of long tubules and vesicles extending to the posterior end of the cell body, returning to the opposite direction and eventually merging with the reservosome. (G) Our model also suggests that cruzipain molecules, as well as other proteases, are processed and leave the Golgi complex. (H) Vesicles containing these molecules also interact with the endocytic pathway and are transported to reservosomes. These images were made based on micrographs of transmission electron microscopy.
Figure 7
Figure 7. Frame view of paraflagellar rod animation during flagellar beating in comparison to deep-etching replicas.
(A and B) Show the flagellum in a straight state and (C and D) in a bent state. (A and C) Schematic 3D representation and (B and D) deep-etching replica images. Axoneme (light pink), filaments that link the PFR to the axoneme (purple), proximal and distal domains of the PFR (red), and the intermediate domain (salmon). These schematic 3D representations were made based on micrographs of transmission electron microscopy (image courtesy of Gustavo Rocha).
Figure 8
Figure 8. Schematic 3D view of the phases of T. cruzi interaction in the invertebrate host.
(A) Insect vector ingesting trypomastigotes present in the blood of the vertebrate host during a blood meal. (B) In the stomach of the insect, trypomastigotes transform into epimastigotes and spheromastigotes. (C) Epimastigotes multiply in the midgut and attach to the perimicrovillar membranes of the intestinal cells. (D) Note that this adhesion occurs predominantly through the region of the flagellum. (E) At the most posterior region, many of the epimastigotes transform into metacyclic trypomastigotes and adhere to the cuticle lining the epithelium of the rectum and the rectal sac of the insect. (F) When the parasites leave the epithelium, the metacyclic trypomastigotes may be eliminated in the urine or feces of the insect. These images were made based on micrographs of transmission electron microscopy and video microscopy.
Figure 9
Figure 9. Schematic 3D view of the phases of interaction of the epimastigote form of T. cruzi with vertebrate cells (macrophage).
(A) Attachment of epimastigotes to the macrophage surface. (B) This attachment triggers the internalization process via phagocytosis with the formation of pseudopods (C) and is followed by the formation of a parasitophorous vacuole. (D–G) Host cell lysosomes migrate toward and fuse with the parasitophorous vacuole, releasing their contents into the vacuole and subsequently digesting the intravacuolar epimastigotes (H). These images were made based on micrographs of transmission electron microscopy and video microscopy.
Figure 10
Figure 10. Schematic 3D view of the phases of interaction of the trypomastigote form of T. cruzi with vertebrate cells (macrophage).
(A) Attachment of the trypomastigote form to the macrophage surface. (B) The process of internalization via phagocytosis begins with the formation of pseudopods and is followed by the recruitment and fusion of host cell lysosomes (C). A parasitophorous vacuole is subsequently formed. The lysosomal content is released into the vacuole, and the parasite is not affected. (D) In the vacuole, the trypomastigote transforms into the amastigote form. (E) This transformation is accompanied by the digestion of the parasitophorous vacuole membrane. (F) The amastigote is released into the cytoplasm of the host cell and divide several times. (G) Following division, the amastigotes transform into trypomastigotes, which show intense and constant movement. (H) The host cell bursts and the parasites reach the extracellular space and, subsequently, the bloodstream. These images were made based on micrographs of transmission electron microscopy and video microscopy.
Figure 11
Figure 11. Schematic 3D view of the phases of interaction of the amastigote form of T. cruzi with vertebrate cells (macrophage).
(A) In this example, attachment of the amastigote form to the macrophage surface is observed to initiate the process of internalization via phagocytosis. (B) The formation of pseudopods is followed by the formation of a parasitophorous vacuole (C). The lysosomes fuse with the parasitophorous vacuole and discharge their contents. (D) Subsequent digestion of the parasitophorous vacuole membrane occurs. (E) Note that the amastigote is released into the cytoplasm of the host cell and divides several times (F). (G) Following division, the amastigotes transform in trypomastigotes, which display intense and constant movement. (H) Finally, the host cell bursts and the parasites are released into the extracellular space and reach the bloodstream. These images were made based on micrographs of transmission electron microscopy and video microscopy.
Figure 12
Figure 12. Schematic 3D view of the phases of interaction of the trypomastigote form of T. cruzi with vertebrate cells (cardiac cells).
(A) Attachment of the trypomastigote form to the surface of heart muscle cells. This attachment initiates the process of invasion and is followed by the formation of a parasitophorous vacuole (B). (C) Inside the vacuole, the trypomastigote transforms into an amastigote form and this transformation is accompanied by the digestion of the parasitophorous vacuole membrane. (D) The amastigote is released into the cytoplasm of the host cell and divides several times (E). (F) Following division, the amastigotes transform into trypomastigotes, which are released into the extracellular space. These images were made based on micrographs of transmission electron microscopy and video microscopy.
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References

    1. Secretaria de Vigilância em Saúde, Ministério da Saúde (2010) Boletim eletrônico epidemiológico: Situação epidemiológica das zoonoses de interesse para a saúde pública. 2: 10–11.
    1. Tyler KM, Engman DM (2001) The life cycle of Trypanosoma cruzi revisited. Int J Parasitol 31: 472–481. - PubMed
    1. Pollock E, Chandler P, Sweller J (2002) Assimilating complex information. Learning Instruction 12: 61–86.
    1. Tversky B, Morrison JB (2002) Animation: can it facilitate? Int J Human Comput Stud 57: 247–262.
    1. McClean P, Johnson C, Rogers R, Daniels L, Reber J, et al. (2005) Molecular and cellular biology animations: development and impact on student learning. Cell Biol Educ 4: 169–179. - PMC - PubMed

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