Desktop version

Home arrow Economics arrow American Trypanosomiasis Chagas Disease, Second Edition: One Hundred Years of Research


Biology of Trypanosoma cruzi and biological diversity

M. de Lana and E.M. de Menezes Machado Federal University of Ouro Preto, Minas Gerais, Brazil

Chapter Outline

Taxonomy 345 Introduction 346 Evolutionary stages 346 Biological cycle 348 Biology in the vertebrate host 348 Cellular adhesion 348

Cellular invasion and formation of the parasitophorous vacuole 350 Trypomastigote-amastigote differentiation 350 Amastigote-trypomastigote differentiation 351 Biology in the invertebrate host 352 Biological diversity of T. cruzi 355 In the vertebrate host 355 In the invertebrate vector 359 Maintaining T. cruzi in the laboratory 359 Acellular culture 359 Cellular culture 360 Cryopreservation 361

Successive and alternative passages in animals and vectors 361 Glossary 362 References 363


Kingdom: Protista

Subkingdom: Protozoa

Phylum: Sarcomastigophora

Subphylum: Mastigophora

Class: Zoomastigophora

Order: Kinetoplastida

Suborder: Trypanosomatina

Family: Trypanosomatidae

Genus: Trypanosoma

Subgenus: Schyzotrypanum

Species: Trypanosoma (Schyzotrypanum) cruzi

American Trypanosomiasis Chagas Disease. DOI:

Copyright © 2017 Elsevier Inc. All rights reserved.


Trypanosoma cruzi, the etiological agent of Chagas disease, or American trypanosomiasis, is a flagellate of the Kinetoplastida order, family Trypanosomatidae, characterized by the presence of one flagellum and a single mitochondrion in which the kinetoplast, a specialized DNA-containing organelle, is situated. This protozoa was discovered by Carlos Ribeiro Justiniano das Chagas, a Brazilian physician, in 1909[1] when he was a member of the Instituto Oswaldo Cruz, Rio de Janeiro, Brazil. The genius of the still very young Carlos Chagas enabled him to describe the etiological agent, the vectors, the principal reservoirs, and mechanisms of infection, as well as several clinical stages of the disease with heart, gastrointestinal, and neurological manifestations.

The consensual genetic characterization of T. cruzi divides this species into six genetic groups, named TcI to TcVI,[2] [3] [4] and an additional DTU was more recently described named TcBat.3,4 Apparently this genetic variability may be associated to parasite virulence as well as pathogenicity and the clinical manifestations of the disease that is also variable.[5] Chagas disease is endemic only on the American continent, especially Latin America, with its vectors present from the south of United States to Argentina. Today, due to immigration, the infection is also present in nonendemic countries like Australia, Canada, Spain, United States, and some Asiatic countries.6 Chagas disease is considered to be responsible for the greatest socioeconomic impact in Latin America due to the loss of productivity with an estimated cost of US$ 1.2 billion annually. In addition the medical costs for treatment of the affected individuals by cardiac and/or digestive pathologies are several times


more expensive.

  • [1] Amastigotes (Fig. 16.1) are round intracellular stages in mammalian cells, displaying ashort inconspicuous flagellum that is not free from the cell body9 when they areobserved on electron microscopy. These forms multiply by longitudinal binary fission.This stage can be reproduced in cellular culture of different types of mammalian cells;they are approximately 25 mm in length and 2 mm in diameter and are infective formammals.
  • [2] Epimastigotes (Fig. 16.2) are 20-40 mm long and are present in the intestinal tract and
  • [3] urine of the insect vector, where they multiply by longitudinal binary fission and present a
  • [4] free flagellum which originates in the anterior position of the nucleus.9 This stage can be
  • [5] reproduced in liquid culture media and is not infective for mammals.
Found a mistake? Please highlight the word and press Shift + Enter  
< Prev   CONTENTS   Next >

Related topics