A New Aspect of Trypanosoma cruzi Life‐Cycle in the Invertebrate Host

Abstract

SYNOPSIS. Trypanosoma cruzi blood trypomastigotes transform, in the stomach of the invertebrate host, into round or pear‐shaped forms. A certain number form attached pairs or large masses of aggregated amastigotes. Cytoplasmic bridges and membrane leaks may be observed between apposed parasites. There are fusion of the organisms, an apparent disorganization of the DNA‐containing organelles and thickening of the borders of the parasite aggregates. From those borders single or small clumps of flagellates begin to detach and liberate. The meaning of this heretofore overlooked sequence of events as well as the possibility of genetic exchange among the parasites in the early stages of development are discussed.

The Development of Trypanosoma cruzi (Trypanosomatidae) in the Reduviid Bug Triatoma infestans (Insecta): Influence of Starvation

“…In the majority of investigations the population of the entire intestinal tract or only of the rectum was considered, and quantitative comparative investigations of the effect of starvation on development in different regions of the intestinal tract are lacking. Not only the population density but also the stages of the flagellate seemed to be affected [17, 211. The different stages of the flagellate in the vector have already been excellently described in the original description [6], and further details have been added especially by Dias [7], Brack [3], Brener [4], and Brener and Alvarenga [5]. However, the factors inducing the development of different stages are largely unknown.…”

Neurotrophin Receptor TrkC Is an Entry Receptor for Trypanosoma cruzi in Neural, Glial, and Epithelial Cells

“…It preferentially invades astrocytes in the central nervous system (CNS), Schwann cells in the peripheral nervous system (PNS), and enteric glial cells in the enteric nervous system (ENS) (11,30,36). Intracellular parasite growth during acute Chagas' disease can lead to partial destruction of the PNS and ENS and cause megacolon and megaesophagus (megaviscera) in patients with chronic Chagas' disease (3,22,29). Therefore, it is critical to understand the molecular mechanisms underlying T. cruzi recognition of host cell receptors that drive entry into cell hosts, a process required for completion of the life cycle in humans and other mammalian hosts.…”

An in vitro comparison of Trypanosoma spp. (subgenus Schizotrypanum) from bats

“…However, other isolates of T. cruzi first developed rounded forms before epimastigotes were produced (Elkeles, 1951;Norman et al, 1959;Wery & de GroodtLasseel, 1966;Petana, 1972). Brener (1972) made a similar observation in the vector, Tr&toma. Brener & Chiari (1965) speculated that this difference in development depended on the strain of Trypanosoma cruzi.…”