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When Dr Carlos Chagas first observed underthe microscope the flagellate that he named Schizot-rypanum cruzi (today known as Trypanosomacruzi), in honor of his master and friend OswaldoCruz, he began to study the biology of this inter-esting microorganism (Chagas 1909). This uniquefact in medicine, a single person’s discovery andreport of the clinical picture of a new disease, witha new etiological agent, its life cycle, its vectorsand wild reservoirs, were later explained by him-self (Chagas 1922): a process that he was able tounderstand after the intense and basic studies onthe biology of this parasite, carried out at theOswaldo Cruz Institute. In Chagas’ own words“...quando no sangue periferico de uma criancafebril, observamos o flagelado patogenico, de suabiologia ja possuiamos nocao completa, adquiridaem demorados estudos anteriores” “...when wefound the pathogenic flagellate in the blood of achildren, we had already a complete notion of itsbiology, acquired under previous and detailed stud-ies” (Chagas 1922).Since then, the intriguing biology of this spe-cial parasite has been studied. Its morphology, de-picted under the optical microscopy of CarlosChagas and Garpar Vianna, was first investigatedunder an electron microscope by Dr Hertha Meyer(Meyer & Porter 1954). Dr Carlos Chagas Filho,Chagas’ son who founded in Rio de Janeiro thefamous Institute of Biophysics that later took hisname, achieved to establish Dr Hertha Meyer inthis Institute during the II World War. She starteda whole school of cell biology of T. cruzi (as wellas other tropical disease parasites), introducing invitro cell culture of muscle and nerve cells, andthe ultrastructure study of all the parasite develop-mental stages (reviewed in De Souza 1984). SinceDr Chagas’ time, some basic questions still chal-lenge the intelligence and curiosity of scientists allover the world. Why and how does the parasiteevolve among three different morphological andfunctional states of differentiation over its life cycle(ama-, epi- and trypomastigotes)? Does the T. cruzislender and stout forms found in blood stream ofdifferent host represent sexual dimorphism or any-thing else? How does T. cruzi enter so many dif-ferent cells? How does at least part of the parasitepopulation that infects a person or animal escapethe vigorous specific immune response elicited inthe host by the infection, leading to the finding ofviable forms during the decades-lasting chronic de-velopment of the disease?During the 90 years that followed since Chagas’classic report of a new disease, much informationwas obtained on the biology and ultrastructure ofits causative agent. Recent reviews from DrWanderley De Souza (1984, 1995) summarize theknowledge in this area. A large knowledge wasobtained on the understanding of its clonal com-position (Heckert et al. 1994, Tibayrenc 1995), aswell as in its population distribution and associ-ated biological and molecular markers (Zingaleset al. 1998). Another important field on parasitebiology investigation concerns its metabolic path-ways (reviewed in Cazzulo 1992), that engages thedesign of new drugs based on differences encoun-tered. Key organelles from which the parasite getsenergy such as acid calcisomes (DoCampo et al.1995) and reservosomes (Figueiredo et al. 1994)are under intense study. The same happens withsome pivotal enzymes for the parasite that are in-volved in energy production (such as glycosomalenzymes, purine and sterol byosynthetic pathways),detoxification (such as trypanothione reductase, or-nithine decarboxylase and S-adenosylmethioninedecarboxylase), or virulence (such as cysteine pro-teases) mechanisms. Second generation anti-try-panocidal drugs will certainly emerge from thisfield of research (Krauth-Siegel & Schoneck 1995,Cazzulo et al. 1997, Croft 1999, Urbina 1999) tosubstitute for the same two old and toxic drugs thatare currently available for clinical use since thesixties (benznidazole and nifurtimox).

Biology and ultra-structure of Trypanosoma cruzi: a 90-years old challenge for scientists