In 1909, a great scientific event occurred in Brazil: the discovery by a Brazilian scientist named Carlos Chagas (Fig. 25.1) of the Ameri can trypanosomiasis (Chagas' disease).4 This is a protozoan infection caused by the flagellate Trypanozoma (Schizotrypanum) cruzi, widespread in the American continent, mainly among small wild mammals (enzootic sylvatic cycle). Bioecologic and socioeconomic factors leave rural poor populations of South and Central America in contact with the sylvatic cycle, where the parasite is transmitted by natural vectors of the infection, determining human Chagas. In 1916, after observing the onset of dysphagia in acute cases, Chagas attempted to correlate this symptom to the disease he had discovered.
In 1912, Arthur Neiva and Belizario Penna5 took a scientific trip through the Brazilian hinterland. They traveled through the interior of Bahia, Pernambuco, Piaui, and Goias. Many cases of dysphagia were found in these states locally named mal de engasgo. In addition to dysphagia, they noted alterations in the heart rhythm, popularly called "vexame," and constipation, "caseira." Megaesophagus and megacolon were extensively studied during the 1930s and 1940s in Brazilian universities. The starting point at Sao Paolo School of Medicine was in 1932 when Amorim and Netto6 published their report describing lesions of the myenteric plexus not only in the esophagus and colon but also throughout the entire digestive tract.
Subsequently Etzel7 demonstrated the pathogenic identity of megaesophagus and megacolon and its systemic character. Several other authors established a link between the megas and Chagas' disease based on clinical and epidemio-logical evidence.
The theory of Chagasic etiology was reinforced by two important studies performed in 1946. De Freitas8 submitted 80 patients with megaesophagus and megacolon to the complement fixation test for Chagas' disease and
observed a 91.2% positive result. Laranja et al9 conducted an identical study on 81 patients with megaesophagus and found 97% positive reactions. This high serologic positivity could never have been a random occurrence and clearly indicated the etiologic relationship between Chagas' disease and the "megas."
Koeberle10-12 provided the definitive anato-mopathologic confirmation of this relationship. His famous studies were performed at the School of Medicine of Ribeirao Preto, University of Sao Paulo, beginning in l955. These studies demonstrated that Chagas' disease causes lesions of the nervous intramural plexuses described earlier. By counting the cells of the esophagus and colon during autopsy on patients with Chagas' disease, Koeberle detected the ubiquitous presence of a variable degree of denervation in the intramural plexuses.
Koeberle's studies on the esophagus and colon were extended to other segments of the digestive tract, as well as to the other organs, demonstrating the presence of universal autonomic dener-
vation in Chagas' disease.13'14 Other authors later confirmed this denervation.15'16 The great contribution made by Koeberle was to regard Chagas' disease as a disorder of the autonomic nervous system.
One of the difficulties in accepting megaesophagus and megacolon as manifestations of Chagas' disease was the fact that these phenomena can be very rare or even absent in some regions where Chagas' disease is endemic. This regional difference in Chagas' disease occurs due to the existence of different strains of Trypanosoma cruzi. Differences among strains can be demonstrated by biologic and biochemical studies of the parasite.1719 In 1959 Rezende20 pointed out the clinical manifestations of the digestive tract of Chagas' disease.
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