Two strains of Trypanosoma rangeli and three strains of Rhodnius prolixus were used in various combinations to transmit the trypanosomes via the reduviid bug. A persisting infection in the midgut lumen posterior to the stomach resulted in all 2,500 bugs being third and fourth instars. Infectious, metacyclic forms developed exclusively in the salivary glands; forms excreted with bug feces were noninfectious to mice. The midgut epithelium was the main barrier to transmission of the parasite. In only 2%-5% of the infected bugs was it penetrated, and no correlation with any parameter tested could be found. The trypanosomes passed through the gut epithelium by an intracellular route; they were contained in a parasitophorous vacuole. The salivary glands of R. prolixus were found to be infected whenever the hemolymph was infected, after a successful penetration of the gut epithelium, or after injection of T. rangeli. On the other hand, hemolymph infections in Triatoma infestans were eliminated within a few days, and the salivary glands of this bug were never invaded. Pathogenic effects of T. rangeli on R. prolixus could be seen in midgut epithelial cells by a loss of cytoplasm and in muscle and salivary gland cells by very high parasite densities. However, as the penetration rate of the gut is low, T. rangeli is not likely to prove to be efficient in natural control of R. prolixus.
Culture forms of Trypanosoma rangeli could be agglutinated with Canavalia ensiformis (Con A) lectin and, less effectively with Pisum sativum agglutinin (PEA), at a concentration of 200 micrograms/ml. Ricinus communis agglutinin I (RCA I) agglutinated trypanosomes only if they were not previously washed with physiological Ringer's solution. Three other lectins did not react with the same parasite forms. Direct or indirect lectin-gold labeling techniques were applied to LR-White embedded thin sections of T. rangeli culture forms and to forms in the gut, hemolymph, and salivary glands of Rhodnius prolixus. Under these conditions, Con A was the only lectin out of 9 that bound to the surface of trypanosomes from culture and from the bug hemolymph. Con A did not react with any midgut or salivary gland forms. The preservation of the biological activity of the lectin-gold complexes that did not bind to the parasite surface was confirmed by reactions with structures of the invertebrate host.
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