Histopathological and functional changes in the pancreas were studied in 94 hamsters infected and reinfected with Trypanosoma cruzi VIC strain and in 73 non-infected normal controls. Infection in each animal was verified by microhematocrit, hemoculture, specific peroxidase anti-peroxidase, polymerase chain reaction and seroagglutination. Blood glucose and insulin were determined. The number of islets per section and the number of islet cells marked with antibodies were counted. Insulitis, neuritis, fibrosis, atrophy and inflammatory infiltrates were evaluated. Experimental chagasic infection caused pancreatitis similar to human Chagas' disease, involving acini, islets and nerves, with atrophy and fibrosis, although without correlation to the number of reinfections. Erratic blood glucose levels and a tendency to hypoinsulinemia were observed in infected animals. During the acute phase, the number of somatostatin and pancreatic polipeptide producer islet cells was lower in infected hamsters, which was eventually related to changes in blood sugar levels and hypoinsulinemia. Our findings favor the hypothesis of the existence of an endocrine form of chronic chagasic infection.

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Trypanosoma rangeli is a kinetoplastid protozoan parasite that has been found in the majority of Latin American countries, overlapping its distribution area with that of Trypanosoma cruzi, the causative agent of Chagas disease. This parasite shares the same reservoirs and vectors as T. cruzi. Triatomines from genus Rhodnius are considered the most susceptible hosts to infection. In this work, we report the susceptibility of different triatomine species (Rhodnius neglectus, Panstrongylus megistus, Triatoma infestans, T. sordida, T. braziliensis, and T. vitticeps) to experimental infection by T. rangeli isolated from Didelphis albiventris in a highly endemic region for Chagas disease. An intense parasitism was evidenced in feces (56% to 81%) of the majority of the species studied on the 10th day after infection, decreasing during the period of the experiment (30 days). T. vitticeps did not present parasites in feces at any time. All triatomine species presented parasites in the hemolymph. In T. vitticeps and P. megistus, this parasitism was scarce (6.3% and 6.6%, respectively). In the other species, the parasitism was variable (62.5% to 100%). Triatomine mortality varied between 3% to 40%, increasing during the infection in all species studied. The lowest mortality was observed for T. infestans. Also, we showed that only trypomastigotes forms from salivary glands, and hemolymph were infective for mice. We conclude that all triatomine species used were susceptible to infection by T. rangeli at different levels. There was no direct correlation between intensity of parasitism and mortality.

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Beginning the study of chronic pathologic changes in pancreas of hamsters experimentally infected with Trypanosoma cruzi Vic strain, hepatocyte metaplasia was observed in one animal from infected group. This is the first report of oncocytes in Chagas' disease, which could be due to aberrant regenerative response to pancreas inflammatory process.