The clinical characteristics of acute and chronic Chagas' disease in central Brazil are described (29 acute cases and 111 chronic cases). The geographical distribution of Trypanosoma cruzi zymodemes in this region was mapped. Zymodeme (Z) 1 was identified in 12 acute cases, Z2 in 13 and repeated xenodiagnosis gave the same zymodeme identification. The clinical pictures of the Z1 and Z2 acute phases were similar. Resistance to benznidazole treatment occurred after either Z1 or Z2 acute infections. Only 14 positive xenodiagnosis were obtained from the 111 chronic phase patients examined. For 12 of these 14 patients the zymodeme was identified. All 12 carried Z2, 10 of whom had mega involvement. There were several possible explanations for the failure to detect T. cruzi Z1 in chronic Chagas' disease with mega syndromes: suggestions were made for follow-up investigations.

The objective of this work was to determine the profile of the cellular defense system during mansonic infection. Specifically, this study assessed the number of hemocytes that were produced and released into the hemolymph in response to the parasitic infection. The quantification of the Biomphalaria glabrata hemocytes was performed on groups of snails at 1, 5, 10, 15, 20 and 30 days post-infection that had been individually infected with 5, 10, 15 or 30 Schistosoma mansoni miracidia. The results revealed that B. glabrata possesses a cellular defense mechanism that is characterized by the release of hemocytes into the hemolymph. The maximum peak of cellular production occurred 24 hours after infection, and there was a significant reduction in the hemocyte concentration over the following 10 days. However, at 15 days post-infection, there was a second increase in the cellular hemocyte production, although this was not as strong as the primary peak. At 30 days post-infection, there was another moderate rise in the cellular hemocyte production. Based on this cellular response profile, the defense system of the snail appears to be effective immediately following infection, but the response does not ensure the destruction of all parasites during the course of the infection.

Experimental models of Schistosoma mansoni infections in mammals have contributed greatly in understanding the pathology and pathogenesis of human infection. The absence of earlier reviews regarding specific strains of the Amazon region prompted research, which the main objective was to describe histopathological lesions in different phases of schistosomiasis in a murine model using PC (Pará) and LILA (Maranhão) S. mansoni strains. One hundred and eighty young female albino swiss mice (Mus musculus) were used and were randomly divided into five groups and controls), according to the number of cercariae injected and the strain adopted. Animals were sacrificed in predetermined periods (35, 56, 112, 156, and 180 days) in an attempt to follow the evolution of the disease in the histological sections of their tissues at different phases of infection. Our findings were compatible with the data already described by others authors using different strains of S. mansoni, making it possible to identify some peculiarities, which are discussed in this work. In conclusion, the strains of parasite used did not modify the histopathological findings in the tissues of infected mice in any significant way when compared with the results of other studies using different strains.