The Effects of Lead Acetate on Host Susceptibility to Trypanosoma Cruzi
Trypanosoma cruzi. a protozoan parasite, causes American trypanosomiasis or Chagas' disease. The infective stage of this parasite resides in the hindgut of the reduviid bug (family Reduviidae), which is both host and vector, and is transmitted to the mammalian host through fecal material released during a blood meal. Chagas' disease, an acute to chronic infection resulting in fever, malaise, and heart and liver enlargement, is becoming a concern in the United States due to the large increase in Latin American immigrants, and the lack of safe and effective therapeutic treatment and vaccination. Another growing concern in the United States involves environmental toxicants and their ability to act as immunosuppressants. Lead is of particular interest because it is widespread in places such as soil, food, water, batteries, paints, and plastics. Studies have shown lead exposure during bacterial and viral infection causes decreases in antibody production, T cell recognition, and macrophage activity—all of which result in decreased host resistance to infection. The present study was conducted to determine the immunosuppressive effects of lead acetate in C57B1/6 mice challenged with the Brazil strain of T\ cruzi. Mice were treated with lead acetate concentrations ranging from 0 to 1000 p.p.m. in their drinking water for three weeks prior to infection. During the fourth week of the experiment, mice were injected with lxlO4 blood-form trypomastigotes (BFTs) of T\ cruzi and lead treatment was continued. Food and water consumption was measured to monitor feeding patterns and lead exposure during infection. Parasitemias were performed at fourteen days post infection and continued at 3 and 4 day intervals throughout the study. Parasite-specific antibody production was determined by an indirect enzyme-linked immunosorbent assay (ELISA) using serum samples collected during high parasite counts. Average daily food consumption showed no statistical differences between lead-treatment groups of mice per replicate experiment. Average daily water consumption and mean weight gain showed no statistical differences among groups in replicates II and III; however, in replicate I significant differences were observed in both variables between mice receiving 100 and 1000 p.p.m. lead acetate concentrations. The highest mean peak parasitemias were observed in mice receiving 100 and 1000 p.p.m. lead acetate, though high lead acetate concentrations did not appear to suppress T\ cruzi-specific antibody production. Although low mortality was observed in lead-treated mice, the results of this study suggest that lead exposure does enhance the susceptibility of mice to infection with T\ cruzi, resulting in high parasitemias.
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