Histopathological and immunocytochemical studies of Trypanosoma musculi infection of mice.

Mice infected with Trypanosoma musculi developed hyperplasia of the spleen, lymph nodes, and liver; in contrast, their thymuses displayed transient involution. All organs returned to normal in a month or less. There was modest anemia, lasting until the parasites were cleared from the bloodstream, followed by a rapid influx of erythrocytes into the blood and a subsequent return to normal erythrocyte numbers. During the first 2 weeks, trypanosomes and trypanosome-derived substances were found in the livers and, in moderate amounts, in the red pulp of the spleens; thereafter, trypanosomes and trypanosome-derived substances gradually decreased in these organs. The lymphoreticular hyperplasia involved a large increase of immunoglobulin G (IgG)-containing cells in the spleens and lymph nodes at 2 weeks of infection. Hyperplasia of immunoglobulin-producing cells correlated with elevation of serum immunoglobulins, especially IgG. Cells producing IgG in the spleens proliferated mainly around the central arterioles of the white pulp, i.e., in the T-cell-dependent areas. The decline of trypanosome-derived substances in the livers and spleens was associated with marked hyperplasia of IgG-containing cells in the spleens and lymph nodes. These results suggest that trypanosome-mediated depression of murine immune responses is attributable to proliferation and terminal differentiation of more-mature lymphoid cells and temporary inhibition of normal maturation of less-mature precursor cells.