Abstract
The effects of subchronic trypanosomiasis upon immune responses were examined in Trypanosoma gambiense infection and in subcurative treatment of T. brucei- and T- equiperdum-infected mice. About 60% of the mice infected with T. gambiense developed a subchronic infection similar to human trypanosomiasis, characterized by the absence of circulating trypanosomes. The animals died between 1 and 12 months after infection with elevated serum immunoglobulin M (IgM) levels (16 times the normal level). After 1 month of infection, the mice showed a normal primary antibody response against sheep erythrocytes, as tested by hemagglutination, despite their high serum IgM levels. After more than 1 month of infection, about 20% of the mice showed depressed hemagglutination titers (25% of control), whereas all relapsed mice that contained circulating parasites showed a pronounced suppression. Elimination of the blood parasites with Berenil treatment restored immune competence, which persisted until the relapse of the animals. Identical results were obtained in T. brucei-infected mice. Berenil treatment abolished the immune depression against sheep erythrocytes, but did not cure the animals, which relapsed with the development of a new state of immune depression. T. gambiense and T. brucei infections were always followed by a marked increase of serum IgM levels. Hypergammaglobulinemia was also induced in relapsing T. equiperdum-infected mice treated with Berenil. No immune depression against sheep erythrocytes could be detected. It appeared that immune depression was not the result of clonal exhaustion (measured by the serum IgM level) but seemed to be closely associated with the presence of living trypanosomes.