Basis of the specificity of rodent trypanosomes for their natural hosts.

The strong natural insusceptibility of mice to infection with the rat-specific Trypanosoma lewisi was investigated in a variety of mouse strains. Parasite elimination by all strains was similar involving a lag phase of about 7 h of constant parasitemia followed by rapid clearance (half-times of 55 and 130 min in different strains). In vitro cultures were utilized to determine whether mouse cells and serum were inherently deficient in supporting T. lewisi or, alternatively, toxic for the parasite; neither was found to be the case. In attempts to prolong T. lewisi survival and growth, mice were treated with various preparations, including T. lewisi sonicates, rabbit antiserum against mouse macrophages, silica dust, normal rat and rabbit sera and crude immunoglobulin fractions, and combinations of silica dust and serum or immunoglobulin fractions. The most striking effects were obtained with combinations of silica dust and serum, resulting in extensive T. lewisi growth and death of a portion of the infected mice. These results, together with microscopic observations, suggested that the principal mechanism responsible for murine resistance to heterologous trypanosomes is a type of antibody-dependent, cell-mediated immunity involving granulocytes and (probably) platelets.