The relationships among parasite growth, responses to infection and host genetic factors were examined in rodents infected with Echinococcus multilocularis. Mongolian gerbils, cotton rats and C57L/J mice were relatively susceptible to the infection, whereas five other inbred strains of mice, and hybrids and backcrosses between C57L/J and C57BL/6J mice were more resistant. In mice, susceptibility to E. multilocularis was controlled by multiple, non-H-2-linked genes, as were pathological, inflammatory and specific (antibody) responses to the infection. These responses were also affected by the degree of parasite growth in individual hosts. Antibodies, natural killer cells and hematological responsiveness were ruled out as contributing to resistance to E. multilocularis. Studies on peritoneal leukocytes from infected animals suggested that infections with E. multilocularis were controlled by cells in two phases: an acute phase involving neutrophils and mononuclear cells and a chronic phase involving eosinophils and mononuclear cells.

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