Abstract
Nonspecific immunity (NSI) was manifested in rats injected intravenously with killed Corynebacterium parvum and challenged with Trypanosoma lewisi, Plasmodium chabaudi, or Babesia rodhaini. The NSI became evident some 5 days after infection as a suppressed parasitemia, a more rapid recovery from patent infection and as enhanced survival among rats infected with B. rodhaini. The C. parvum injections produced anemia and thrombocytopenia with splenomegaly and signs of glomerulonephritis in rats. The signs became evident about 5 days after injection and were accompanied by reduced titers of lytic complement, elevated titers of antibody against fibrinogen products (Anti-F), antibody against soluble serum antigen of malaria and babesiosis (ABSA), and antibody against the third component of fixed complement or immunoconglutinin (IK). These were the autoantibodies associated with anemia and reduced parasitemia of infection-induced NSI. In as much as immunoconglutination of blood cells or parasites coated with complement fixing immune complexes was implicated as a functional mechanism in infection-induced NSI, it is possible that these same factors might function in C. parvum induced NSI.
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