High primary doses of Trichinella spiralis administered orally to Kenyan baboons (Papio anubis) induced a marked but unpredictable eosinophilia which started 2–3 weeks after infection and persisted as erratic waves for at least 6 months. Low primary oral doses induced no eosinophilia but a later, high challenge gave an accelerated eosino-philic response, although the peak was lower than in high primary infection. Intravenous injection of infective T. spiralis larvae resulted in a predictable, rapid eosinophilic response which persisted for several weeks. Intravenous injection of a particulate material, Sepharose, gave no oesinophilic response.
Percutaneous Schistosoma mansoni infection of baboons resulted in a two-stage eosinophilic response: an initial rise occurred about ⅔ of the way through the pre-patent period and was followed by a second rise at the onset of patency. After peaking, the eosinophilia waned erratically over the next 3 or 4 weeks.
A strong antibody response, measured by countercurrent imnruno-electrophoresis, was given in oral infections with T. spiralis, but intravenous injections elicited little or no antibody formation. Parasitological evidence indicated no cross-resistance to S. mansoni in baboons injected with T. spiralis 9 days previously. Thus, the intravenous injection of infective T. spiralis larvae appears to be a suitable method of inducing experimentally a non-specific eosinophilia to investigate possible immune mechanisms to S. mansoni in the baboon.