SUMMARYThe chemiluminescent characteristics of enriched (>95%) peripheral blood polymorphonuclear leukocyte populations (PMN) from normal and feline leukaemia virus (FeLV)-infected cats were investigated. FeLV-infected cats demonstrated a significantly lower (P < 0.001) PMN chemiluminescent response when compared to the response of normal age-matched controls. Normal PMN treated with FeLVinfected cat serum exhibited a depressed response in comparison to control cells. A titration of serum from infected cats supplemented with normal serum revealed a titratable suppression of chemiluminescence with increasing concentration of serum from the infected cats. However, PMN from FeLV-infected cats treated with normal serum displayed a slight increase in chemiluminescence over the same cells in autologous serum. The addition of inactivated FeLV to normal PMN caused a titratable decrease in chemiluminescence.

A series of experiments was conducted to determine the time required to induce absolute immunity to three species of Eimeria in young broiler chickens continuously exposed to the parasite. Acquisition of immunity was measured by cessation of oocyst production in each bird. Initial experiments were performed in broilers beginning at age 7 days with continuous oocyst administration for 28 days with E. tenella, E. maxima, or E. acervulina. Evaluation of oocyst production demonstrated a major decline in oocyst output of E. maxima and E. tenella by 2 weeks, with cessation by 25 days. Exposure to E. acervulina caused cessation of oocyst production by day 16. To study whether chickens of different ages varied in their capacity to immunize within this time frame, 1-day-old birds also were studied. For E. tenella, exposures also were initiated in 14- and 21-day-old birds. This study demonstrated that regardless of the age of the broiler, all were capable of establishing complete protective immunity to E. tenella, E. maxima, and E. acervulina under continuous exposure within 25, 24, and 16 days, respectively.

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BALB/c mice were exposed to the enteric parasite Eimeria falciformis to produce a natural acquired immunity. The mice were then depleted of their effector T-cell function by in vivo administration of a cytotoxic Thy-1.2 mouse monoclonal antibody. T-cell depletion was demonstrated by a reduction in concanavalin A-induced proliferation of splenic lymphocytes in treated mice compared with that in controls. Twenty-four hours following T-cell depletion, the mice were challenged with 5,000 oocysts of E. falciformis. Daily total oocyst counts were done for each mouse from days 6 to 21 following challenge. Our studies demonstrated that depleting mice of their effector T-cell function following establishment of immunity caused an abrogation of protective immunity to this parasite.

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