Viscerotropic velogenic Newcastle disease in turkeys: immune response following vaccination with either viable B1 strain or inactivated vaccine.
When used as a vaccine, live letogenic B1 Newcastle disease virus (NDV) protects turkeys against challenge-exposure to viscerotropic velogenic NDV (VVNDV). Low-level passively-immune poults were vaccinated one, two, or three times at various intervals and their immunity challenged at various times from 1 to 10 months of age. Newcastle disease virus was isolated readily from either the blood, trachea, or vent of turkeys in all challenge groups (through 5 months of age) on the 3rd to 6th days postchallenge (PC) but after 14 days PC was isolated rarely. Virus was isolated from turkeys that had high titers of serum hemagglutination-inhibition antibodies at the time of challenge. The anamnestic antibody response appeared to be stronger in poults that had low antibody titers prior to challenge-exposure to VVNDV. In a small-scale study with an inactivated VVNDV vaccine, vaccinated poults were protected against challenge with the homologous viscerotropic virus. Parallel control studies on the infectivity of viscerotropic NDV for turkeys indicated that resistance to VVNDV increased with age.
Response of congenitally immune chicks to viscerotropic velogenic Newcastle disease virus.
Separate groups of chicks of hen hyperimmune to viscerotropic velogenic Newcastle disease virus (VVNDV) were challenge-exposed to VVNDV by intraocular route at 1 day and 34 days old. Their response was evaluated by clinical symptoms, hemagglutination-inhibition (HI) titers, and virus isolations. Chicks exposed at 1 day old excreted VVNDV from the vent for up to 60 days; their active mean HI titers remained low (10-40); and deaths from VVNDV occurred early (5-16 days) and late (28-55 days). Chicks challenge-exposed at 34 days old excreted virus from the vent for 10 days; active HI titers developed quickly and remained high (891-1177); and deaths and signs of VVNDV occurred early (5-13 days).
The antioxidant effects of phospholipids on perilla oil
Antioxidant effect of phospholipids on the oxidation of refined perilla oil (PO;α-18:3, 54.5%; 16:0, 7.2%; 18:0, 2.6%; 18:1, 18.6%; 18:2, 15.5%), tocopherol-free (POF) and tocopherol-enriched (POR) perilla oil were investigated by measuring weight-gains and by the oven test at 37°C. The oxidative stability of PO was especially increased by additions of phosphatidylethanolamine (PE) and phosphatidylserine (PS), but phosphatidylcholine (PC) scarcely showed an antioxidant effect. The oxidative stability of POF was markedly low, and none of the phospholipids (PC, PE, PS) showed an antioxidant effect on the oxidation of POF. The stability of POR was lower than that of PO regardless of its higher tocopherol contents. However, the oxidation of POR was significantly suppressed by additions of PE and PS, as was observed with PO. PC showed a small antioxidant effect on the oxidation of POR. Therefore, it seems that the antioxidant effects of phospholipids, especially of PE and PS, was due to the presence of tocopherols in the perilla oil.