Three groups of SPF pigs aged 6-7 weeks were vaccinatel resj:oDtively with DVD (5) pepared by 10% of infected spleen in cattle, with BVD (0 prepared by two passages in DT cells, and with DVD (0+ LPC miflrie.
The two groups of pigs respeetively vaccinated with BVD (5) or DVD (I) were clinicallynornall, but the DCI) (0=LPC mixture group showed 1-2 days of slight fever reaction pcttvaccination.
Those tested pigs were challenged with ALD virulent virus 6 weeks pcetvaccination, The pigs vathnaal with BVD (5) or DVD (I) showed fecer reaction aft ALD challenge and some pigs anorexia but recovered socn, On the contiay pigs vaccinatel with BVD (0-i-LPC mixture were quite normal aft challenge. The pigs vaccinated with BVD (5) or DVD (1) did not produce HC antibcdy kefc’xe ALD challenge. But pigs with BVD (0÷LPC vaccination produced ne HC antibody 6 days U postvathnation and had a high titer of Log 3.01 just before challenge.
The pigs vaccinatel with DVD (5) or BVD (0 virus rapidly induced HC antibody aft challenge. Average HC antibody titer in these two groups were 1.5 and 2.24 one week, 2.83 and 2.86 two weeks, and 3.13 and 2.96 three weeks pxtehallenje. While most pigs of BVD (T’)+LPC group kept the same titer around 3.31 aft challenge. BVD antibody titer was rapidly prcduced in pigs vacdnatel with BVD (5) or BVD (I) aft HC challenge and reached 3.85 or above three weeks posthallenge. But pigs vacdnatl with BVD (I) group and only did reach 1,83 three weeks pcetchallenge. The reason might be that the challenge ALD virus was influence-i by existing HC neutralizing antibody. Similar pathological changes were found in BVD (5), BVD (0 or BVD (fl+LPC groups. Tonsils and lynphoid tisst of all vaccinatel pigs were p-ominenly lymphoid hyerplasia, but with occasional heraorrhage in lymphoid tissue.