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The intention of this collaborative project was eradication of pestivirus from the Norwegian cattle population of about 30,000 dairy and beef herds, primarily by identification and culling of persistently infected (PI) animals. Testing was performed in four tiers, with examination for pestivirus antibodies by indirect ELISA in (1) bulk milk, (2) pooled milk from primiparous dairy cows and (3) pooled blood from young stock. The herds positive in the third tier were examined for pestivirus antigen in blood from all antibody-negative individuals by -antigen-capture ELISA, and these animal composed tier (4). Following culling of the PI animals, a herd was considered free from pestivirus when pooled blood from young stock was antibody-negative on two sampling occasions three months apart. Number of herds with PI animals peaked at about 3000 (10 per cent) in the 2nd project year, then decreased steadily; only three herds (0.01 per cent) contained PI animals 10 years later. Solid, continuous information flow to all relevant partners was crucial to project success. The project saved losses of between 50 million and 200 million Norwegian crowns (NOK) annually (approximately 4.5 million to 18 million GBP). Project running costs for 10 years were 52.4 million NOK. Following project completion, surveillance of the Norwegian cattle population for pestivirus has continued.

Two trials were designed to investigate whether bovine viral diarrhoea virus (BVDV) could be transmitted after the birth of persistently infected calves, even if they were removed immediately after birth. In trial 1, 11 calves were actively exposed to fetal fluids and uterine lochia collected from cows that had delivered calves persistently infected with type 1 BVDV. One calf that was exposed to a sample taken on the day of calving seroconverted. In trial 2, six calves were housed in stables where persistently infected calves were being born and then removed immediately from their dams and from the stable unit within two to three hours. One of four calves in close contact with the cows after delivery seroconverted and one of two calves housed within the same stable unit became infected.

Twenty-two heifers were infected intranasally with non-cytopathic bovine viral diarrhoea virus (BVDV) between days 74 and 82 of pregnancy. All animals had developed serum antibodies against BVDV 5 weeks later. No clinical effects were seen in the heifers, and they all delivered a live calf. The newborn calves were generally small, appeared unthrifty as typical 'poor doers', and some developed secondary infections with diarrhoea and signs of respiratory disease. Eighteen of the 22 calves were born without antibodies against BVDV and were persistently infected (PI) with the virus. One was weak at birth and died the following day. Four calves were born with serum antibodies against BVDV and with no detectable virus. Three of these showed signs and/or pathological changes indicating disease in the central nervous system. Otherwise, there were no obvious clinical differences between these calves and the PI calves, nor were there any apparent significant differences in blood parameters between these groups. In general, the calves showed low gamma-globulin values and thrombocytopaenia, but moderately increased fibrinogen values and relatively normal lymphocyte numbers.

Neutralising serum antibodies against bovine virus diarrhoea virus (BVDV) were monitored for three years in 35 cattle that were infected with the virus as calves; 24 of the calves were inoculated intramuscularly or intranasally, and 11 contracted the infection naturally. All the experimentally infected calves seroconverted within 14 to 28 days after inoculation, and all the animals still had high serum levels of antibodies to BVDV three years after infection. Determinations of antibody levels in milk and blood samples excluded the possibility that the calves had been reinfected with BVDV during the study.

Fifty-eight dairy herds, suspected to be recently infected with bovine virus diarrhoea virus (BVDV) due to a rise in BVDV antibodies in bulk milk, were followed over a two-year period. In 34 (59%) of these 58 herds (Group 1), pooled milk samples from heifers or pooled blood samples from calves were negative for BVDV antibodies. In this group as many as 53 and 76% of the herds again had antibody-negative bulk milk one and two years after the positive sample, respectively. Of the remaining herds, 5 and 17% had negative samples after one and 2 years respectively. Possible explanations for the limited duration of antibodies against BVDV in bulk milk are discussed. In 65% of the herds in Group 1, animals had been purchased and introduced into the herd, or the herds had been exposed to other forms of contact representing a risk of infection with BVDV. In the remaining 35% of the herds in this group, no explanation for the rise in BVDV antibodies in the bulk milk could be found. In this study the introduction of seropositive animals into the herd, and infection inducing seroconversion in one or more animals as the only result, seem to be the most probable explanations for the rise in antibody levels observed in Group 1.

During one breeding season, 2335 female goats in 39 herds in different parts of Norway were examined for pestivirus infection and for reproductive performance. Before breeding, all animals were examined for neutralizing antibodies against the NADL strain of pestivirus, 83 (3.6 per cent) positive animals in 12 herds being demonstrated. The herd prevalences ranged from 1 to 63 per cent. Antibody titres varied from 1 in 4 to 1 in 2048. Of 1816 females in 30 herds for which post-breeding information was available, a total of 178 (9.8 per cent) animals in 25 of the herds demonstrated gestation failure. Three of these goats began to produce antibodies against the NADL strain during gestation. Sera from the 83 animals with NADL antibodies were titrated for neutralizing antibodies against three additional strains of pestivirus, the highest geometrical mean titre being found for antibodies against a Norwegian bovine strain.