Enzyme-linked immunosorbent assays for the detection of immunoglobulin M (IgM), IgA, IgGl, and IgG2 antibodies against bovine respiratory syncytial virus (BRSV) were used to measure antibody responses of calves after experimental or natural infection with BRSV. Serially collected sera, lung lavage samples, nasal and eye secretions, and feces were tested for the presence of these antibodies. Lung lavage fluids and nasal secretions were further examined for the presence of virus. After experimental infection of 3-to 4-week-old, colostrumdeprived (seronegative) calves, the virus was detected from days 3 to 8 post-initial inoculation day (PID). An immune response was first detected 8 to 10 days PID, when BRSV-specific IgM and IgA appeared nearly simultaneously in serum, secretions, and feces. BRSV-specific IgGl appeared only in serum on days 13 to 17 PI), and IgG2 was first detected in sera from 1 to 3 months PID. Specific IgM and IgA were detectable in the different samples for various periods. In the respiratory and eye secretions, IgA usually remained detectable for long periods, that is, for up to 3.5 months or longer. In lung lavage samples, BRSV-specific IgG1 was only incidentally demonstrated and appeared to be blood derived. The immune response of a 5-month-old calf strongly resembled that of the 3-to 4-week-old calves (feces excepted), indicating that an age effect on the immune response to BRSV is unlikely. After experimental infection of colostrum-fed, seropositive calves, both local and systemic antibody responses were largely or totally suppressed. The degree of suppression seemed to be related to the lçvel of preinoculation virus-specific serum IgGl. Of ail isotypes, IgM was least affected. Colostrum-fed animals shed virus in about equal amounts and for the same length of time as colostrumdeprived calves. Clinical signs were mild in both groups. After reinfection, no virus shedding was detected In either colostrum-deprived or colostrum-fed calves. In both groups, a secondary immune response developed, characterized by strong and rapid (from about day 6 PID) mucosal and systemic IgA responses, but reaching higher titers in colostrum-deprived calves. Also, strong mucosal, but not serum, IgM responses were observed, which, however, did not develop faster than those observed after primary infection. Naturally infected calves, showing severe signs of respiratory disease, had various levels of, most likely, maternally derived antibodies on the first day of illness. Mucosal and systemic antibody responses of various heights and durations were observed, but in general these responses were stronger than those observed after experimental infection. The results point to an important role for loéal IgA, rather than for serum IgGl, in the protection against BRSV infection. The capacity to mount a local memory IgA response seems especially important. Priming for such a mucosal memory response is possible even when the primary immune response is severely suppressed because of the presence of maternal antibodies.

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Epidemiological aspects of bovine viral diarrhoea virus (BVDV) infections were studied longitudinally in a large dairy herd for three years. At the start of the study, practically all the cows more than four years old had BVDV antibody titres, whereas the younger stock were almost all seronegative. The spread of the virus was monitored in a part of the population that contained only transiently viraemic cattle and in another part that contained persistently viraemic calves. Among the lactating cows the virus circulated for two-and-a-half years, although they had no direct contact with persistently viraemic cattle during this period. The highest transmission rate occurred when a large number of susceptible heifers was added to the population of cows that contained transiently viraemic cattle. The circulation of BVDV among the lactating cows ceased while 27 seronegative cows were still present. Both findings are in accordance with predictions from simple epidemic models. The susceptibility of the cows that remained seronegative was confirmed experimentally. In contrast with the limited circulation of BVDV caused by transiently viraemic cattle, virtually all susceptible cattle that came into contact with a persistently viraemic calf became seropositive within three months. Transplacental BVDV infections were not detected in the calves born to cows that had antibodies against the virus due to an infection that had occurred at least four years earlier. Transplacental transmission of BVDV did not occur in most of the pregnant cows that were infected before approximately the 60th day of gestation, but when cows became infected later in gestation the virus virtually always invaded the fetus.(ABSTRACT TRUNCATED AT 250 WORDS)

Specific pathogen-free calves were inoculated intranasally with one of seven strains of bovine herpesvirus 1.1 (BHV 1.1) to identify a highly virulent strain for use in vaccination-challenge experiments. The calves were monitored clinically and virologically. Clear differences in virulence between the strains were observed. The Iowa strain was the most virulent; the four calves infected with the strain had the most severe clinical signs; two of them died and viraemia was detected in three of them. To evaluate the immunogenicity of the seven strains all the calves were challenged 16 weeks later with the Iowa strain. The calves of a control group showed the typical signs of a BHV1 infection, whereas all the other calves were protected against disease and shed little or no virus. Hence, the differences in virulence were not associated with differences in immunogenicity. After the calves had been treated with dexamethasone, differences were observed between the strains in the amount of virus that was excreted.

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