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Calves exposed by intravenous or intradermal inoculation with Herpes simplex virus (HSV), types 1 and 2, remained clinically normal and HSV was not recovered from nasal secretion nor blood samples. However, the clinical response of calves pre-inoculated with HSV, to Bovid herpesvirus-2 (BH-2) challenge infection was much milder than that in the challenge control calves, and the titer of BHV-2 by skin titration underwent a significant (2-2.5 log units) reduction in the HSV pre-inoculated calves. Inoculation of calves with live HSV provided a much greater protection against BHV-2 challenge infection compared with the results of previous experiments in which a Triton X100-inactivated HSV antigen was used. It was speculated that the possibility of HSV replicating in cattle must still be considered an open question.

Pregnant cows were given the first injection of an inactivated bovine rotavirus vaccine approximately 4 weeks before calving and a second injection just before calving. This led to the enhancement of rotavirus antibody titers in their colostrum as well as in the milk for at least 5 days after parturition. Thus, when newborn calves were fed with the mammary secretions obtained from the vaccinated cows daily for 5 consecutive days they were fully refractory to experimental infection with 81/36F bovine rotavirus. By contrast, the calves which were given the mammary secretions from unvaccinated cows, had clinical signs consistent with rotavirus infection and viral shedding. Based on these results it is suggested that vaccination of cows according to the scheme followed in this experiment, i.e., two injections within the last month of pregnancy, might be a valid approach which depending on confirmation under field conditions, could help reduce the incidence of rotavirus-induced diarrhea in newborn calves.

Concentrated antigen of Herpes simplex virus (HSV) types 1 and 2, previously inactivated with Triton 100X, were inoculated into calves. Thirty-two days later the calves were challenge exposed either by the intradermal or the intravenous route with Bovid herpesvirus 2 (BHV 2). The HSV-immune calves responded to BHV 2 infection with clinical signs which were much less severe that those observed in the challenge control calves. The skin lesions in the calves exposed to intravenous inoculation of BHV 2, were fewer in the calves in the HSV-immune group, whereas they were heavily disseminated, covering the skin of the entire body, in the control calves. In the case of calves which received BHV 2 intradermally, the titer of the virus underwent a reduction of more than one log unit in the pre-immunized calves. The most significant serologic finding was that the HSV-preimmunized calves produced antibody to the BHV 2 challenge virus at an earlier time than did the control calves. The immunologic relationship between BHV 2 and HSV was confirmed by the results of this study.

Nine calves, six of which had been infected with strain 85/BH 16TV and three with strain 85/BH 232TN of Bovid herpesvirus-4 (BHV-4), were treated with dexamethasone (DMS) three months after infection. DMS administration did not induce any clinical signs of disease, but BHV-4 was isolated from the nasal swabbings of all calves for a maximum of 8 days after the start of DMS treatment. The virus was also isolated from the nerve tissues, nasal mucosa, lymph nodes, lung and spleen of 4 calves that were killed at different stages (3, 5, 7 days) of the DMS treatment. Intranuclear inclusions associated with cellular shrinkage were found in the neural tissues of calves killed either 3 or 5 days after the start of DMS treatment. Unexpectedly, a latent infection by infectious bovine rhinotracheitis (IBR) virus was reactivated. The virus was isolated from the nasal swabbings of two calves and also from the brain, cerebellum and nasal mucosa of one calf killed 5 days after the start of DMS treatment.