Neural changes in recurrent infection of infectious bovine rhinotracheitis virus in calves treated with dexamethasone.

Recurrent infection by infectious bovine rhinotracheitis (IBR) virus was induced in calves by dexamethasone (DM) treatment (given 5 days) at 5 months after primary infection. The virus appeared in nasal secretions of the calves on the 4th day after initiation of DM treatment and continued until the 9th day. The calves were killed on the 1st, 3rd, 4th, 5th, 6th, 7th, 8th, 10th, and 11th days after DM treatment was started for examination by histopathologic and immunofluorescent antibody techniques. The most significant neural change was trigeminal ganglionitis with neuronophagia, which was observed from the 3rd to the 11th day. Significantly, the extent of changes in the trigeminal ganglion and medulla oblongata corresponded to the amount of DM treatment administered. The IBR virus antigen was first observed in the trigeminal ganglion cells, and thereafter, it was detected in the Schwann cells, satellite cells, neuroglia cells, and nasal mucosa until the 10th day. These observations indicate that the IBR virus is capalbe of producing a persistent infection in the trigeminal ganglion and that trigeminal ganglionitis may be a characteristic lesion for inducing the reactivation of lagent IBR virus.     

Recrudescence of infectious bovine rhinotracheitis virus and associated neural changes in calves treated with dexamethasone

Reactivation of infection bovine rhinotracheitis (IBR) virus in calves administered dexamethasone (DM) was studied in 2 experiments. At 2, 3, 5, 15, or 30 months after inoculation of the Los Angeles strain of IBR virus, IV injections of DM were given for 5 consecutive days to induce a recurrent infection (experiment 1). Three months after the 1st treatment, a 2nd recurrent infection was induced, using DM with the same doses as used in experiment 1. The virus was excreted from nasal secretions from the 4th to the 10th day after initial treatment with DM, and from the 6th to the 9th day after the 2nd treatment. On pathologic examination, trigeminal ganglionitis, consisting of many proliferated microglia and inflammatory cells, was observed in all DM-treated calves. Moreover, degeneration of the ganglion cells and neuronophagia were prominent features in the calves after the 2nd recurrent infection. These observations indicated that the trigeminal ganglion may be one of the latent sites of IBR virus in calves after intranasal infection and that calves can develop a recrudescent infection after DM treatment several times during their lifetime.     

Persistence of antibodies and anamnestic response in calves vaccinated with inactivated infectious bovine rhinotracheitis virus and parainfluenza-3 virus vaccines

Persistence of antibodies in calves vaccinated with 2 types of inactivated infectious bovine rhinotracheitis (IBR) virus and parainfluenza-3 (PI-3) virus vaccines were determined. Calves seronegative for IBR and PI-3 viruses were inoculated with 2 doses of inactivated IBR virus-PI-3 virus vaccines administered 2 weeks apart. Blood samples were obtained from the calves for serum at 2 weeks, 6 months, and 1 year after vaccination. The serums were tested by serum-neutralization tests. Antibody response to the vaccines persisted on a declining scale for 1 year. The anamnestic responses to the vaccines were determined by inoculating the same calves with a booster dose of vaccine 1 year after the original 2 doses were given. Blood samples were obtained from the calves for serum 2 weeks later. The serums were tested by serum-neutralization tests. The single booster dose of vaccine elicited an anamnestic response to both IBR and PI-3 viruses.     

Evidence for defective neutrophil function in lungs of calves exposed to infectious bovine rhinotracheitis virus

Calves were exposed to an aerosol of infectious bovine rhinotracheitis (IBR) virus followed five days later by an aerosol of Pasteurella haemolytica. The animals were subjected to bronchoalveolar lavage before IBR and four days after, and again at 0, 4, 24, and 48 hours following Pasteurella haemolytica challenge. The results of these experiments suggest that neutrophil infiltration into the lung, in response to the presence of the bacteria was delayed thereby allowing the bacteria to become established in the lung. Neutrophils in infected animals displayed little random migration in vitro and did not respond to a chemotactic stimulus. It was also found that alveolar macrophages from virus-infected animals were not able to produce neutrophil chemotactic factors. These data suggest that the decrease in neutrophil chemotaxis and the lack of chemotactic factor production by the alveolar macrophage following infection with infectious bovine rhinotracheitis virus may predispose infected cattle to a secondary bacterial infection.     

Nitrogen metabolism of calves inoculated with bovine adenovirus-3 or with infectious bovine rhinotracheitis virus

Beef calves were inoculated with bovine adenovirus-3 or infectious bovine rhinotracheitis virus. After inoculation, plasma fibrinogen increased, serum phosphorus decreased, and nitrogen and phosphorus digestibility decreased compared with preinoculation values. Urinary N excretion increased when calves developed rectal temperatures greater than 39.7 C. Results indicated that clinical infection of calves with infectious bovine rhinotracheitis virus increases urinary N excretion and reduces N and phosphorus balance, and that clinical and subclinical infections with either virus reduce dietary N digestibility.     

Necrotic oophoritis in heifers vaccinated intravenously with infectious bovine rhinotracheitis virus vaccine during estrus

Twenty-two Hereford heifers were injected IM with prostaglandin F2 alpha a, 11 days apart to synchronize estrous cycles. Twelve of 14 heifers that had signs of estrus were inoculated IV with 1 of 3 modified-live infectious bovine rhinotracheitis virus vaccines, and 2 were assigned to a nonvaccinated control group. Also, 6 of the 8 anestrous heifers were inoculated IV with 1 of the 3 vaccines on the fourth day after the last prostaglandin injection and the other 2 were assigned to the nonvaccinated group. Vaccine virus was isolated from the blood and nasal and vaginal secretions from the vaccinated heifers on postvaccination days 4, 7, and 9. On postvaccination day 9, all heifers were ovariectomized and ovarian tissues were processed for virus isolation and histologic examination. Vaccine virus was isolation and histologic examination. Vaccine virus was isolated from ovarian tissues of some heifers in each of the vaccine groups. Necrotic oophoritis characterized by multifocal areas of ovarian tissue necrosis, hemorrhage, and mononuclear lymphocytic infiltration was observed. The corpora lutea and surrounding ovarian tissues taken from vaccinated heifers in each group had varying amounts of necrotic and inflammatory change, but the changes appeared to be more severe in 1 group than in the other 2. Virus also was isolated from 2 of the controls; these heifers apparently became infected with vaccine virus that had been excreted from the vaccinated animals.     

Leukocyte changes and interferon production in calves injected with hydrocortisone and infected with infectious bovine rhinotracheitis virus.

Correlations between leukocyte counts and serum interferon titers were determined in calves given hydrocortisone (HC) and infectious bovine rhinotracheitis (IBR) virus. Calves were injected with either 1 mg or 3 mg of HC/kg of body weight every 8 hours for a total of 9 injections each. Control calves were given placebo injections. Viral inoculation was given IV 10 hours after the 1st dose of HC or placebo was given. By the time of viral inoculation, all calves injected with HC had developed neutrophilia, and the calves injected with 3 mg of HC also developed leukocytosis, lymphopenia, and eosinopenia; total leukocyte counts in calves injected with 1 mg of HC were increased, but not as much as in other HC-treated calves. Leukocyte counts in calves given placebo remained essentially unchanged before viral inoculation. At 1 day after IBR virus was inoculated, the number of circulating lymphocytes in HC-treated calves and control calves was decreased by more than 50%, on the average, of the counts taken before the HC injections or inoculation of virus. A significant negative correlation existed between the numbers of circulating lymphocytes and serum interferon titers at 1, 2, and 3 days after inoculation with IBR virus. The interferon response of calves undergoing lymphocyte suppression due to HC was not impaired, but was enhanced.     

Vaccination to protect calves against infectious bovine rhinotracheitis

A commercially available inactivated vaccine against infectious bovine rhinotracheitis (BHV1) was tested to assess its ability to immunise young seronegative calves and protect them against challenge with a virulent strain of BHV1. Calves showed seroconversion after one or two doses of vaccine. A two-dose and three-dose vaccination regimen each afforded calves significant protection against challenge as judged by the development of clinical symptoms. Vaccinated calves were on average 7 to 10 kg heavier than control calves 24 days after challenge, a statistically significant difference. Vaccination had no significant effect on the virus excretion pattern after challenge.     

Effects of infection with parainfluenza-3 virus and infectious bovine rhinotracheitis virus on neutrophil functions in calves

Calves were challenge exposed in separate experiments with parainfluenza-3 (PI-3) virus or infectious bovine rhinotracheitis (IBR) virus. Blood neutrophils were assayed for functional activity every other day for at least 3 weeks by random migration, Staphylococcus aureus ingestion, antibody-dependent cell-mediated cytotoxicity, cytochrome-c reduction, iodination, and native chemiluminescence. Exposure to PI-3 virus resulted in a brief febrile response and no other clinical signs. Alterations in total or differential WBC counts were not detected. Chemiluminescence and iodination activities were reduced from activities before exposure. Exposure to IBR virus resulted in mild clinical signs and a febrile response of several days' duration. Total WBC and mononuclear cell counts were reduced. Random migration was reduced, whereas S aureus ingestion was enhanced. We concluded that infection of calves with IBR virus and PI-3 virus might directly or indirectly result in alterations of neutrophil function. The functional alterations apparently are different for each virus. These virus-induced alterations in neutrophil function might predispose calves to secondary bacterial pneumonia.     

The pathology of concurrent bovine viral diarrhoea and infectious bovine rhinotracheitis virus infection in newborn calves

Concurrent bovine viral diarrhoea (BVD) and systemic infectious bovine rhinotracheitis (IBR) are reported from two neonatal (11 and 15 days old) calves. The diseases occurred sporadically in a large-scale herd which may have been due to the calves' heterogeneous immunobiological status. Gross pathological and histopathological examinations revealed focal interstitial pneumonia with acidophilic intranuclear inclusions in the alveolar epithelial cells and necrotic foci in the liver with a few intranuclear inclusions in the hepatocytes. There were subserous haemorrhages in the forestomachs and intestine, necrotic changes in the rumen, enteritis, lymphocytic necrosis in the Peyer's patches, and fibrinoid necrosis in the wall of some of the neighbouring blood vessels. BVD virus was demonstrated by immunofluorescence (IF), whereas IBR virus by electron microscopy, immunofluorescence and virus isolation.     

Effect of infectious bovine rhinotracheitis virus immunization on viral shedding in challenge-exposed calves treated with dexamethasone

Calves not vaccinated with infectious bovine rhinotracheitis virus (IBRV) became latently infected when challenge exposed and treated with dexamethasone (DM). Calves that shed IBRV after DM treatment were considered to be latently infected. Vaccination with a temperature-sensitive intranasal vaccine or with formalinized IBRV in Freund's complete adjuvant (IBRV-FCA) protected some, but not all, calves against latent infection--indicating a role for the immune response in preventing latent infection. That all latently infected calves were not detected after DM treatment was indicated by the fact that after a 2nd DM treatment of 3 calves treated 6 months previously and not found to shed virus, 1 of the calves was latently infected. Latently infected calves were inoculated with successive doses of IBRV-FCA and treated with DM. Nonvaccinated calves shed virus, whereas vaccinated calves similarly treated did not shed virus. Because both groups had a comparable cell-mediated immune response, as determined by blastogenic response to IBRV, but the vaccinated group had significantly higher virus-neutralizing antibody titers, a role for humoral antibody in preventing viral shedding was indicated.