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.     

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.     

Neural changes in vaccinated calves challenge exposed with virulent infectious bovine rhinotracheitis virus

Recurrent infection in calves vaccinated with infectious bovine rhinotracheitis-(IBR) modified live virus was induced by dexamethasone (DM) treatment given 49 days after challenge exposure with virulent IBR virus. Nonchallenge-exposed IM and intranasally vaccinated calves did not excrete the virus after DM treatment; however, IM and intranasally vaccinated and subsequently challenge-exposed calves excreted the challenge-exposure virus into the nasal secretions 5 to 11 days and 6 to 10 days after the DM treatment, respectively. The calves were killed 15 to 18 days (experiment 1) and 14 days (experiment 2) and DM treatment was started and then were examined by histopathologic and fluorescent antibody techniques. All DM-treated calves that were inoculated with the vaccinal virus and challenge exposed with the virulent virus developed nonsuppurative trigeminal ganglionitis and encephalitis. On the contrary, the DM-treated nonchallenge-exposed vaccinated calves did not have lesions in the peripheral nervous system and CNS. Infectious bovine rhinotracheitis virus antigens were not observed in tissues of any of the calves examined (experiments 1 and 2) by fluorescent antibody techniques. These observations indicated that the modified live IBR virus neither produced lesions nor induced latent infection and that modified live IBR virus vaccination did not protect the calves against the establishment of a latent infection after their exposure to large doses of the virulent IBR virus.     

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.     

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.     

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.     

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.     

Comparative studies of strains of infectious bovine rhinotracheitis virus isolated from latently infected calves

Three strains (479 C, 778 TL, 982 LE) of infectious bovine rhinotracheitis (IBR) virus isolated from latently infected calves were compared with the prototype strain of IBR virus (LA strain) in studies which included restriction endonuclease analysis, experimental infection, and reciprocal cross protection tests in cattle. From the restriction endonuclease analysis it appeared that the 3 "latent" viruses were derived from the same isolate, and that it differed slightly from the LA strain. However, latency does not seem to have affected the pathogenicity or the immunogenicity of the virus. This is demonstrated by the identical clinical and virologic response of calves subjected to experimental infection with the various strains under study, and by the finding that when the LA strain and a "latent" strain (982 LE) were tested in cross protection tests in cattle, they proved to be mutually protective.     

Enhancement of infectious bovine rhinotracheitis virus replication with corticosterone

Infectious bovine rhinotrachetis virus (IBRV) progeny was increased ten to 12 fold in bovine turbinate (BT) cells treated with 10^?3 M corticosterone acetate (CCA) as demonstrated by plaque assay. Autoradiographic studies demonstrated an increased binding of ³H-corticosterone (³H-CS) in IBRV infected cells and the fractionation of labelled cells revealed 78–80% of the total hormone associated with the cytoplasmic components. Incorporation of ³H-uridine and ³H-valine precursors into cells treated with the hormone demonstrated up to 16-fold increase in RNA and protein synthesis which was inhibited by the addition of actinomycin D. The data suggest that increased rate of macromolecular synthesis in IBRV infected cells treated with the corticosteroid may result in the enhancement of virus production.