Abstract. A type of bovine herpesvirus, BHV-1.3, causes encephalitis in calves, whereas BHV-1.1 causes respiratory disease. Three colostrum-deprived calves and two colostrum-fed calves were inoculated with BHV-1.3 by intranasal aerosolization. Two colostrum-deprived calves were inoculated with BHV-1.1 by intranasal aerosolization. BHV-1.3-inoculated calves demonstrated severe encephalitis with minimal respiratory lesions, and BHV-1.1 -inoculated calves demonstrated severe respiratory lesions and no clinical signs of neurologic disease. Calves fed colostrum that contained virus neutralizing antibodies were protected against neurologic disease. Colostrum-fed BHV-1.3-inoculated calves did not develop disease although they did become infected; virus was shed in respiratory secretions for 10-1 3 days postinoculation, similar to infected colostrum-deprived calves. BHV-1.3 was reactivated from a latent state from one colostrum-fed calf after administration of dexamethasone 60 days postinoculation. Histopathologic examination of the three colostrum-deprived BHV-1.3-inoculated calves revealed severe lesions of encephalitis. One of the two BHV-1.1-inoculated calves had one focal lesion of encephalitis. Virus was isolated from brain tissue of colostrum-deprived BHV-1.3-inoculated calves and from one BHV-1.1 -inoculated calf. Immunohistochemical staining for BHV-1 antigen was observed in neurons from the colostrum-deprived BHV-1.3-inoculated calves.

A sensitive method for simultaneously detecting and discriminating between bovine herpesviruses types 1 and 5 (BHV-1 and BHV-5) was developed using a nested polymerase chain reaction (PCR) technique. Following amplification using type-common primers derived from gC sequences, amplification using type-specific nesting primers produced different-sized bands specific to the corresponding types, as demonstrated by blot hybridization. Less than 0.1 plaque-forming units (PFU) of each virus and 75 fg or less of viral DNA were routinely detected. The PCR technique amplified correct product from 4 BHV-5 isolates and from 48 BHV-1 isolates, all from the United States, and did not amplify heterologous herpesviruses. The PCR technique was more sensitive than virus isolation in detection of BHV-1 or BHV-5 in nasal secretions from experimentally and naturally infected calves, and it detected BHV-1 or BHV-5 in trigeminal ganglia from these calves.

Malignant neoplasia in 4 alpacas was characterized by acute onset of clinical signs and rapidly deteriorating condition. Postmortem examination revealed metastatic or multicentric neoplasia in the abdominal organs of alpacas 1, 3, and 4 and an extensive thoracic mass in alpaca 2. Immunohistochemical stains supported a diagnosis of B-cell lymphosarcoma in alpacas 1-3 and a neuroendocrine neoplasm in alpaca 4.

Abstract. Calves were intranasally challenged with bovine herpesvirus 5 (BHV5) and followed for the development of viral infection, clinical encephalitis, histologic lesions in the brain, and viral sequences in the trigeminal ganglia. Calves that were previously vaccinated with bovine herepesvirus 1 (BHV1, n ϭ 4) or previously infected with BHV1 (n ϭ 5) or that had not been exposed to either virus (n ϭ 4) were compared. No calf developed signs of encephalitis, although all calves developed an infection as indicated by nasal secretion of BHV5 and seroconversion to the virus. Histologic lesions of encephalitis consisting of multifocal gliosis and perivascular cuffs of lymphocytes were observed in calves not previously exposed to BHV1. BHV5 sequences were amplified from the trigeminal ganglia of calves previously vaccinated and from calves not previously exposed to BHV1; calves sequentially challenged with BHV1 and later BHV5 had exclusively BHV1 sequences in their trigeminal ganglia. Administration of dexamethasone 28 days after BHV5 challenge did not influence clinical disease or histologic lesions in either previously unexposed calves (n ϭ 2) or previously immunized calves (n ϭ 2), although it did cause recrudescence of BHV5, as detected by nasal virus secretion.Bovine herpesvirus 5 (BHV5) has been isolated from outbreaks of naturally occurring encephalitis 2,4,5,10 and has experimentally induced the same disease. 3,10 The prevalence of this virus is unknown because the disease is sporadic, with only 4 isolations of the virus in various parts of the United States. 1 Determination of the prevalence of this virus as well as the conditions under which it is able to induce disease is important because of the potential for fatal outbreaks of encephalitis in the United States and throughout the world. 2,5,10 Currently, serologic methods cannot distinguish between infections with BHV5 and bovine herpesvirus 1 (BHV1, commonly termed infectious bovine rhinotracheitis virus [IBRV]); 7 thus, isolated viruses must be analyzed using molecular techniques. 1 Because of the close genetic and antigenic relationship between BHV1 and BHV5, prior infection with or vaccination against BHV1 may protect against encephalitis caused by BHV5. The interaction between these 2 viruses, if any, in disease has not been investigated. In addition, the role of latency of BHV1 or BHV5 has not been investigated with respect to disease or protection against encephalitis.A model has been developed to study BHV5-induced encephalitis in 1-2-day-old colostrum-deprived calves. Calves in this model develop a fulminant in- Received for publication February 25, 1998. fection of the brain and exhibit rapidly progressing behavioral changes, leading to terminal recumbency. 3 Although this model works well to study the effects of BHV5 in very young calves, fatal encephalitis in the field is typically seen in calves Ն6 months of age. The present work summarizes the course of an experimental infection with BHV5 in 5-6-month-old calves, both with and without p...

Findings suggest that llamas may be infected with BVDV but have few or no clinical signs. Inoculation of llamas during gestation did not result in fetal infection or persistent BVDV infection of crias. Seroprevalence to BVDV in llamas and alpacas is apparently low. The most likely source for BVDV infection in camelids may be cattle.