Background: Bovine encephalitis herpesvirus, or bovine herpesvirus type 5 (BoHV-5), a member of the family Herpesviridae,
subfamily Alphaherpesvirinae, is long recognized as the causative agent of bovine herpesvirus encephalitis. The disease
caused by BoHV-5 is characterized by signs of nervous impairment, consequent to non-suppurative meningoencephalitis.
Although bovine herpetic encephalitis is a rare event in herds from the Northern Hemisphere, BoHV-5 infections are an important
cause of central nervous system disease in cattle in Brazil and Argentina. Recovery of animals from clinical illness has been
documented before, both in naturally infected animals and experimentally infected individuals.
Case: During an experiment of experimental inoculation of a virulent isolate of BoHV-5, clinical signs of neurological disease were
detected in three out of four calves experimentally inoculated with bovine encephalitis herpesvirus (bovine herpesvirus type 5;
BoHV-5; strain EVI88/95). Clinical signs varied from slight prostration (1 calf) to severe signs of nervous impairment which lasted
from 3 to 14 days (in 2 calves) from the beginning of clinical signs to death. Despite the neurological signs, one of the calves with
mild clinical signs recovered: on day 14 p.i, this animal showed apathy, bruxism, dysphagia, pressing of the head against the walls
of the bay, hyper salivation, tongue paralysis, hypermetria, and transient blindness but the signs become gradually milder and
the health status of the animal improved until day 21 p.i. Recovery was complete ten days after the development of clinical signs
and no evident sequelae were noticed up to day 180 when the remaining calves were culled. At necropsy, the prominent
macroscopical finding was a large atrophic area at the left frontal lobe of the cortex. Another atrophic area was evident on the
parietal lobe, at the level of the mamillary bodies, revealing a yellow-orange cystic area on the basis of cerebrum, involving the
nucleus caudatus and the putamen. At histopathology, large areas on the affected frontal cortex were infiltrated by macrophages
containing haemosiderin and some plasma cells BoHV-5 infection was confirmed by viral isolation from nasal and ocular swabs
during acute infection from day 1 p.i. until day 19 p.i., with titres up to 104,5 TCID 50/50 μL, form all inoculated animals. BoHV-5
was also isolated from many organs, especially from the brain, of the animals which died on the acute phase of infection;
however, no infectious virus could be recovered from tissues collected at necropsy from the calf at 180 p.i.
Discussion: These findings suggest the possible association of BoHV-5 with atrophic lesions in the brain, a finding which had
not been previously linked to BoHV-5 infections. Therefore, animals that recover from clinically evident BoHV-5 infection under
field conditions may also bear brain lesions that would remain undetected if the calf is not culled; yet these may be detected only
months or years later, at slaughter. These results are of interest for the South American countries where infections with BoHV-5
are highly prevalent.
