Pseudorabies virus (PRV) latency was investigated, using polymerase chain reaction (PCR). A PCR protocol was developed that specifically amplified a 217-base pair sequence within the gene encoding the essential glycoprotein gp50 of PRV. Using this PCR procedure, the gp50 sequence was amplified from tissues of pigs infected with various doses of PRV (Becker strain). At postinoculation day 64, viral isolation was performed on nasal swab specimens and homogenates of tonsils and trigeminal nerve ganglia obtained from 11 PRV-convalescent, seropositive pigs. Results were negative in all cases. By use of PCR, 11 of 11 pigs had PRV-positive trigeminal nerve ganglia and brain stem, 10 of 11 pigs had PRV-positive tonsils, and 9 of 11 pigs had PRV-positive olfactory bulbs.

The sense of smell in dogs infected with canine distemper virus (CDV) was examined by use of EEG olfactometry, behavioral olfactometry, and electro-olfactography. Infection with CDV was confirmed by a direct immunofluorescence technique in 8 active cases and was suggested by clinical history compatible with canine distemper 10 to 26 weeks earlier in 6 cases. Pathologic alterations of the olfactory mucosa in 3 clinically affected dogs was examined by light microscopy. Infection with CDV was found to be associated with anosmia and lack of recorded responses on electro-olfactogram in 8 of 8 dogs with clinical signs of acute distemper from naturally acquired infections. Anosmia was found in 5 of 6 dogs that had recovered from acute distemper 10 to 26 weeks earlier. The sixth dog had hyposmia, with abnormalities on the electro-olfactogram. Histologic examination was not performed on the 6 dogs that had recovered. Histologic lesions observed at necropsy in 3 dogs that had had clinical signs of acute distemper were those of subacute purulent rhinitis and atrophy of the olfactory epithelium. Altered olfactory function could be explained by mucopurulent exudate blocking odors from olfactory receptors in the acutely affected dogs, but alteration of olfactory function in the dogs that had recovered without clinical evidence of rhinitis could not be explained.

This study was carried out to nvestigate the NPY-immunohistochemical characteristics of the olfactory bulb in the striped field mouse(Apodemus agrarius). The animals were anesthesized with thiopental sodium and perfused with 4% paraformaldehyde through left ventricle and aorta. Brains were removed and tranfered 10%, 20% and 30% sucrose. Sections were then cut on a cryostat into 40 micro meter-thick. The tissue immunostained with avidin-biotinylated complex method. The main olfactory bulb consisted of seven circumferential laminae: and olfactory nerve fiber layer, a glomerular layer with glomeruli surrounding by periglomerular cells, an external plexiform layer having granule and tufted cells, a mitral cell layer, a narrow internal plexiform layer, a granule cell layer forming several cell rows and alayer of white matter. The accessory olfactory bulb had four layers: an olfactory or vomeronasal nerve fiber layer, a glomerular layer consisting of small glomeruli, a mixed layer not distinguishing the external plexiform/mitral cell/granule cell layers and a granule cell layer. Most of NPY-immunoreactive(NPY-IR) neurons in main olfactory bulb were localized in the deeper portion of granule cell layer, white matter and anterior olfactory nucleus. In addition, some NPY-IR neurons were identified in the external plexiform layer. The shape of NPY-IR neurons of all olfactory bulb were predominant round or oval, sometime multipolar in shape. And most NPY-IR processes were parallel to long axis of white matter. In accessory olfactory bulb, NPY-IR neurons were not found in all region.