NECROTIC OOPHORITIS IN GILTS ASSOCIATED WITH EXPERIMENTAL INOCULATIONOF A VIRAL GENE-DELETION MUTANT PSEUDORABIES VACCINE

Previous work on the reproductive effects of various herpesviruses has demonstrated adverse effects on reproductive function in several host species. Although herpesviral vaccines are used in several species to ameliorate the clinical effects of infection, pathogenicity for repro ductive tissue, associated with diminished reproductive efficiency, ha s been reported to be retained in a live-attenuated vaccine strain of the herpesvirus, bovine herpesvirus-l. The objective of this study was to determine if a gene-deletion mutant, thymidine kinase negative, ps eudorabies virus retained acute pathogenicity for the reproductive tra ct of swine following intravenous inoculation during estrus. Estrous c ycles of nulliparous gilts were synchronized by administration of a go nadotropin and daily exposure to a boar. During estrus, six gilts were inoculated intravenously with twice the recommended intramuscular dos e of a commercially available viral gene-deletion mutant pseudorabies vaccine. Six control gilts in estrus were sham inoculated intravenousl y with vaccine diluent during estrus. All animals were euthanatized 10 days postinoculation, and the ovaries and uterus were collected for h istopathology following gross examination. All reproductive tracts wer e grossly normal. Histologically, four of six treated gilts had a mild to moderate, multifocal, necrotizing oophoritis, with the lesions lim ited to corpora lutea and the adjacent stroma. Ovaries of control gilt s exhibited no necrotizing lesions. Both control and pseudorabies vacc ine-inoculated gilts had occasional minimal focal mononuclear infiltra tes in the ovaries. These data show that live attenuated viral gene-de letion mutant pseudorabies vaccine administered to swine during estrus can result in acute pathogenicity in ovarian corpora lutea. No endocr inologic data is available in these pigs, so the impact on pregnancy m aintenance is unknown.