The pathogenesis of pseudorabies (Aujeszky\u27s disease) virus infection of the reproductive tracts of boars and gilts

Effects of pseudorabies virus (PRV) infection were studied on the reproductive tracts of young boars and pregnant gilts. The boars were challenged with virulent PRV which was inoculated intrapreputially (IP) in some and intranasally (IN) in others. Pseudorabies virus was isolated from the prepuce of two intrapreputially inoculated boars twelve days post-inoculation (PI), but not from the semen of any boars. Microscopic changes were typified by lympho-histiocytic aggregates, and were primarily limited to the prepuce and penis. Microscopic lesions in central nervous system (CNS) of these boars were characterized by a lympho-histiocytic meningoencephalitis and ganglioneuritis. All of the boars experienced poor semen quality PI for a period of one to two weeks. Semen changes were observed 10-14 days PI, they were characterized by bent, coild and reverse tails. Head abnormalities were manifested four weeks after inoculation. The changes were typified by knobbed (cystic acrosome), detached and double heads;In one group of boars, reactivation of PRV occurred following castration. This shedding of virus from the nasal cavity was attributed to stress which occurred following surgery. This does indicate that boars with positive serum neutralization titers for PRV if latently infected may shed virus when the appropriate stressful situation occurs;Pregnant gilts were intranasally inoculated with PRV. Four gilts aborted 4-15 days PI and PRV was isolated from the fetal membranes. This suggests that this strain of PRV crosses the placenta. In eight intrauterinely inoculated gilts none aborted, but inclusion bodies were presented in the tonsil, nasal turbinates and adrenal glands. This provides good evidence of hematogenous spread of virus after local multiplication;Ten pregnant gilts were inoculated intranasally with PRV on the 45th day of gestation. Four gilts aborted 6-12 days PI. Pseudorabies virus was isolated from the trigeminal ganglia, spleen, lungs, uterus and fetal membranes. The placenta contained multiple intranuclear inclusion bodies in trophoblastic cells. Viral particles could be demonstrated by electron microscopy. The presence of virus in these tissues suggests that there was a hematogenous spread of virus and that this virus crosses the placenta