Submitted to: Pig Veterinary Society International Congress Proceedings
Publication Type: Proceedings
Publication Acceptance Date: July 10, 1996
Publication Date: N/A
Technical Abstract: In 1991, the porcine reproductive and respiratory syndrome (PRRS) virus (PRRSV) was first isolated and demonstrated to cause the maternal reproductive failure associated with PRRS epizootics. Since then, the PRRSV-induced maternal reproductive failure has been reproduced with different field isolates in laboratories around the world; however, the pathogenesis of the virus-induced reproductive failure is only partially understood. This study was designed to investigate the mechanism(s) of PRRSV-induced maternal reproductive failure and the relationship between the time of maternal infection and the onset of fetal infection during early and late gestation. Sows were oronasally exposed to PRRSV at either 30 or 90 days of gestation and were euthanized at selected times thereafter. Their fetuses were examined for the presence of transplacental infection and microscopic examination was completed on selected fetal and placental tissues. Transplacental infection was determined by testing fetal sera and tissues for PRRSV using a susceptible cell line, MARC-145. Gross and microscopic fetal lesions that developed following late-gestation maternal infection indicated fetal vascular lesions may play a major role in the virus-induced reproductive failure. In addition, an apparent difference exists between the incidence of fetal infection when sows are challenged with virus at 30 days of gestation vs 90 days of gestation, i.e., a 25% vs. a 100% incidence of fetal infection; however, the study is still in progress and the final results will be reported.