Detmer, Susan E.2016-07-132016-07-132016-062016-07-13June 2016http://hdl.handle.net/10388/7344Despite nearly 25 years of research, pathogenesis of fetal death in PRRS still remains unclear. This large-scale study is aimed to provide overarching insight into the process of infection within uterus and fetus. Hypotheses of this thesis are that PRRSV-specific pathological lesions, their severity, replication in susceptible cells, and cell death are significantly associated with PRRSV infection both on maternal and fetal side, and fetal death. The objectives of this thesis were to assess potential associations between specific histopathological lesions, numbers of CD163, CD169, apoptotic cells and areolae at the maternal-fetal interface (MFI) and PRRSV RNA concentration in the fetuses and the MFI. Dams and their litters were humanely euthanized and necropsied 21 days later. Samples from the maternal-fetal interface (uterus with fully attached placenta) and fetal thymus were collected for analysis by RT-qPCR to quantify PRRSV RNA concentration. The corresponding paraffin-embedded uterine section was subjected to immunohistochemistry for PRRSV nucleocapsid N protein, CD163, CD169, cathepsin and TUNEL assay for apoptosis. Our findings confirm type 2 PRRSV infection in pregnant gilts induces significant histopathological lesions at MFI, but they are not associated with the presence of PRRSV in the MFI and fetal thymus at 21 days post infection. Fetal pathological lesions are associated with the presence of PRRSV in the MFI and fetal thymus, and meconium staining of fetuses is significantly associated with the presence of both fetal and umbilical lesions observed 21 days post infection. Studies presented in this thesis confirm that although type 2 PRRSV infection in pregnant gilts in the third trimester of gestation induces significant pathological lesions at the maternal-fetal interface, fetal and umbilical pathology together with PRRSV viral load in the fetus and increased cell death at the MFI contribute to fetal compromise and death. This study also found that only an increase in numbers of CD163 positive macrophages in the endometrium in concert with the decrease in the numbers of CD163 positive macrophages in the fetal placenta significantly increased the probability of PRRSV infection of the fetus.application/pdfPorcine reproductive and respiratory syndromePRRSfetusuterusplacentaendometritisvasculitisCD163CD169areolaeapoptosis.Thesis2016-07-13