Submitted to: American Association of Swine Veterinarians Annual Meeting
Publication Type: Proceedings
Publication Acceptance Date: 3/2/2002
Publication Date: 3/2/2002
Citation: LAGER, K.M., BUTLER, J.E. EFFECT OF FETAL PRRSV INFECTION ON THE DEVELOPMENT OF THE PORCINE IMMUNE SYSTEM. PROCEEDINGS OF THE AMERICAN ASSOCIATION OF SWINE VETERINARIANS ANNUAL MEETING. 2002. p. 299-300. Interpretive Summary:
Technical Abstract: Porcine reproductive and respiratory syndrome (PRRS) is the number one infectious disease problem for US swine. It is caused by the PRRS virus (PRRSV) which is capable of causing in utero infections. This study tested the probability that fetuses infected during midgestation could develop a state of immunotolerance against PRRSV. Gilts underwent surgery at about 50 days of gestation and all fetuses in one uterine horn received an intraamniotic injection of either NADC-8 wild-type parent virus (n=6 litters) or NADC-8 attenuated virus (n=8 gilts). A pair of gilts from each group was euthanized at 3, 6, and 9 weeks-post-inoculation (wpi) and the 4th pair of gilts in the attenuated virus group was allowed to farrow. Sera from the fetuses/pigs were tested for PRRSV and specific antibody. In the wild-type group all principal fetuses and all but one of the control fetuses were either dead or infected with wild-type PRRSV. There was a marked contrast in litters inoculated with attenuated-PRRSV. Only 3 of the 6 litters necropsied and only one of the litters allowed to farrow contained any infected fetuses/pigs. These fetuses and pigs were normal in appearance and most of the older infected fetuses and some of the congenitally-infected pigs had PRRSV-specific antibody. This study suggests that the likelihood of porcine fetuses developing a PRRSV immunotolerant state would be remote because virulent virus will usually kill the fetus and if the virus would be less virulent, then the fetus would seroconvert in utero or postpartum.