Author
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Lager, Kelly |
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Mengeling, William |
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Brockmeier, Susan |
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Submitted to: Veterinary Microbiology
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 5/16/1997 Publication Date: N/A Citation: N/A Interpretive Summary: Porcine reproductive and respiratory syndrome (PRRS) is one of the most significant diseases facing the swine industry today. It was first identified in 1987 in the United States and its cause, the PRRS virus, was discovered in 1991. Field reports of PRRS outbreaks on swine farms typically describe late-term reproductive losses and respiratory disease in swine of all ages. The disease outbreak may last for several months before the reproductive losses decline to normal or near normal levels. However, the respiratory disease may persist in a herd for some time depending on husbandry practices. Field reports indicate sows may develop a protective immune response following clinical disease because sows will usually breed back following their recovery from the PRRS disease and have a normal litter. In this study we were able to demonstrate that gilts can develop protective PRRS virus immunity within 83 days of "vaccination." Vaccination consisted of an exposure to field PRRS virus by way of the gilt's nose and mouth at 30 days of gestation or by way of an intrauterine exposure following natural breeding. The same field strain of virus was used for challenge; meaning this was a homologous or "same virus" challenge of protective immunity. Results from this study indicate sow vaccination programs could have some efficacy, however we do not know the level of cross-protective immunity that could or could not develop among different PRRS virus strains. In addition, the early gestation virus exposure just after breeding did not dramtically affect conception nor did it affect the developing fetuses. However, virus exposure at 30 days of gestation resulted in some fetal infection but much less than when gilts were exposed to virus late in gestation. Technical Abstract: Thirty-three pregnant gilts were allotted to 6 experimental groups. Gilts in groups 1, 3, and 5 were exposed to the NADC-8 isolate of porcine reproductive and respiratory syndrome virus (PRRSV) at 1, 30, or about 90 days of gestation (DG), respectively; these groups were designed to serve as virus-exposed control groups. Groups 2 and 4 were exposed to virus at 1 and 30 DG, respectively; these exposure times were used as an immunization against a subsequent homologous virus challenge at or about 90 DG. Group 6 was the sham-infected control group. Groups 1 and 2 were exposed to PRRSV by way of an intrauterine inoculation following natural breeding at 1 DG. All virus exposure at 30 and 90 DG was via the oronasal route. Gilts were either necropsied on or about 111 DG (groups 1 to 5) or allowed to farrow (group 6). Presence or absence of transplacental infection was determined by detecting virus in the serum of fetuses at necropsy or in the serum of piglets within 12 hours of birth. Of the virus-exposed control groups, transplacental infection was not detected in group 1, gilts exposed to virus at 1 DG; however, it was detected in groups 3 and 5, gilts exposed to PRRSV at 30 or about 90 DG, respectively. In the homologous challenge groups, transplacental infection was not detected in group 2, gilts exposed to virus at 1 and about 90 DG; however, it did occur in group 3, gilts exposed to virus at 30 and about 90 DG. Transplacental infection in group 3 was attributed to the 30 DG virus exposure and not to the 90 DG virus exposure. No transplacental infection was detected in the control group. In summary, this study demonstrates swine can develop a homologous protective immunity, and the NADC-8 isolate of PRRSV used in this study can cause reproductive failure in gilts following oronasal exposure at 30 and 90 DG. |
