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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #95204


item Lager, Kelly

Submitted to: Ph D Dissertation
Publication Type: Other
Publication Acceptance Date: 8/8/1998
Publication Date: N/A
Citation: N/A

Interpretive Summary: Porcine reproductive and respiratory syndrome (PRRS) is a disease of swine that was first recognized in North Carolina in 1987 as a few cases of acute reproductive failure (abortions, weak pigs, stillborn pigs) and severe respiratory disease in young pigs. Since then it has become one of the most economically important diseases that affects swine around the world. The disease is caused by the PRRS virus that was discovered in 1991. This dissertation describes a collection of studies that help explain the pathogenesis or causes of PRRS virus-induced maternal reproductive failure, that demonstrate protective immunity can develop in sows, that the likelihood of virus transmission between infected and noninfected adult swine is low, and that piglets suckling immune dams can still become infected with PRRS virus. Results from these controlled animal experiments answer numerous questions about the mechanisms of PRRS virus-induced disease and provide some building blocks on which swine practitioners can design strategies for the control and prevention of PRRS.

Technical Abstract: This dissertation compiles studies beginning in 1992 that investigated the pathogenesis of porcine reproductive and respiratory syndrome (PRRS) virus (PRRSV)-induced maternal reproductive failure utilizing an experimental model that involved exposure of gilts and sows to PRRSV at various stages of gestation. Results indicated that PRRSV may have little detrimental effect on conception or embryonic development. However, as gestation progresses the incidence of transplacental infection increases and the fetus becomes more susceptible to the lethal effects of an intrauterine PRRSV infection. Homologous protective immunity was demonstrated that developed within 90 days after exposure to PRRSV and persisted for at least 600 days. In contrast, heterologous protective immunity may have limited cross-protection and duration, this may be due to antigenic relatedness of the challenge and vaccine virus. The cause of reproductive failure may be attributed to a virus-induced vasculitis that involves maternal and fetal tissues. The severity of vascular lesions is variable among fetuses within a litter and among gilts within the same treatment group. This may account for the diverse range of clinical signs attributed to PRRSV in the field. Additional studies demonstrated passively acquired immunity conferred limited protection to piglets, however, it did not prevent piglets from being infected and transmitting virus to contact controls. PRRSV is a primary swine pathogen that is capable of causing severe reproductive losses. Fortunately, a protective immune response can be induced with vaccine that may aid in the prevention and control of PRRS.