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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #67546

Title: PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME: UPDATE AND OVERVIEW OF THE REPRODUCTIVE DISEASE

Author
item Lager, Kelly
item Mengeling, William

Submitted to: American Association of Swine Practitioners Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 3/5/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Porcine reproductive and respiratory syndrome (PRRS) is a virus-induced disease of swine which is responsible for major losses within the swine industry. Although the predominant clinical signs of reproductive failure and respiratory disease can be experimentally reproduced, the pathogenesis of this multi-faceted disease is only partially understood. Control and treatment regimes have been based on empirical data; however, the discovery of the PRRS virus (PRRSV) in 1991 opened the door for experimental studies investigating the pathogenesis and epizootiology of the disease and the development of a modified-live vaccine. Producers still undergo PRRS epizootics and apparent chronic infections within their herds despite the best control plans. Additional information is needed on how the PRRSV is able to infect swine, persist in swine, and cause disease. This proceedings reviews our current pathogenesis studies in sows and provides data useful to veterinarians in their day-to-day battle against PRRS. Studies involving sows previously infected with PRRSV (for 3-10 weeks) suggest the virus does not readily transmit to contact controls. We have demonstrated that sows develop a natural immunity to PRRS and this immunity may last for the life of the sow. Exposure to one strain of PRRSV may lead to cross protection against a different strain of virus; however, the protection may be limited. During late gestation transplacental infection occurs within 2 weeks of maternal infection and subsequent fetal death may be due to viral effects on fetal and/or uterine vasculature.