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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #65618

Title: COMPARISON AMONG STRAINS OF PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME VIRUS AS TO THEIR ABILITY TO CAUSE REPRODUCTIVE FAILURE

Author
item Mengeling, William
item Vorwald, Ann
item Lager, Kelly
item Brockmeier, Susan

Submitted to: American Journal of Veterinary Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/21/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary: Porcine reproductive and respiratory syndrome (PRRS) is believed by many to be the most important virus-induced disease currently faced by the U.S. swine industry. The PRRS virus causes reproductive and respiratory tract disease, potentiates the clinical effects of other swine pathogens, and threatens the international trade of pork and pork products. In this study we have demonstrated that strains of PRRS virus differ in their ability to cause disease and that some relatively mild strains may be used as vaccines to protect against the more severe effects of other strains. The control of PRRS through vaccination and other measures will save the U.S. swine industry millions of dollars annually and help ensure our access to international markets for our pork and pork products.

Technical Abstract: Differences in the relative virulence of 4 selected strains of porcine reproductive and respiratory syndrome virus (field strains VR-2385, VR-2431, NADC-8, and vaccine strain RespPRRS) for maternal reproduction were tested by evaluating the consequences of oronasal exposure of pregnant gilts to the respective strains on or about day 90 of gestation. All of the strains crossed the placenta to infect fetuses in utero. However, the consequences of such infection were strain dependent. Virus was isolated from presuckling serum samples of 66 of 120 (55%) liveborn pigs, and from serum or other samples of 7 of 10 (70%) stillborn pigs and 10 of 60 (16.7%) late-term dead fetuses of 16 principal gilts (4 gilts exposed to each strain). Antibody for PRRSV was detected in presuckling serum samples of 19 liveborn pigs and serum or thoracic fluids of 9 stillborn pigs and late-term dead fetuses. Conversely neither PRRSV nor homologous antibody was detected in any of the same types of samples collected from pigs and fetuses of 4 control gilts (gilts not exposed to PRRSV but otherwise treated similarly). Late-term fetal death provided the best measure of relative virulence and the number of such fetuses ranged from 0 for the 4 litters of control gilts and the 4 litters of gilts exposed to strain RespPRRS to 38 (of a total of 51 pigs and fetuses) for the 4 litters of gilts exposed to strain NADC-8. Most (15 of 16) principal gilts were show to be viremic following virus exposure and many (9 of 16) were still infected on or about day 49 postexposure as evidenced by detecting infectious virus in alveolar macrophages collected at necropsy.