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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #105986


item Lager, Kelly
item Mengeling, William
item Wesley, Ronald

Submitted to: Canadian Journal of Veterinary Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/3/2002
Publication Date: 5/1/2003
Citation: Lager, K.M., Mengeling, W.L., Wesley, R.D. 2003. Strain predominance following exposure of vaccinated and naive pregnant gilts to multiple strains of porcine reproductive and respiratory syndrome virus. Canadian Journal of Veterinary Research. 67:121-127.

Interpretive Summary: Porcine reproductive and respiratory syndrome (PRRS) is currently the most significant disease affecting the U.S. swine industry. It is caused by the PRRS virus (PRRSV) for which several modified-live vaccines have been produced. Controlled studies indicate these vaccines are efficacious in preventing or reducing the PRRS disease on a farm; however, some field reports suggest vaccine use does not always meet producer's expectations. There are probably many factors why vaccines may not perform as well on the farm when compared to laboratory conditions; one of these may be due to how well vaccines cross protect among the different strains of PRRS virus circulating in the field. A series of studies to evaluate cross-protection among PRRS virus strains were completed. Results from these studies suggest that one PRRSV strain used as a vaccine could cross protect against other virus strains, but one vaccine may not cross protect against all strains. These results emphasize the importance of biosecurity on the farm, i.e., one should try to prevent the introduction of a new PRRSV strain into the herd since there may be little or no cross protection against this strain.

Technical Abstract: Two studies were performed in order to test the relative ability of different strains of porcine reproductive and respiratory syndrome virus (PRRSV) to replicate and cross the placental barrier in pregnant gilts. Study 1 comprised 6 nonvaccinated gilts. Study 2 comprised 8 nonvaccinated gilts and 12 gilts that were vaccinated twice before conception. On, or about, gestation day 90 all gilts were simultaneously exposed to 20 field strains of PRRSV (all strains were distinguishable by restriction fragment length polymorphism (RFLP) patterns). Gilts of study 1 were euthanized on day 7 postpartum. Gilts of study 2 were euthanized on, or about, gestation day 111. All gilts, pigs, and fetuses were tested for the presence and type of strain of PRRSV. Of 128 samples shown to contain PRRSV, 118 contained a single strain, 4 contained 2 strains, and 2 contained a strain or strains for which the RFLP pattern was undecipherable. Only 8 of the 20 strains were isolated from nonvaccinated gilts and their litters. And only 2 of the 20 strains (notably 2 of the same strains isolated from nonvaccinated gilts and their litters), were isolated from vaccinated gilts and their litters. Moreover, 1 of the 2 strains accounted for most (31 of 37; 84%) of the isolates from the vaccinated group. Collectively these results indicate that strains differ in their ability to replicate in pregnant gilts and cross the placental barrier. And they suggest that maternal immunity, although sometimes insufficient to prevent transplacental infection, can exert additional selective pressure.