|Benson, James - IOWA STATE UNIV, AMES, IA|
|Yaeger, Michael - IOWA STATE UNIV, AMES, IA|
Submitted to: Swine Health and Production
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 1, 2000
Publication Date: N/A
Interpretive Summary: Porcine reproductive and respiratory syndrome (PRRS) is a swine disease caused by the PRRS virus (PRRSV) which was discovered in 1991. It is the number one infectious disease concern for United States pork producers making control and prevention of PRRS a top priority. Commercially available vaccines have been developed and are used successfully in many situations, however, they may not protect all swine under all conditions. One of the many factors that contribute to why a vaccinated animal may not be protected against virus challenge could be the magnitude of the actual virus challenge. The objective of this study was to evaluate the relative susceptibility of vaccinated and nonvaccinated pregnant swine to low, medium, and high challenge doses of PRRSV. In this study it appeared that vaccinated animals had more resistance to virus challenge than nonvaccinated animals and that vaccine induced protective immunity could be eovercome with increased doses of challenge virus. These findings support the use of vaccine by veterinarians for improving herd resistance against PRRSV infection. However, vaccinated animals may not be fully protected and it is very important to keep new virus strains out of the herd through strict biosecurity. On average, about one third of a litter was infected with PRRSV indicating that multiple fetuses/weakborn pigs should be submitted to a diagnostic laboratory to assure that infected animals are represented in the sample population.
Technical Abstract: The relative susceptibility of vaccinated and nonvaccinated pregnant swine to varied challenge doses of porcine reproductive and respiratory syndrome virus (PRRSV) was tested. Fifteen nonpregnant gilts obtained from a PRRS free herd were vaccinated twice with a modified-live PRRSV vaccine prior to artificial insemination. Once pregnant, these gilts and 16 pregnant nonvaccinated gilts from the same herd were randomly divided into control, low, middle, or high dose groups and intramuscularly inoculated at 90 days of gestation with either a sham inoculum (control group) or challenge virus inoculum consisting of approximately 10**2 (low dose group), 10**4 (middle dose group), or 10**6 (high dose group) CCID50 of the NADC-8 PRRSV strain. Fetal death and viremia was found in 4 of 4, 3 of 3, and 3 of 4 litters in the low, middle, and high challenge dose groups of the nonvaccinated animals, and in 0 of 4, 1 of 2, and 1 of 4 litters in the low, middle, and high challenge dose groups of the vaccinated animals. No fetal death or viremia was identified in control groups. Among infected litters, no significant difference in the percentage of infected fetuses per litter was observed regardless of vaccination status or challenge virus dose. Vaccine induced protective immunity appeared to protect eight of 10 litters from reproductive failure, but may be overcome with increased (10**4 CCID50) doses of challenge virus. The lowest studied PRRSV exposure dose (10**2 CCID50) did cause reproductive failure in naive, unvaccinated animals. The percentage of infected fetuses per litter has significant diagnostic implications; i.e., multiple fetuses/weakborn pigs should be sampled from each affected litter to assure that infected animals are represented.