Porcine reproductive and respiratory syndrome continues to be a major health problem in the U.S. pork industry. First reported in America in 1989 and in Europe in 1990, PRRS produces respiratory distress, increased mortality rates, abortions and reduced weight gain.
The immune response against PRRS virus is ineffective at rapidly resolving viral infection, resulting in a prolonged viremia and persistent infection in lymphoid tissues. While individual farms have been able to eliminate PRRS virus, endemically infected herds still pose an exposure risk to neighboring PRRS-negative swine populations.
To move forward with eradication programs, appropriate and cost-effective control protocols are needed. While PRRS’ clinical presentation may include both a reproductive and a respiratory component, 88 percent of the total cost is due to the virus’ effect in post-weaning pigs.
Therefore, breeding herd stabilization, as measured by absence of vertical virus transmission (sow to pig) thereby producing PRRS-negative weaned piglets, is a control program’s initial goal.
Under field conditions, the strategic combination of mass vaccination using modified-live virus PRRS vaccine and pig-flow management has been a successful approach to controlling PRRS virus transmission in acutely infected herds. However, these studies were observational in nature and lacked controls. A University of Minnesota College of Veterinary Medicine research team conducted two large-scale, controlled studies to evaluate the benefits and limitations of the therapeutic use of a PRRS MLV vaccine on pig populations already infected with PRRS virus, which more typically reflects real-world situations.
The research was conducted in two phases. The first consisted of mass vaccination of PRRS-infected pigs; the second phase included inoculating pigs of different virus-exposure status with a highly virulent PRRS virus isolate.
Phase 1: Vaccination of PRRS-infected Pigs
The first study evaluated the effects of PRRS MLV vaccination on a population infected with a homologous (same origin) isolate. The experiment included positive- and negative-control groups, intense diagnostic monitoring and strict control of several factors such as infection time, feeding, genetics, health status and management. There were 80, 6- to 8-week-old PRRS-naïve pigs per group (Groups A through D). They were intranasally inoculated with PRRS virus VR–2332, the parental strain of Ingelvac PRRS MLV vaccine. The negative-control group had 12 pigs (Group E).
At seven days post-inoculation pigs in Groups B, C and D were vaccinated intramuscularly with Ingelvac PRRS MLV vaccine. Pigs in Group C were revaccinated at 37 days post-inoculation, and pigs in Group D received three doses of the vaccine at seven, 37 and 67 days post-inoculation.
To evaluate viral transmission, sentinel pigs were introduced periodically to each group. Those pigs were slaughtered 30 days after introduction. To evaluate virus persistence, 10 pigs per group were slaughtered and sampled at different times post-infection. At 98 days post-inoculation, 10 pigs per group were transported to the University of Minnesota’s isolation facilities. Previously exposed (infected and vaccinated) pigs and negative controls were intranasally inoculated with PRRSV MN 184, a highly pathogenic isolate able to induce severe clinical signs that is heterologous (different origin) to both the original challenge inoculation virus and the vaccine virus. (See Table 1 for the study’s design.)
Phase 1 Results
Mass vaccination significantly reduced the number of persistently infected pigs at 127 days post-inoculation. Vaccination did not eliminate wild-type PRRS virus; however, administration of two or three doses of MLV vaccine prevented viral shedding after 97 days post-inoculation. Previous exposure to wildtype and vaccine viruses reduced clinical signs and enhanced growth following heterologous challenge but did not prevent infection.
The results of Phase 1 suggest that therapeutic vaccination may help reduce PRRS-related economic losses, but it’s unlikely that such a homologous relationship between vaccine virus and field virus would occur in commercial swine production environments.
Phase 2: Heterologous PRRS
Phase 2 attempted to develop a more relevant field-based challenge model. It not only included infection and later application of different mass vaccination protocols to a large population infected with a PRRS virus isolate that was heterologous to the MLV vaccine, but it also simulated the introduction of a highly virulent heterologous isolate to previously infected and/or vaccinated pigs.
The experimental design of Phase 2 was similar to Phase 1, with some differences; Phase 2 included a Group F with 20 pigs that only received one dose of Ingelvac PRRS MLV vaccine. Pigs were intranasally inoculated with PRRS virus MN 30-100 isolate. At seven days post-inoculation, pigs were vaccinated intramuscularly with Ingelvac PRRS MLV vaccine. Positive tissue samples were tested by strain-specific PCR to differentiate the modified-live virus from MN 30-100. Previously exposed (infected and vaccinated) and negative control pigs were inoculated with PRRSV MN 184, but this time a naïve pig was introduced to every room with five inoculated pigs three days after the MN 184 challenge.
Phase 2 Results
The proportion of persistently infected pigs and transmission from inoculated pigs to sentinels are shown in Table 2. MN 30-100 (the challenge virus given prior to vaccination) was the predominant PRRS virus isolate detected by strain-specific PCR in tissue samples from persistently infected pigs in all the groups, as well as from infected sentinel pigs. No statistical differences of group average viral load were detected within sampling days. However, administration of MLV vaccine prevented viral shedding after 127 days post-inoculation. Following the subsequent MN 184 inoculation, PRRS virus was detected in serum of pigs from all groups (Groups A through F) at three and seven days after inoculation.
However, the proportion of viremic pigs in the first-time exposed group (Group E+) was statistically higher than in the previously exposed groups at seven days after MN 184 challenge. All sentinel pigs in all groups became infected after being in contact with MN 184 inoculated pigs. Groups A, B, C, D or F showed no severe clinical signs, but high fever, anorexia and two deaths were registered in group E+ (non-vaccinated and first-time exposed group).
Therapeutic vaccine intervention prevented viral shedding to PRRS-naïve pigs and significantly improved the clinical response against a highly virulent heterologous challenge; therefore, therapeutic vaccination could be used in combination with other strategies to reduce duration of PRRS virus transmission and to increase the resistance of pig herds under certain scenarios in the field.