Monitor outcomes to ensure long-term PRRS control success. Track diagnostic results and pig performance data across sow, grow-finish, and whole production systems to detect low-level virus circulation, guide decisions, and move herds toward stable or negative status.
The Guilty Gilt Guide was written with a clear objective – to maximize the whole-herd performance of pig populations by helping gilts to reach their full reproductive potential and produce healthy pigs that reach their full genetic potential during grow-finish.
The open reading frames (ORF)5 represents approximately 4% of the porcine repro- ductive and respiratory syndrome virus (PRRSV)-2 genome (whole-PRRSV) and is often determined by the Sanger technique, which rarely detects >1 PRRSV strain if present in the sample.
Porcine reproductive and respiratory syndrome virus (PRRSV) is an important swine pathogen affecting the global swine industry.
This study evaluated porcine reproductive and respiratory syndrome virus (PRRSV)-2 modified live virus (MLV) vaccine against heterologous single and dual challenge of Korean PRRSV-1 and PRRSV-2. Pigs were administered PRRSV-2 MLV vaccine intramuscularly at 21 days of age and inoculated intranasally with both genotypes at 56 days of age. Vaccination of pigs with PRRSV-2 MLV vaccine resulted in reduction of viral loads of both PRRSV-1 and PRRSV-2 after heterologous single and dual challenge with PRRSV-1 and PRRSV-2. In addition, pigs vaccinated with PRRSV-2 MLV vaccine exhibited higher frequencies of PRRSV-1 and PRRSV-2 specific interferon-γ secreting cells (IFN-γ-SC) and showed a significant reduction in lung lesions and PRRSV nucleic acid within the lung lesions after single and dual challenge compared with unvaccinated challenged pigs. Taken together these results demonstrated that vaccination of pigs with PRRSV-2 is efficacious in protecting growing pigs from respiratory disease against heterologous single and dual PRRSV-1 and PRRSV-2 challenge.
Type 2 porcine reproductive and respiratory syndrome (PRRS) virus (PRRSV) was first isolated in Korea in 1994. The commercial PRRS modified live vaccine (Ingelvac® PRRS MLV, Boehringer Ingelheim Vetmedica Inc., St. Joseph, Missouri, USA) based on type 2 PRRSV, was first licensed for use in 3- to 18-week-old pigs in Korea in 1996. The objective of the present study was to evaluate the efficacy of this 20 year old commercial PRRS modified live vaccine (MLV) against two recent PRRSV isolates. Two genetically distant type 2 PRRSV strains (SNUVR150004 for lineage 1 and SNUVR150324 for lineage 5), isolated in 2015, were used as challenge virus. Regardless of the challenge virus, vaccination of pigs effectively reduced the level of viremia, the lung lesions, and of the PRRSV antigen within the lung lesions. The induction of virus-specific interferon-γ secreting cells by the PRRS vaccine produced a protective immune response, leading to the reduction of PRRSV viremia. There were no significant differences in efficacy against the two recently isolated viruses by the PRRS MLV based on virological results, immunological responses, and pathological outcomes. This study demonstrates that the PRRS MLV used in this study is still effective against recently isolated heterologous type 2 PRRSV strains even after 20 years of use in over 35 million pigs.
Cell-mediated immunity (CMI), IL-10, and the protective efficacy of modified-live porcine reproductive and respiratory syndrome virus (PRRSV) vaccines (MLV) against co-challenge with PRRSV-1 and PRRSV-2 (HP-PRRSV) were investigated. Seventy, PRRSV-free, 3-week old, pigs were allocated into 7 groups. Six groups were intramuscularly vaccinated with MLV, including Porcilis (PRRSV-1 MLV, MSD Animal Health, The Netherlands), Amervac (PRRSV-1 MLV, Laboratorios Hipra, Spain), Fostera (PRRSV-2 MLV, Zoetis, USA), Ingelvac PRRS MLV and Ingelvac PRRS ATP (PRRSV-2, Boehringer Ingelheim, USA), and Prime Pac PRRS (PRRSV-2 MLV, MSD Animal Health, The Netherlands). Unvaccinated pigs were left as control. Lymphocyte proliferative response, IL-10 and IFN-γ production were determined. At 35 days post-vaccination (DPV), all pigs were inoculated intranasally with 2 ml of each PRRSV-1 (105.4 TCID50/ml) and PRRSV-2 (105.2 TCID50/ml, HP-PRRSV). Following challenge, sera were quantitatively assayed for PRRSV RNA. Pigs were necropsied at 7 days post-challenge. Viremia, macro- and microscopic lung lesion together with PRRSV antigen presence were evaluated in lung tissues. The results demonstrated that, regardless of vaccine genotype, CMI induced by all MLVs was relatively slow. Increased production of IL-10 in all vaccinated groups was observed at 7 and 14 DPV. Pigs in Amervac, Ingelvac MLV and Ingelvac ATP groups had significantly higher levels of IL-10 compared to Porcilis, Fostera and Prime Pac groups at 7 and 14 DPV. Following challenge, regardless to vaccine genotype, vaccinated pigs had significantly lower lung lesion scores and PRRSV antigens than those in the control group. Both PRRSV-1 and PRRSV-2 RNA were significantly reduced. Prime Pac pigs had lowest PRRSV-1 and PRRSV-2 RNA in serum, and micro- and macroscopic lung lesion scores (p < 0.05) compared to other vaccinated groups. In conclusion, PRRSV MLVs, regardless of vaccine genotype, can reduce viremia and lung lesions following co-challenge with PRRSV-1 and PRRSV-2 (HP-PRRSV). The main difference between PRRSV MLV is the production of IL-10 following vaccination.
In this study, we analyzed PRRS virus (PRRSv) specific lymphocyte function in piglets vaccinated with Ingelvac PRRSFLEX EU® at two and three weeks of age in the presence of homologous maternal immunity. Complete analysis of maternal immunity to PRRSv was evaluated postpartum, as well as passive transfer of antibodies and T cells to the piglet through colostrum intake and before and after challenge with a heterologous PRRSv at ten weeks of age. Maternal-derived antibodies were detected in piglets but declined quickly after weaning. However, vaccinated animals restored PRRSv-specific antibody levels by anamnestic response to vaccination. Cell analysis in colostrum and milk revealed presence of PRRSv-specific immune cells at suckling with higher concentrations found in colostrum than in milk. In addition, colostrum and milk contained PRRSv-specific IgA and IgG that may contribute to protection of newborn piglets. Despite the presence of PRRSv-specific Peripheral Blood Mononuclear cells (PBMCs) in colostrum and milk, no PRRSv-specific cells could be detected from blood of the piglets at one or two weeks of life. Nevertheless, cellular immunity was detectable in pre-challenged piglets up to 7 weeks after vaccination while the non-vaccinated control group showed no interferon (IFN) γ response to PRRSv stimulation. After challenge, all piglets developed a PRRSv-specific IFNγ-response, which was more robust at significantly higher levels in vaccinated animals compared to the primary response to PRRSv in non-vaccinated animals. Cytokine analysis in the lung lumen showed a reduction of pro-inflammatory responses to PRRSv challenge in vaccinated animals, especially reduced interferon (IFN) α levels. In conclusion, vaccination of maternally positive piglets at 2 and 3 weeks of age with Ingelvac PRRSFLEX EU induced a humoral and cellular immune response to PRRSv and provided protection against virulent, heterologous PRRSv challenge.