#11-113

Complete

Date Full Report Received

04/16/2013

Date Abstract Report Received

04/16/2013

Investigation

Institution:
Primary Investigator:

We believe that achieving control of PRRSV will require the industry to develop the capacity to easily, efficiently, and continuously surveil herds for PRRSV. The objective of the research was to explore one possible surveillance option.
In four PRRSV vaccinated commercial swine herds, oral fluid samples were collected from 600 litters (150 samples from each of the 4 herds) 24 hours prior to weaning and serum samples from their dams two days post weaning. All sows had received at least 4 doses of PRRSV vaccine.

Once collected, samples were completely randomized and tested for PRRSV (RT-qPCR and sequencing) and PRRSV antibodies. In addition, PRRSV ORF5 sequencing was attempted on RT-qPCR-positive samples. Virus and antibody assay results were analyzed for associations with farm, sow parity, litter size, time, and infection status.
Testing of pre-weaning oral fluid samples (n = 600) and sow serum samples (n = 600) by PRRSV RT-qPCR resulted in 9 positive oral fluid samples. No PRRSV RT-qPCR-positive serum samples were observed. The positive results were confirmed by blind re-testing at a second laboratory.

Conclusions and observations:
1. PRRSV can be present in litters of clinically normal pigs in well-vaccinated herds at very low levels. That is, the incidence of infection in sampled litters was 1.5%. A striking feature was the highly sporadic nature of the infection. That is, infected litters were “hidden” among a majority of PRRSV-negative litters.
2. The obvious question is, “Where did the virus come from?” The sequence analyses showed that the virus was wild-type virus (not vaccine virus).
No viremic sows were detected, but sow serum samples from RT-qPCR-positive litters showed significantly higher (p < 0.05) mean serum IgG (1.73 vs. 0.98) and commercial kit (1.97 vs. 0.98) S/P ratios, but no difference in IgM or IgA responses. These data fit the previous observation that re-exposure of vaccinated or PRRSV-infected animals did not produce anamnestic IgM or IgA responses, but did produce an anamnestic IgG response.
Although the antibody responses indicated that both the sows and their litters had been infected, the source(s) of the virus was not revealed by these data. Nor is it possible to determine whether the sows were infected before or after the piglets.
3. Collection and testing of oral fluids from litters immediately prior to weaning was useful for the detection of PRRSV. The utility and limitation of this approach should be evaluated in other herds, particularly in herds that are moving toward PRRSV elimination.