Virological and serological characterization of vaccinated and non-vaccinated piglet subpopulations coming from vaccinated and non-vaccinated sows.

The present study describes the virological and serological profiles of PCV2 vaccinated (V) and non-vaccinated (NV) piglet subpopulations coming from V and NV sows in a PCV2 subclinically infected farm. Four hundred seventy-six piglets born from V or NV sows were further subdivided in a total of four groups: NV sows-NV pigs (NV-NV), NV sows-V pigs (NV-V); V sows-NV pigs (V-NV) and V sows-V pigs (V-V). Seventy-five pigs were randomly selected at the beginning of the trial from each group and they were bled at 4, 8, 12, 16, 21 and 25 weeks of age. All animals included in the trial were weighed at 4 and 25 weeks of age and their average daily weight gain (ADWG) was calculated. Serum samples obtained at different time points were used to assess PCV2 infection (viremia) and the level of antibodies by means of immunoperoxidase monolayer assay (IPMA) against this pathogen. IPMA titers (classified in high, medium or low) and PCR results (positive or negative) were analyzed using a multiple correspondence and K-means cluster analysis. According to these tests, animals included in the study were classified into the following four clusters: (1) 93 piglets that were viremic mainly from 12 to 25 weeks of age and with PCV2 antibody titers increasing over time; (2) 75 piglets with late PCV2 infection and seroconversion (later than 16 weeks of age); (3) 26 piglets with high but decreasing PCV2 antibody titers and low percentages of PCV2 PCR positive serum samples; and (4) 105 piglets with medium and high IPMA titers throughout the trial and sporadic PCR positive samples. The defined subpopulations of piglets were observed in all experimental groups (NV-NV, NV-V, V-NV and V-V) although in variable percentages. Thus, animals from clusters 1 and 2 belonged mainly to the NV-NV and V-NV groups and animals from clusters 3 and 4 were distributed mainly into the NV-V and V-V groups. Finally, the ADWG of pigs belonging to clusters 3 and 4 was significantly higher (p=0.02) than that of pigs belonging to clusters 1 and 2. Within each cluster, no statistically significant differences were found in ADWG between treatment groups.