In a field trial on a farm with a severe PMWS problem, the piglets of 8 sows were followed until 12 weeks of age. None of the piglets derived from the dams with highest PCV2-antibodies developed PMWS, and 60% of the piglets that did develop PMWS were derived from the dams with the lowest PCV2 serum antibody levels (Allan et al., 2002). Another European field study investigated the effect of the sow on PMWS in a cohort study in 3 sow herds with a high postweaning mortality due to PMWS (Hassing et al, 2003). A total of 1,183 piglets derived from 125 sows were included in this study. It was found that the offspring from sows with high antibody levels against PCV2 at farrowing had a higher risk of dying after weaning. The risk of dying was also dependent on increasing IPMA titers against PCV2 from weaning until 4 weeks after weaning (Hassing et al., 2003).
Harms et al. (2002) used a total of 124 pigs with highly variable PCV2-antibody titers and inoculated 51/124 with PCV2 and coinfected 47/124 with PRRSV and PCV2 at different ages (3, 6 and 11 weeks of age). Piglets with a PCV2 ELISA S/P ratio of 0.6 were protected by PCV2 replication and development of PMWS (Harms et al., 2002).
Allan et al. (2002) published an experimental study in which ten piglets derived from 2 dams with high PCV2 titers (determined by IFA) and ten piglets derived from 2 dams with low PCV2 titers were weaned at 2 days of age and infected with PCV2 at 3 weeks of age. Piglets derived from the low PCV2 titer dams had significantly reduced daily weight gain and a higher incidence of PCV2 antigen in lymphoid tissues as determined by IHC (Allan et al., 2002).
Fenaux et al. (2004) demonstrated that pigs vaccinated with PCV2 and challenged with the same strain were protected. McKeown et al. (2005) determined the effects of PCV2 maternal antibodies on the immune response to experimental PCV2 infection. Twenty-four piglets were divided into 4 groups on the basis of the ELISA titers of PCV2 maternal antibodies: group A (n = 6; negative), group B (n = 5; low antibody levels), group C (n = 8; high antibody levels), and group D (n = 5; high antibody levels). Piglets in groups A, B, and C were inoculated with PCV2 at 0 DPI and challenged with PCV2 at 42 DPI. Group D pigs were not exposed to PCV2 at 0 DPI but were challenged at 42 DPI. The authors concluded that protection against PCV2 infection conferred by maternal antibodies is titer dependent: higher titers are generally protective, but low titers are not (McKeown et al., 2005).
Pigs that have a lower birth and weaning weight are more frequently affected by PMWS (Corrégé et al., 2001) and 7 of 10 pigs in a PMWS affected herd with insufficient colostral transfer as defined by refractometer reading did not survive to weaning (Moll 2004). Unfortunately, PCV2 antibodies in the piglets or dams were not determined in those studies.
By using the gnotobiotic pig model, Meerts et al. (2005) found that variation in the onset of adaptive immunity may account for variation in PCV2 replication in pigs. In particular, absence of PCV2 neutralizing antibodies may be an important factor in the development of a increased virus replication (Meerts et al., 2005).
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