Flow strategies to minimize infection at breeding may provide better control.
Porcine circovirus type 2 (PCV2) is the causative agent of Porcine Circovirus-Associated Disease (PCVAD). PCVAD causes significant economic losses to producers from increased mortality and culling rates to poor growth in growing pigs. The introduction of commercial vaccines against PCV2 has been universally successful in minimizing economic losses in growing pigs.
The effect of PCV2 in breeding herds has not been identified. There have been numerous field reports of PCV2- related reproductive failures as early as 1999. These reports suggest increased rates of mummified and stillborn fetuses. The impact of PCV2 on breeding herds may not be as dramatic as other diseases, such as porcine reproductive and respiratory (PRRS), but evidence suggests it can play a role in economic losses.
Case Study No. 1
A large North American PRRS-free breeding herd had a significant increase in mummies in the fall of 2008. The mummies increased from approximately 2% to over 10% for a 10-week period. Sows farrowed at the expected time (114 to 115 days of gestation), but had variable numbers of mummified and liveborn pigs. The number of stillbirths was normal.
The striking part of the presentation was despite high numbers of mummified pigs in a litter, the pigs that were born alive were normal and survived to weaning at a rate that was similar to the rate prior to the outbreak.
In U.S. breeding herds, the differential diagnoses for an increase in mummies include porcine parvovirus, swine influenza virus, PRRS and PCV2.
The herd experiencing the outbreak was part of a larger system that had common feed, management and housing conditions; these items could be removed from consideration as a cause of the mummified fetuses. Interestingly, there was an increase in the number of irregular returns to estrus per week starting in week 15, 2008, 22 weeks before the increase in mummies was observed.
With the increase in mummies, a series of diagnostics were conducted. Three cases were submitted to veterinary diagnostic labs over a period of about one month. The initial diagnostics were a set of 20 mummies; these samples were positive by polymerase chain reaction (PCR) for PCV2. They were negative for all other diseases that cause mummification. All of the fetuses had distended abdomens that were suggestive of heart failure.
A second set of fetuses sent to the diagnostic lab were positive for PCV2. A third set of samples on stillborn fetuses demonstrated severe myocardial damage due to PCV2.
Numerous control measures were attempted during the outbreak to help resolve the mummified fetuses. Upon the outbreak of increased mummies, vaccination of gilts three weeks prior to entry into the breeding herd was reinitiated, and mass vaccination of the entire sow herd was undertaken with a killed PCV2 vaccine.
Statistical process control (SPC) analysis suggested that vaccination was not successful in lowering the number of mummies, as no SPC signals were generated from either the mass vaccination or the vaccination of gilts prior to breeding. The herd had maintained pre-breeding PCV2 vaccination as a preventative.
The intervention strategies used in this herd were not effective in eliminating clinical signs and did not prevent clinical signs in three other herds from the same gilt source. These herds all receive gilts in a similar manner to Farm 1. One herd from the same source was unaffected. It receives gilts at about 150 lb., or nine weeks younger than the other farms in the flow. This farm has never experienced an increase in fetal mortality as represented by increased mummies or irregular returns.
These data suggest that flow strategies, such as when gilts are introduced into the breeding herd, could have a large role in the PCV2-associated reproductive failure. It appears that when gilts are introduced to the breeding herd at a young age, they have enough time to recover after exposure at entry prior to being bred, and this puts their fetuses at risk of infection.
Although PCV2 may not be a common cause of reproductive failure in North American breeding herds, it can have devastating consequences. Routine control measures, such as vaccination, do not appear to be effective in eliminating clinical signs within the breeding herd. Flow strategies to minimize infection of animals at the time of breeding may be necessary to provide better control. None of the available commercial vaccines completely eliminate viremia (infection in the bloodstream), and it appears that even low rates of PCV2 infection are capable of producing some reproductive losses associated with PCV2.