PCV2 mass vaccination in gilts and sows to overcome PDNS

Finishing pigs from a 10,000-sow multisite herd in the east of England were routinely presenting with red to purple macules and papules. These skin lesions would eventually coalesce, forming an irregular patch of dermatitis primarily on the skin behind the hindlegs and the perineum. Approximately 1% of the finishers in the all-in, all‑out system displayed these clinical signs.

The total wean-to-finish monthly mortality rate would range from 5% to 10% (average 7.7%) with dead pigs having variable body condition scores and dying from a combination of acute or chronic, and specific or non-specific, clinical issues.

Tail biting cases in finishers had also increased. These health and production concerns had been ongoing for 12 months.

The gross lesions observed during necropsy of chronically ill pigs were haemorrhagic and necrotising dermatitis; cutaneous pallor; depleted or enlarged congested lymph nodes; and pale, swollen kidneys with or without cortical petechiae.

These single-parity breeding operation sites had been outsourcing their replacement gilts from a rearing facility that had not been administering porcine circovirus type two (PCV2) vaccine at the time of selection, but vaccinating them only at weaning. PCV2 vaccination was not part of the existing sow health programme either – only in their progeny, which would receive a single dose at weaning.

Diagnostic investigation and results

Blood samples, as well as some sectioned, formalin-fixed lymph nodes, kidney and skin tissues, were sent to the laboratory to confirm PCV2 involvement through quantitative PCR and histopathology.

DNA copies detected in most of the blood samples submitted were greater than or equal to 5 log GE/mL of serum. While only moderate lymphocyte depletion was observed in histopathology of the submitted lymph nodes, a marked fibrino-necrotising glomerulonephritis, as well as non-purulent interstitial nephritis, were seen in the examined sections of the kidney. Severe fibrinoid necrotising vasculitis with haemorrhages were noted from the sampled dermis and subcutis.

The diagnosis of porcine dermatitis and nephropathy syndrome (PDNS) was satisfied through necropsy, serum and histopathological examinations, which correlated with the observed clinical signs, the level of the viral genome detected in the serum, as well as on the gross and microscopic lesions consistent of a PCV2 infection.

Intervention and outcome

The recommended practical interventions of a few scientific studies^1-3 were slightly modified and implemented. In addition to the continuing PCV2 vaccination of piglets at weaning, a one‑off PCV2 mass vaccination (Ingelvac CircoFLEX) of sows across the existing breeding sites was rolled out.

A one-shot PCV2 vaccination, at least three weeks before breeding, was also introduced as part of the vaccination programme for all incoming gilts.

Comparing the data six months before with six months after the intervention, distinct improvements were seen in the post-weaning health and production performance of the weaners, and the succeeding batches weaned out of their PCV2-vaccinated dams.

The PDNS cases ceased, post-weaning monthly mortality rate dropped by approximately 35% – from 7.7% to 5% – and the average finisher weight increased from 81kg to 88kg dead weight. The feed conversion ratio improved from 2.72 to 2.49.

A notable improvement in breeding performance was also observed – especially in the worst-affected, 1,320-sow herd as shown in Table 1.

Discussion

The diagnosis of PCV2-associated PDNS in this pig operation was initially attributed to vaccine inefficacy and vaccination failure. However, recent epidemiological studies showed that PCV2-associated diseases have been increasing over the past few years; this was due to the inevitable changes in the infection dynamics of PCV2⁴.

The use of highly efficacious PCV2 vaccines in progeny herds across the globe for more than a decade has resulted in a significant decline of viral load in a herd⁴. This could lead to seronegative finisher pigs, so when replacement animals are selected from this herd, it is highly likely that a PCV2-naive gilt will be infected on introduction into a PCV2-endemic breeding herd.

PCV2 infection could then be perpetuated, hence creating an unstable breeding herd where transplacental or in utero infection can occur^4-6.

In this particular case, it was believed that among those unvaccinated outsourced replacement gilts, some might have already been harbouring PCV2. Virus shed from those PCV2-infected gilts could spread to the rest of the selected naive stock leading to a single-parity herd with individual sows having variable levels of PCV2 protection.

This scenario potentially resulted in transplacental transmission and post-farrowing subsequent PCV2 horizontal transmission, and early infection among susceptible littermates, prior to the programmed PCV2 vaccination at weaning^4-6. Aside from PDNS, PCV2-related immunosuppression was believed to be another contributing factor in the morbidity and mortality observed in the herd⁷.

Although the breeding performance was not the main driver for Ingelvac CircoFLEX mass vaccination in this operation, fertility was not as good as it should have been, as shown in Table 1. Interestingly, a significant improvement occurred in breeding herd performance parameters six months post-intervention, which was the only notable course of action implemented at the time.

It is known that PCV2 has a negative effect on reproduction^5,6, so the PCV2 vaccination applied to the existing and replacement animals must have provided some relatively immediate, yet remarkable, benefits similar to what have been described in the literature^5,8.

Conclusion

Based on the results of the implemented PCV2 vaccination in the incoming gilts and the one-off sow mass vaccination, it is highly likely that PDNS-afflicted finishers were infected prior to PCV2 vaccination (at weaning).

Hence, the initial suspicion that vaccine inefficacy was the primary issue appears to not be the case – rather, it was PCV2 instability in the breeding herd, as influenced by insufficient or lacking PCV2 protection in replacement gilts, that was the underlying cause of the PDNS in finishers, thereby highlighting the importance of PCV2 vaccination in replacement animals and in a breeding herd at risk of perpetuating PCV2.

In future cases, placental umbilical cord serum or piglets’ pre-vaccination serum samples can be collected and submitted for PCV2 qPCR testing to prove the occurrence of transplacental transmission.