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The porcine dermatitis and nephropathy syndrome (PDNS) is a clinically and pathologically well-defined condition that primarily affects fattening pigs (between 2 and 6 months of age). This disease causes highly characteristic vascular lesions, considered as a consequence of an immunologically mediated type III hypersensitivity reaction, i.e., caused by the deposition of immune complexes in the walls of blood vessels. Since the disease was first described in 1993, researchers have attempted to link PDNS to various pathogens. Although there is no definitive evidence confirming its aetiology, porcine circovirus 2 (PCV2) has been the main pathogen linked with the development of this disease over the past two decades.

Porcine Circoviruses (PCVs) belong to a family of highly ubiquitous viruses, meaning they are found at very high prevalence in swine populations. Typically, their presence does not cause any apparent disease, so their detection in clinical cases does not guarantee an association with pathology. The association of PCV2 with PDNS is based on the fact that this pathogen is frequently identified in studied cases. Additionally, supporting the hypothesis, pigs affected by PDNS often exhibit very high antibody titres against PCV2. However, 10 years ago, a new porcine circovirus, PCV3, was discovered and identified in PDNS cases, suggesting that it may also cause this syndrome.

Previous studies have investigated the presence of PCV2 or PCV3 in this context, but some of these did not analyse both viruses, and others lacked strict pathological inclusion criteria. In the present study, 102 retrospective cases of acute PDNS were collected using strict diagnostic criteria (Figure 1) to investigate the presence of all PCVs (also including PCV1 and PCV4) through qPCR or conventional PCR tests. Additionally, RNAscope®, a technique for detecting genetic material in histological sections (in situ hybridization), was used to localize the PCV2 and PCV3 genomes within PDNS lesions.

All studied cases tested positive for PCV2 (102/102; 100%), while only 30/102 (29.4%) were positive for PCV3. No other PCVs were detected in any of the cases. Furthermore, the PCV2 load was higher than that of PCV3 in all cases. While no genetic material from PCV3 was detected in the lesions by in situ hybridization, the PCV2 genome was found in approximately half of the cases, albeit in low quantities, within the characteristic PDNS lesions.

The presence of PCV2 in all studied cases supports the conclusion that this virus is the most likely causative pathogen associated with PDNS. In contrast, PCV3 was found at a prevalence similar to that observed in healthy animals (between 5% and 60%, depending on different studies). However, the presence of both viruses within the lesions was not consistently observed. This may be because, by the time the lesions and, consequently, the disease develops, the viral particles are no longer present, having been cleared by the immune system.

_{Figure 1. PDNS characteristic histologic lesions. A) Leukocytoclastic arteritis. The wall of the artery undergoes necrosis and there is presence of fibrin and abundant leukocytes. B) Fibrinous and necrotising glomerulonephritis. The renal glomeruli are also affected, displaying a marked exudation of fibrin into the Bowman’s space.}