Pathogenesis of postweaning multisystemic wasting syndrome reproduced by co-infection with Korean isolates of porcine circovirus 2 and porcine parvovirus.

Thirty-two colostrum-deprived conventional pigs aged 28 days were co-infected with Korean isolates of porcine circovirus 2 (PCV2) and porcine parvovirus (PPV) and observed for up to 35 days post-inoculation (dpi). Histopathologically, granulomatous inflammation, with or without intracytoplasmic inclusion bodies, was present in lymphoid tissues (e.g., lymph nodes, thymus, spleen and tonsil) from 20 dpi, being most severe at 24 dpi. PCV2 and PPV DNA were detected in the lymph nodes from 3 to 35 dpi by in-situ hybridization, but the labelling for both viruses was particularly intense and widespread at 20 and 24 dpi. A close relationship between the cells labelled for PCV2 and those labelled for PPV was revealed by examination of serial sections from lymph nodes, and PCV2 and PPV were also detected in peripheral blood monocytes from 3 to 35 dpi. Other tissues and cells in which PCV2 and PPV DNA were detected included macrophages in the tonsil, thymus, spleen, lung, liver, kidney and heart. Significantly more PCV2-positive cells than PPV-positive cells were detected in the lymph nodes at 5 to 35 dpi. The pathogenesis of postweaning multisystemic wasting syndrome (PMWS) reproduced in this study may be suggested thus: initial viral entry through tonsillar macrophages, followed within 3 days by viraemia; PCV2 and PPV replicate, at least to some extent, in circulating peripheral monocytes, contributing to the cell-associated viraemia and to viral distribution throughout the lymphoid tissues.