Porcine Parvovirus - Lesions

Lesions

Neither macroscopic nor microscopic lesions have been reported for nonpregnant pigs. It is conceivable that cellular infiltrations subsequently described for fetuses could be induced by infection during the perinatal interval.

Macroscopic lesions have not been reported in pregnant dams; however, microscopic lesions have been seen in tissues of gilts killed after their fetuses were infected by transuterine inoculation of virus. Gilts that were seronegative when their fetuses were infected at 70 days of gestation had focal accumulations of mononuclear cells adjacent to the endometrium and in deeper layers of the lamina propria when they were killed 12 and 21 days later. In addition, there were perivascular cuffs of plasma cells and lymphocytes in the brain, spinal cord, and choroid of the eye. When fetuses were infected earlier in gestation (35, 50, and 60 days) and their dams were killed 7 and 11 days later, the lesions were similar. However, uterine lesions were more severe and also included extensive cuffing of myometrial and endometrial vessels with mononuclear cells. Only focal accumulations of lymphocytes were seen in uteruses of gilts that were seropositive when their fetuses were infected.

Macroscopic changes of embryos are death followed by resorption of fluids (Fig. 4) and then soft tissues (Fig. 5). Virus and viral antigen are widely distributed in tissues of infected embryos and their placentas, and it is probable that microscopic lesions of necrosis and vascular damage, subsequently described for fetuses, also develop in advanced embryos.

There are numerous macroscopic changes in fetuses infected before they become immunocompetent (Fig. 6). These include a variable degree of stunting and sometimes an obvious loss of condition before other external changes are apparent; occasionally, an increased prominence of blood vessels over the surface of the fetus due to congestion and leakage of blood into contiguous tissues; congestion, edema, and hemorrhage with accumulation of serosanguineous fluids in body cavities; hemorrhagic discoloration becoming progressively darker after death; and dehydration (mummification). Many of these changes also apply to the placenta. Microscopic lesions consist primarily of extensive cellular necrosis in a wide variety of tissues and organs (Fig. 7A). Inflammation and intranuclear inclusions also have been described.

In contrast, macroscopic changes have not been reported for fetuses infected after they become immunocompetent for PPV. Microscopic lesions are primarily endothelial hypertrophy and mononuclear cell infiltrations consistent with an immune response. Meningoencephalitis characterized by perivascular cuffing with proliferating adventitial cells, histiocytes, and a few plasma cells was seen in the gray and white matter of the cerebrum and in the leptomeninges of PPV-infected stillborn pigs. These lesions were believed to be pathognomonic for PPV infection. Similar lesions have been observed in PPV-infected, live fetuses collected late in gestation (Fig. 7B).

Both general types of microscopic lesions (i.e., necrosis and mononuclear cell infiltration) may develop in fetuses infected near midgestation when the immune response is insufficient to provide protection.