Porcine parvovirus
![Figure 1. Cell cultures infected with PPV. (A) Cytopathic effect, secondary fetal porcine kidney cells, 120 hours after infection (×250).[41] (B) Hemadsorption, secondary adult porcine thyroid cells, guinea pig erythrocytes, 22 hours after thyroid cells were infected and then subcultured (May-Grünwald-Giemsa; ×100).](/uploads/202502/03/Diseases_of_Swine_17-14357.png)


![Figure 5. Segment of uterus opened to show necrotic remnants of a partially resorbed PPV-infected embryo
(arrows) and associated extraembryonic membranes of a gilt experimentally infected oronasally immediately after breeding and killed 22 days later; remnants are laden with virus and viral antigen. Bar = 1 cm.[81]](/uploads/202502/03/Diseases_of_Swine_17-54357.png)
Porcine parvovirus (PPV) causes reproductive failure of swine characterized by embryonic and fetal infection and death, usually in the absence of outward maternal clinical signs. The disease develops mainly when seronegative dams are exposed oronasally to the virus anytime during about the first half of gestation, and conceptuses are subsequently infected transplacentally before they become immunocompetent. There is no definitive evidence that infection of swine other than during gestation is of any clinical or economic significance. The virus is ubiquitous among swine throughout the world and is enzootic in most herds that have been tested. Diagnostic surveys have indicated that PPV is the major infectious cause of embryonic and fetal death. In addition to its direct causal role in reproductive failure, PPV can potentiate the effects of porcine circovirus type II (PCV2) infection in the clinical course of postweaning multisystemic wasting syndrome (PMWS).