Porcine parvovirus (PPV), a virus in the species Ungulate protoparvovirus 1 of genus Protoparvovirus in the virus family Parvoviridae, 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).
Signs and symptoms
Acute infection of postnatal pigs, including pregnant dams that subsequently develop reproductive failure, is usually subclinical. However, in young pigs and probably in older breeding stock as well, the virus replicates extensively and is found in many tissues and organs with a high mitotic index. Viral antigen is especially concentrated in lymphoid tissues (Fig. 3A, B). Many pigs, irrespective of age or sex, have a transient, usually mild, leukopenia sometime within 10 days after initial exposure to the virus. PPV and other structurally similar viruses have been identified in the feces of pigs with diarrhea. However, there is no experimental evidence to suggest that PPV either replicates extensively in the intestinal crypt epithelium or causes enteric disease as do parvoviruses of several other species. PPV also has been isolated from pigs with lesions described as vesiclelike. The causal role of PPV in such lesions has not been clearly defined.
The major and usually only clinical response to infection with PPV is maternal reproductive failure. Pathologic sequelae depend mainly on when exposure occurs during gestation. Dams may return to estrus, fail to farrow despite being anestrus, farrow few pigs per litter, or farrow a large proportion of mummified fetuses. All can reflect embryonic or fetal death or both. The only outward sign may be a decrease in maternal abdominal girth when fetuses die at midgestation or later and their associated fluids are resorbed. Other manifestations of maternal reproductive failure, namely, infertility, abortion, stillbirth, neonatal death, and reduced neonatal vitality, also have been ascribed to infection with PPV. These are normally only a minor component of the disease. The presence of mummified fetuses in a litter can prolong both gestation and the farrowing interval. Either may result in stillbirth of apparently normal littermates, whether or not they are infected.
There is no evidence that either fertility or libido of boars is altered by infection with PPV.
Cause
PPV is classified in the genus Parvovirus (Latin parvus = small) of the family Parvoviridae. All isolates of PPV that have been compared have been found antigenically similar if not identical. PPV is also antigenically related to several other members of the genus. However, its identity can be established by relatively stringent serologic tests such as virus neutralization (VN) and hemagglutination inhibition (HI).
Biophysical and biochemical properties
The biophysical and biochemical properties of PPV have been extensively studied and are summarized as follows. A mature virion has cubic symmetry, two or three capsid proteins, a diameter of approximately 20 nm, 32 capsomeres, no envelope or essential lipids, and a weight of 5.3 × 106 daltons. The viral genome is single-stranded deoxyribonucleic acid (DNA) with a molecular weight of 1.4 × 106 (i.e., about 26.5% of the weight of the complete virion). Buoyant densities (g/mL in cesium chloride) of complete infectious virions, incomplete "empty" virions, and extracted virion DNA are 1.38–1.395, 1.30–1.315, and 1.724 respectively. Viral infectivity, hemagglutinating activity, and antigenicity are remarkably resistant to heat, a wide range of hydrogen ion concentrations, and enzymes.