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 (Cartwright and Huck 1967; Mengeling 1978b; Thacker and Leman 1978; Vannier and Tillon 1979; Mengeling et al. 1991).
ETIOLOGY
PPV is classified in the genus Parvovirus (Latin parvus = small) of the family Parvoviridae (Siegl 1976; Bachmann et al. 1979). All isolates of PPV that have been compared have been found antigenically similar if not identical (Cartwright et al. 1969; Johnson and Collings 1969; Morimoto et al. 1972a; Johnson et al. 1976; Ruckerbauer et al. 1978). PPV is also antigenically related to several other members of the genus (Cotmore et al. 1983; Mengeling et al. 1986, 1988). However, its identity can be established by relatively stringent serologic tests such as serum neutralization (SN) and hemagglutination inhibition (HI).
Biophysical and Biochemical Properties
The biophysical and biochemical properties of PPV have been extensively studied (Siegl 1976; Molitor et al. 1983; Berns 1984) 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 × 10 daltons. The viral genome is single-stranded deoxyribonucleic acid (DNA) with a molecular weight of 1.4 × 10 (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.
Replication
Replication of PPV in vitro is cytocidal and characterized by "rounding up," pyknosis, and lysis of cells (Fig. 17.1A). Many of the cell fragments often remain attached, eventually giving the affected culture a ragged appearance. Intranuclear inclusions develop (Cartwright et al. 1969) but they are often sparsely distributed (Rondhuis and Straver 1972). Infected cultures may hemadsorb slightly (Cartwright et al. 1969) (Fig. 17.1B). Cytopathic changes are extensive when cell culture-adapted virus is propagated under appropriate conditions. However, on initial isolation several serial passages of the virus (Cartwright et al. 1969) or, better, the infected culture may be necessary before the effects are recognized. The use of immunofluorescence (IF) microscopy greatly increases the likelihood of detecting minimally infected cultures (Lucas and Napthine 1971; Mengeling 1975).
Primary and secondary cultures of fetal or neonatal porcine kidney cells are most often used for propagation and titration of PPV, although other kinds of cultures are also susceptible (Pirtle 1974). Replication is enhanced by infection of mitotically active cultures (Mayr et al. 1968; Cartwright et al. 1969; Bachmann 1972; Hallauer et al. 1972). Many cells in such cultures are in the S phase (i.e., the DNA synthesis phase) of their cell cycle, wherein the DNA polymerases of cell origin needed for viral replication are available (Tennant 1971; Siegl and Gautschi 1973a, b).