W. L. Mengeling

“ EPIDEMIOLOGY Porcine parvovirus is ubiquitous among swine throughout the world. In major swine-producing areas such as the midwestern United States, infection is enzootic in most herds, and with few exceptions sows are immune. In addition, a large proportion of gilts are naturally infected with PPV before they conceive, and as a result they develop an active immunity that probably persists throughout life. ”

“ Low levels of antibody found to be protective allow speculation that, once the immune system has been primed with PPV, subsequent exposure to virulent virus during gestation is unlikely to result in transplacental infection even if antibody from vaccination is no longer detected (Mengeling et al. 1979) .
Vaccination is recommended also for seronegative sows and boars. Seronegative sows are usually found only in PPV-free herds; in such cases, inactivated vaccine is indicated. Experience has shown that few herds can be expected to remain free of PPV even if access is carefully controlled. ”

“ 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. ”

“ The primary significance of passively acquired antibody is that it interferes with the development of active immunity. High levels of such antibody can prevent infection, and lower levels can minimize dissemination from infected pigs (Suzuki and Fujisaki 1976; Paul et al. 1980) . Consequently, some groups of gilts are not fully susceptible to infection and dissemination of virus until either shortly before conception or during early gestation. ”

“ Infected cells commonly seen in the lung of fetuses that develop a high titer of antibody for PPV probably represent this stage of replication (see Fig. 17.8C) . Affected cells subsequently round up, become pyknotic, and disintegrate with release of virus and viral antigen (Fig. 17.2B) . Other cells in the culture that are not at the appropriate stage to support viral replication continue to phagocytize and accumulate viral antigen in their cytoplasm (Fig. 17.2C) . ”

“ 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) . ”

“ Gilts should be either naturally infected with PPV or vaccinated for PPV before they are bred. To promote natural infection, a common practice is to arrange contact between seronegative gilts and seropositive sows, with the expectation that one or more of the sows will be shedding virus. Moving gilts to a potentially contaminated area, either currently or recently inhabited by seropositive swine, also can be recommended. ”

“ Several mummified fetuses (<16 cm in length) or lungs from such fetuses, if sufficiently developed, should be submitted to the diagnostic laboratory. Larger mummified fetuses (i.e., more than about 70 days of gestational age) (Marrable and Ashdown 1967) , stillborn pigs, and neonatal pigs are not recommended for submission unless they are the only samples available. If infected, their tissues will usually contain antibody that interferes with laboratory tests for either virus or viral antigen. ”

“ These lesions were believed to be pathognomonic for PPV infection (Narita et al. 1975) . Similar lesions have been observed in PPV-infected, live fetuses collected late in gestation (Hogg et al. 1977; Joo et al. 1977) (Fig. 17.7B) .
Both general types of microscopic lesions (i.e., necrosis and mononuclear cell infiltration) may develop in fetuses infected near midgestation (Lenghaus et al. 1978) when the immune response is insufficient to provide protection. ”

“ Hemadsorption, secondary adult porcine thyroid cells, guinea pig erythrocytes, 22 hours after thyroid cells were infected and then subcultured (May-Grünwald-Giemsa; ×100) . Several investigators have used IF microscopy to follow the development of PPV in cell culture (Cartwright et al. 1969; Lucas and Napthine 1971; Mengeling 1972; Siegl et al. 1972; Bachmann and Danner 1976) . In general, the sequence of events is as follows. Viral antigen is detected in the cytoplasm of cells soon after infection if the inoculum contains a high titer of virus and viral antigen. ”

“ Vaccines are used extensively in the United States and in several other countries where PPV has been recognized as an economically important cause of reproductive failure. All federally licensed vaccines marketed in the United States are inactivated. ”

“ 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. ”

“ Ruckerbauer et al. 1978) and age (Morimoto et al. 1972a) of the donor—may quantitatively affect results. The HA test is most commonly conducted at room temperature, at approximately neutral pH, and with guinea pig erythrocytes. ”

“ These are normally only a minor component of the disease. The presence of mummified fetuses in a litter can prolong both gestation (Narita et al. 1975) and the farrowing interval (Mengeling et al. 1975) . Either may result in stillbirth of apparently normal littermates, whether or not they are infected.
17.3. Cryostat-microtome sections of tissues from PPV-infected 8-week-old pigs, examined by IF microscopy (×312.5) . (A) Viral antigen in germinal center, tonsil. (B) Viral antigen in osteogenic layer of periosteum, rib: a = connective tissue, b = cortical bone, c = marrow cavity. ”

“ Parvoviruses as contaminants of permanent human cell lines. III. Biological properties of the isolated viruses. Arch Gesamte Virusforsch 38:369-382.
Hogg, G. G.; Lenghaus, C.; and Forman, A. J. 1977. Experimental porcine parvovirus infection of foetal pigs resulting in abortion, histological lesions and antibody formation. J Comp Pathol 87:539-549.
Hohdatsu, T.; Baba, K.; Ide, S.; Tsuchimoto, M.; Nagano, H.; Yamagami, T.; Yamagishi, H.; Fujisaki, Y.; and Matumoto, M. 1988. Detection of antibodies against porcine parvovirus in swine sera by enzyme-linked immunosorbent assay. ”