return to Swine Manual index


Porcine parvovirus (PPV) can cause reproductive failure in naïve dams. It is characterized by the occurrence of large numbers of mummified fetuses, an increase in the number of returns to estrus, small litters, failures to farrow, decreased farrowing rate, and rarely abortion.


Porcine parvoviral infection (PPV) is endemic in most swine herds. It usually is subclinical and a very common infection. Prior to porcine reproductive and respiratory syndrome (PRRS), PPV was probably the most commonly diagnosed infectious cause of reproductive failure in swine. Reproductive failure is much more likely to occur in gilts than in sows. PPV occurs worldwide in major swine-raising countries.

Historical information

The earliest publication about PPV occurred in 1967. Within a few years the disease was identified as a major cause of reproductive failure. Much of the research on PPV was done in the 1970s and 1980s. Most details regarding the virus and the disease it causes are now known. Losses from PPV now are well controlled, largely by vaccination, and clinical effects of PPV are now less prevalent.

Many manifestations of reproductive failure seen with PPV accompany other reproductive diseases of swine and should not be considered pathognomonic for PPV.


The disease is caused by a porcine parvovirus (PPV). All isolates are similar antigenically. PPV is quite resistant to environmental degradation and many disinfectants. It persists for at least 4 months on contaminated premises. The virus hemagglutinates many kinds of erythrocytes, a feature useful in its laboratory identification. Porcine parvovirus does not cause diarrhea in swine although related parvoviruses do so in several other species.


Parvoviral infection is endemic in most swine herds. Following infection, virus is shed in the secretions and excretions from the animal for approximately two weeks. An infected dam will disseminate virus in feces and fluids, including placental fluids and mummified fetuses. Fetuses infected during gestation can be born as infected, immunotolerant piglets that can pass the virus intermittently or continuously but the significance or likelihood of this phenomenon is unknown. Because parvovirus is quite resistant to environmental influences, contaminated facilities are an important source of exposure.

Oronasal transmission can occur among susceptible swine of all ages. Surprisingly, surveys show that many herds with endemic infection contain some animals that are susceptible.

Transplacental infection of embryos and fetuses is the result of dams failing to develop an active immunity prior to pregnancy. Passive immunity persists in some gilts beyond the time they are old enough to be bred. This interferes with their development of an active immune response to natural or vaccine exposure (active immunity usually develops following exposure of gilts to parvovirus in the environment as passive immunity wanes). Gilts with little or no immunity can be infected during their first pregnancy. If infected during pregnancy, virus may cross the placenta and infect some, or all, of their embryos or fetuses.

It is likely that PPV can be transmitted through semen or artificial insemination since it has been isolated from the semen of naturally infected boars. Also, boars may transmit virus mechanically.


Pregnant, infected dams develop a viremia during the acute phase of PPV infection. Virus then may cross some or all of the separate placentas of developing embryos or fetuses. Fetal infection during the first 35 days of gestation causes death and resorption of embryos, resulting in irregular returns to estrus or reduced litter size. Infection between 35 and 70 days of gestation results in fetal death and mummification. Since fetuses become immunologically competent by about the 70th day of gestation, fetuses older than that may successfully resist infection and survive.

After one embryo or young fetus is infected, the virus may slowly spread through the uterus and infect some or all of the others. The direct effect of PPV on the uterus, as can be seen microscopically in experimental dams, probably contributes to reproductive failure.

The death of embryos and fetuses is attributed to the direct destructive effect of parvovirus on their organs and tissues. Many kinds of cells are affected, especially mitotically active capillary endothelium and neurons. Extensive endothelial cell damage may be reflected in damage to many organs.

Clinical signs

In most swine a transient leukopenia occurs within ten days of infection with PPV. However, this and any other indication of infection are inapparent in all swine except developing fetuses. Infection of a naïve herd of pregnant females results in irregular return of bred animals to estrus, increased numbers of mummified fetuses, smaller litter size, increases in animals checked positive for pregnancy that fail to farrow, and prolonged gestation lengths. The increase in mummified fetuses after a normal gestation period is the hallmark of PPV. Abortions attributable to this virus are rare.


Gross lesions are not apparent in the dams. The most important lesion observed with parvoviral infection is mummified fetuses. In experimentally infected dams, nonspecific microscopic and gross lesions are described but are of no diagnostic value.


The lack of illness in the dams, coupled with increased mummies, irregular return to estrus and decreased litter size, primarily in gilts, is suggestive of PPV infection. A tentative diagnosis can be confirmed by demonstrating PPV antigen in the lungs of several mummified fetuses using immunofluorescent microscopy. The preferred specimen for diagnosis is the lung tissue from several mummified fetuses less than 16 cm long. Larger fetuses are not satisfactory since their tissues may contain antibody that interferes with the procedure.

It is possible but rarely practiced, to isolate the virus and identify it by hemagglutination and hemagglutination inhibition (HI) tests. Virus isolation usually is more difficult and time consuming than diagnosis through demonstration of viral antigen in fetal cells.

Sometimes antibody can be demonstrated in fluids or sera from stillborn pigs or presuckle neonatal live pigs. While this may indicate intrauterine infection with PPV, there is considerable likelihood of false positive serologic reaction from these specimens. Serology from breeding animals may be difficult to interpret since cross-sectional sampling will often reveal a wide range of titers. Demonstration of seroconversion in many gilts and sows with paired serology also may be used for a positive diagnosis but acute samples are often not available. Conversely, the absence of titers may aid in exclusion of PPV as the cause. If mummies are not available for evaluation, efforts should concentrate on gilt serology, comparing titers from unmated gilts to those exhibiting signs of infertility.


Probably the best way to prevent PPV infection is to vaccinate all susceptible breeding stock twice, 2 weeks apart, several weeks before breeding. Killed vaccines are available and effective. They should stimulate an active immunity in the dams that will protect the developing fetuses. Alternatively, seronegative stock can be exposed to a herd of seropositive older stock and used for breeding only after seroconversion. Some of those should be shedding virus that would stimulate development of an active immunity. There is no effective treatment for PPV infection.