Porcine parvovirus

General information

Porcine parvovirus (PPV) infection is not a common cause of reproductive failure in breeding pigs throughout Australia as most pork producers now vaccinate for this disease. It is a complicated disease and well researched. A commercial vaccine is available to prevent PPV.

How porcine parvovirus causes disease

Porcine parvovirus is probably present in most piggeries, but producers should be aware that some piggeries are completely free of PPV. PPV-induced reproductive failure occurs when susceptible (non-immune) gilts and sows are infected during pregnancy. PPV does not cause disease at any other time apart from pregnancy. Natural infection in the pigs occurs following ingestion or inhalation of the virus. The PPV then circulates in the bloodstream, and in the pregnant pig crosses the placenta and infects the developing embryos and foetuses.

Following natural infection, active immunity develops that probably lasts for the pig's lifetime. If active immunity occurs before pregnancy, the developing piglets (embryos and foetuses) are not affected. At birth, the piglets receive maternal immunity in the colostrum from the sow and this maternal immunity lasts till up to 20 weeks of age. The greater the level of active immunity in the sow, the more maternal immunity she passes onto her piglets. Thereafter, natural infection with PPV can occur.

A pig recently infected with PPV excretes the virus in saliva and faeces for about two weeks following infection. The virus is hardy and can survive for up to 100 days outside the pig.

The boar can also be infected with PPV but does not produce any clinical signs. He can excrete the virus following infection and can pass it onto sows and gilts at mating.

Signs of disease

Porcine parvovirus causes reproductive failure in the non-immune pregnant pig. If infection occurs at days 0-30 of pregnancy, embryonic mortality can occur, resulting in returns to service and decreased litter size. The most obvious feature following infection at 30-70 days of pregnancy is the birth of mummified piglets. Mummification is the process of sterile digestion of the tissues of the piglets that die in the uterus after the skeleton has started to solidify. PPV-infection is also associated with stillbirths and weak-born pigs if infection occurs in the later stages of pregnancy. Abortion can also be the result of PPV-infection, but is not a common clinical sign of this disease. Overall, PPV-infection decreases the number of pigs born per sow per year.

The pattern of PPV-infection in a pig herd is of two types: endemic and epidemic. Endemic infection is continually present in the pig herd, causing a low but still significant level of continual reproductive loss. Endemic PPV-infection is most likely to be seen in the gilts that have not developed active immunity prior to mating. This endemic type of PPV is more commonly associated with large pig herds as they have a larger gilt population.

Epidemics can last 1-3 months, and its severity depends on the number of non-immune pregnant breeders in the herd. An epidemic will be more severe in a herd free of PPV-infection than in an endemically infected herd, but epidemics can occur in endemically infected herds every 3-4 years. Following an epidemic, endemic infection will occur for a variable period of time.

The high culling rate of sows and boars in modern pig units facilitates the disappearance of PPV. In effect, a pig herd could have a new population of breeding pigs every 3-4 years.


PPV-infection can be diagnosed by the presence of high levels of antibody (active immunity) in blood samples from breeding pigs. The isolation of PPV can be attempted from mummified foetuses, stillborn and weak-born piglets. The clinical symptoms of return to service, mummification and stillborn pigs are indicative of PPV-infection. However, other fertility diseases can produce similar clinical signs.


A commercial vaccine is available to prevent PPV-induced reproductive failure.

In a herd infected with PPV it is important that gilts attain active immunity before mating to ensure that they are protected during pregnancy. Infected herds with a large proportion of gilts to sows may not have active immunity to PPV. In some cases, these breeders have not come in contact with PPV as a gilt or at subsequent outbreaks in a piggery.

A number of methods can be used to produce active immunity in gilts prior to mating. Housing unmated gilts in uncleaned pens recently vacated by batches of older gilts may provide a contaminated PPV-environment. The feeding of dung from older gilts to young gilts has been suggested (feedbacking); however, this is not legal in all states of Australia. Likewise, following an outbreak of PPV- induced reproductive failure in a herd, the dung from affected gilts and sows can be fed to non-immune gilts and sows that are not pregnant. In some herds, mummified foetuses are used for feedbacking to non-pregnant gilts and sows to produce active immunity. This method is illegal in some Australian states because it is considered swill feeding, so check with your herd veterinarian. However, not all mummification of foetuses is due to PPV, and this practice of feedbacking is not totally reliable and can actually spread other diseases through the breeding herd.

A vaccination program provides the best method for preventing PPV-induced reproductive failure. The PPV status of a pig herd can be ascertained by blood sampling a cross section of the breeding herd. Blood samples can also be taken from unmated gilts to determine at what age they are losing their maternal immunity. This information is valuable if implementing a vaccination program for PPV for the first time.

In a herd being vaccinated for the first time, all breeding pigs, boars, sows and gilts should receive two doses of vaccine four weeks apart. A booster dose of vaccine is given every six months. Alternatively, in sows, the booster dose can be given at each weaning. Replacement gilts and boars require two doses of vaccine four weeks apart prior to mating, followed by the six-monthly booster dose.

Further information

Last updated 20 September 2010