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Porcine Parvovirus (PPV)

Porcine Parvovirus Infection

(209) Porcine Parvovirus Infection (PPV) is the most common and important cause of infectious infertility. Porcine parvovirus is a fairly tough virus that multiplies normally in the intestine of the pig without causing clinical signs. It is world-wide in its distribution.

If you test for it in your pig herd it is almost certain it will be present. It is therefore an infection you have to live with and manage. Whereas most viruses do not survive outside the host for any great period of time PPV is unusual in that it can persist outside the pig for many months and it is resistant to most disinfectants. This perhaps explains why it is so widespread and so difficult to remove from the pig environment.

To understand the role of PPV in reproduction it is important to realise that reproductive infection usually occurs without disease, but sometimes there is infection with reproductive disease. PPV is transmitted either by mouth or through the nose passing into the intestine where it multiplies and is passed out in faeces. If a pig becomes infected for the first time when it is not pregnant there are no clinical signs.

However, if the animal is pregnant and exposed for the first time in the first 55 days or so of pregnancy, the virus crosses the placenta killing piglets selectively. If the foetus is infected at less than 35 days of age, before there has been an opportunity for bone development, death results, followed by complete absorption and ultimately a small litter is born. If infection takes place between 30 and 55 days of pregnancy the foetuses die and they become mummified. Do not assume that all mummified pigs are caused by PPV infection. This is often not the case.

It takes 10-14 days from first infection for PPV to reach the piglets inside the uterus. From 70 days of age the immune system of the piglet has started to develop and it can therefore respond and protect itself from the virus. Thus if pregnant animals are infected for the first time after approximately 55 days of pregnancy there will be little evidence of disease. This is quite different to PRRS infection, which kills the foetus only after 70 days of age inside the womb and therefore very late mummified pigs are seen in this disease. Once inside the womb PPV spreads slowly from one foetus to another and as a result the sizes of mummified pigs will vary within the litter.

Clinical signs
Acute outbreaks of disease

  • Infection itself causes no clinical symptoms other than the presence of mummified pigs at farrowing. In acute outbreaks of disease the following occurs:
  • Small litters associated with embryo loss before 35 days
  • Mummified pigs of varying size, (30-160mm).
  • Increased numbers of stillbirths. These are associated with the delay in the farrowing mechanism which occurs because of the presence of the mummified piglet.
  • Abortions associated with PPV infection are uncommon.
  • There may be an increase in low birth weight piglets but neonatal deaths are not affected.
  • The acute disease episode often lasts for up to 8 weeks then wanes for 4-6 weeks, followed by smaller bouts of mummified pigs for a further 4-6 weeks.
  • The virus can take up to 4 months to infect all sows in a susceptible previously uninfected herd.
Sporadic disease in enzootic herds
  • This is seen in individual females which are infected for the first time. It is usually confined to gilts.
Records can assist in the diagnosis of PPV disease and the differences between the normal herd and the diseased herd are shown in Fig.6-4.

In acute herd outbreaks of disease involving many animals, litter size is reduced with the percentage of litters totalling less than 9 increasing from about 10 up to 40%. The numbers of mummified pigs, particularly associated with small litters are elevated and sows not in-pig may increase from 2 to 6%. Sows found not in-pig are due to either total embryo absorption before 35 days or complete foetal death and a pseudo-pregnancy.

In some cases the sow reaches the point of farrowing with normal udder development, even to the extent of producing milk, but there are no live births. An injection of prostaglandin to bring about farrowing yields mummified pigs that have been present inside the womb. These animals would not otherwise farrow because a live foetus is necessary to initiate farrowing. The above picture is only seen at this level in a susceptible herd, that is, with 50-70% of sero-negative breeding females. Such episodes are likely to occur in non-vaccinated herds every 3-4 years and arise because virus circulation ebbs and flows. During periods of low or no PPV activity a susceptible population gradually emerges.

Figures 6-4 and 6-4a

PPV infection results in high antibody levels in the serum which persist for long periods. You should appreciate that such levels do not necessarily mean that there is or has been a reproductive problem or a higher level of protection. For example, a titre of 1:2 will be equally as protective as a titre of 1:80,000. Blood sampling all the sows in a herd on one occasion only indicates the percentage of animals that have been exposed to parvovirus at some previous period which gives you an idea of the overall breeding herd immunity or susceptibility. Once an animal has been exposed to PPV it remains immune for the rest of its life.

From a practical standpoint the breeding herd may be in one of three phases.

  1. Serologically negative. In this situation all females are highly susceptible to infection and reproductive failure. This is an unusual situation but can occur occasionally in small herds, from which the virus can die out. In such herds if parvovirus is introduced there is a massive outbreak of reproductive disease: repeats, mummifications, not in pig and possibly a few abortions. Such herds should be vaccinated immediately.
  2. Endemic infection. Here PPV is continually circulating and 50-90% of animals are immune. However infection can take place in the early to mid pregnancy period in any negative animals and therefore there is a variable amount of disease. This was the typical picture prior to the availability of vaccines in large non-vaccinated herd. Intermittent outbreaks of disease occur, particularly in gilts and second parity females. As viral activity increases, so does immunity across the herd. When there are large numbers of immune animals there is little infection and the herd immunity gradually drops as old immune sows are culled.
  3. Disease in replacement gilts. This is common because at least 50% of gilts at point of mating may not have met PPV and therefore are susceptible. Up to a third of such animals may become infected in the first half of pregnancy resulting in reproductive failure.
Key points to parvovirus infection
  • The virus is widespread throughout all pig populations but it may disappear in small herds (<100 sows).
  • Infection is endemic (present all the time) in most pig units.
  • Once a pig is exposed there is a lifelong immunity.
  • Reproductive problems may appear every 3-4 years in a herd if vaccination is not carried out.
  • Parvovirus infection in a susceptible female can cause death of the embryo with absorption or death of the foetus with mummification.
  • The major signs are therefore small litter sizes, mummified pigs of different sizes, and increases in pseudo-pregnancies and not-in-pigs.
  • Abortion due to PPV is uncommon.
  • Maternal immunity may persist up to 7 months of age but only in a few gilts. (This interferes with vaccine response).
  • Up to 50% of gilts may be sero-negative at point of mating.

In the absence of any other signs of illness in the breeding females, PPV disease can be suspected by increases in mummified pigs and small litter sizes.

The important features are disease and death in the embryo and foetus from approximately 15-70 days of pregnancy. The mummified pigs can be examined by fluorescent antibody test in the laboratory to confirm the infection. Serology will not help because many sows are positive and normal.

Key points for recognising PPV disease

  • Small litters associated with variable sized mummified pigs occurring mainly in unvaccinated gilts or gilts vaccinated while still protected by maternal antibody.
  • Increased percentage of repeats.
  • No other signs of ill health in the breeding female or in individual affected animals.
  • Some gilts or sows progress to the point of farrowing but produce no live pigs.
  • A history of no vaccination programme in gilts..
  • Examine all afterbirths from sows carefully to see whether there are small mummified pigs present which vary in size.
  • Submit small mummified pigs (less than 150mm) from small litters to a laboratory for fluorescent antibody tests. These will confirm whether the foetus has died from PPV infection or not.
Similar diseases

An acute outbreak could be confused with aujeszky's disease (AD) (PR), PRRS, leptospirosis or certain forms of influenza but with PPV there are no other clinical signs in adult breeding stock, newborn piglets are healthy and fully active, and there are few or no abortions. It could also be confused with SMEDI due to enterovirus infection but this is uncommon and laboratory tests can differentiate them.


  • There is no treatment.
Management control and prevention
  • In an acute outbreak immediately vaccinate the breeding herd to prevent infection in those animals that are still sero-negative. Discuss with your veterinarian. Remember it will take 10 days for the first dose of vaccine to take effect.
  • If a sero-negative gilt is given a single dose of vaccine, the immune system is primed and a low antibody level is produced (1:64). Vaccination and stimulation of immunity by natural infection is sufficient to protect the litter from disease. It takes 10-14 days following infection from PPV to cross the placenta and infect the embryos or foetuses. If the infected breeding female has been vaccinated at some time in the past then when exposure to PPV takes place, there is rapid re-stimulation of the immune system (within 5-7 days). This is sufficient to prevent disease and to stimulate a permanent immunity.
  • Fig.6-5 shows the levels of disease in 69 herds over a 10 year period, prior to vaccination and over an eight year period following a single injection of suvaxyn parvo vaccine to gilts only. These results show that disease can be controlled by a single dose of vaccine even though serological tests demonstrated that PPV continued to circulate in all the herds. Discuss your vaccination policy with your veterinarian. Your situation may be different and he/she may advise two doses of vaccine followed by a once or twice yearly booster.

Parvovirus cannot be eradicated from a herd.


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