December 2020

Pork producers and veterinarians need to be aware that the porcine parvovirus (PPV) has been evolving into new strains.

The evolution of PPV and its implications for swine health management are discussed by Professor André Felipe Streck of the Institute of Biotechnology at the University of Caxias do Sul in southern Brazil.

It has been more than 50 years since it was shown that PPV causes stillbirths, mummified piglets, embryonic death and infertility, and we have had parvovirus vaccines to use in our swine breeding herds for at least the last 40 years. Does PPV still need to be investigated?

Yes. Porcine parvovirus is changing. With Professor Uwe Truyen in Leipzig, Germany, we performed some studies focused mainly on evolutionary aspects of the virus and observed the occurrence and distribution of new antigenic types. In my opinion, new PPV vaccines are needed that may induce a greater immune response and cover all of the prevalent strains.

You mentioned discovering new strains, have there been significant genetic changes in the virus since PPV was first reported in the mid-'60s?

The main divergence of this virus was introduced in the last 40 years. Most importantly, in recent years, new amino acids have been found in the external capsid, the part of the virus that has contact with the immune system of the host. In other words, we can see new antigenic profiles of this virus. These antigenic profiles were observed in strains from several countries, mostly in Europe.




Has this emergence of new variants coincided with an increase in submissions to diagnostic laboratories involving porcine parvovirus?

Yes, here in Brazil, we can observe a higher incidence in positive cases of porcine parvovirus and of mummification in our herds. Talking to colleagues from other countries, it is seen there as well. Usually we observe PPV in, say, 30-40 percent of our foetuses. That is a very huge number of incidents, especially if we remember that some diagnoses gave false negative results because the mummified samples reaching the laboratory were too autolysed. To test a mummified foetus you need someone to collect the foetus and bring it immediately to a freezer, then send it quickly to the lab. Sometimes this process can take some days or even some several weeks to perform, which can mean a foetus arrives in a condition that is no longer good for testing.

Have there been significant developments in PPV diagnosis in recent years?

The big difference with diagnosis of PPV came when we started to perform PCR for it in the '90s. That helped us a lot to discover new strains. Recently, the use of real-time PCRs has been important for showing the amount of DNA of this virus. With the technique, we can establish whether PPV was the primary cause of this mummification.

How and where is PPV infection seen in practice?

The only well established clinical sign of a PPV infection is maternal reproductive failure. In sows and gilts the important sign is mummification. At early gestation, infection can result in embryonic death followed by reabsorption of fluids and the soft tissues. From day 35 on, there can be mummification of a dead foetus. By 70 days of gestation, the foetuses already have some immune system and may resist virus infection. In infected litters it is common that not all foetuses are affected in the same way. Many times we have seen mummification in only a few foetuses and others in the litter manage to survive. When you see litters in which there are some mummified foetuses along with stillborn pigs and healthy, live piglets, that are coming from gilts, that’s the big hallmark of porcine parvovirus.

All the evidence tells us that porcine parvovirus occurs in at least two-thirds of sow herds in just about every country where pigs are produced. We can not really think about stamping it out, therefore we must live with it. In practice today, what is needed to a protect a sow herd against PPV?

First, vaccination must be continued. Here in Brazil, swine producers only vaccinate when they have cases of mummification. After a while they stop the vaccination again. Obviously, this causes a great circulation of the virus in their herds and the risk of reproductive failure. Second, in addition to the further development of vaccine technology and new technologies for the diagnostics of PPV, we must always monitor the field strains to understand the relationship with the vaccine used and also with pathogens. With this, we will be one step ahead of new infections.

Are the long established vaccines still effective for those new PPV strains?

I always say that the established PPV vaccines are still effective and we need to practise regular vaccination, but the process of vaccine product improvement should be continuous since we see that the virus also has a continuous evolution.

André Felipe Streck