Effects on pig production from the type-2 porcine circovirus (PCV2) are well described, causing large increases in wasting, poor production and high mortality. But we now have a number of effective vaccines against the virus.

Vaccination -- why is it proving so successful?

The virus is small and as a result has to be relatively simple. It is not enveloped or covered in a protective layer and therefore its outer capsid protein layer is very exposed and strongly immunogenic. The virus also appears to be easily inhibited by circulating antibodies, when it is released outside the cell and found in the blood (viraemia).

However, in the susceptible pig, the virus damages the immune system it grows in the cells which would normally stimulate an immune response and would produce antibodies and defensive cells to fight against it.

PCV2 is a DNA virus and the capsid protein is formed by a piece of DNA termed the open-reading frame 2 (ORF2). All the vaccines are based on this. The vaccines are either a killed whole virus (Circovac Merial) or a conjugated virus based on a non-pathogenic virus PCV1, but with the ORF2 DNA inserted into it to produce the capsid protein (Suvaxyn PCV2 Fort Dodge/Pfizer). Others have inserted the ORF2 into a baculovirus system to produce a purified capsid protein, which is then included into the vaccine (Ingelvac CircoFlex - Boehringer Ingelheim; Circumvent PCV - Intervet/Schering-Plough).

All of the vaccines appear to give a good immunological response, but each has its own advantages and disadvantages. Some of the adjuvants that carry the antigen are quite irritant and have been associated with injection-site reactions. In fact a powerful adjuvant is not really necessary in this case, unlike those commonly used with mycoplasma vaccines. The capsid protein is a good antigen and stimulates the antibody response to stop the viraemia, which is associated with all the major damage to the pig's health and mortality. By contrast, Mycoplasma hyopneumoniae lives on the surface cells in the respiratory tract and does not circulate in the bloodstream, so it is a completely different target.

Why do we have sow and piglet vaccines?

The sow vaccine, Circovac, was the first vaccine to appear in many countries. Its concept was that the piglet has an early exposure to the virus (which was the case at the start of the outbreaks of PMWS) and maternally-derived antibodies would therefore offer the best protection. As the virus grows in the piglet's cells and is released into the blood stream, the maternal antibodies would neutralise it and stimulate the piglets own immunity. It has also been reported to improve reproduction and the number of live piglets.


With the development of natural immunity in many herds the pattern of infection appears to have shifted, so that the viraemia takes place much later, often in the finishing barns. By then, the levels of maternal antibodies have declined and may not be sufficient to stop the development of the disease. The sow vaccine approach appears to work better where the viraemia and mortality due to the disease is below 10 weeks of age. Recent work in multi-site production in Spain showed that the peak viraemia and mortality occurred much later, at about 14 weeks, than on mainly single-site production units in Denmark where the peak age was 10-11 weeks.

Piglet vaccines can be given as early as two weeks of age, but commonly at weaning. Usually, immunity will start at about two weeks after vaccination. Therefore they offer protection from four to six weeks old until slaughter. It explains their popularity, especially in multi-site producing countries such as the USA and Canada. In the UK, where most of the big producers are multi-site, approximately 67% of piglets coming through are being vaccinated.

What are the cost/benefits of vaccination?

I think even the vaccine companies were surprised by the uptake of the vaccines, especially the piglet ones. In North America, piglet vaccines were marketed since November 2006 and the total percentage of pigs vaccinated is approximately 90% of the population. In Europe one can easily predict that they will be as successful as the mycoplasma vaccines. Sow vaccination is approximately one-third the cost of piglet vaccination on a herd basis, as there are fewer animals to vaccinate, but the returns on piglet vaccines are also good because of their outstanding long-term efficacy.

In a recent check on herds using piglet vaccines I found that even those with very mild infections (no mortality) had increased average production/pig by 2.5kg liveweight, which easily covers the cost of vaccination. Eevery one per cent increase in mortality is accompanied by another 0.5kg of average weight loss, so the cost/benefit grows very rapidly. It just shows what effect fighting the viraemia has on growing pigs.

What about the future -- are mutant strains expected?

This is always difficult. A mutation from PCV2a to PCV2b has been discovered, which seems to be more pathogenic. However, all the vaccines are based on PCV2a and they seem to work incredibly well. Currently, there is no information to suggest that circo-vaccines work less efficiently against any of the virus variants. It is worth mentioning that the viral capsid-protein mutations are still below 10% different.

PCV2 is a different virus to PRRS virus, which is an enveloped, RNA virus, where we have seen a much greater diversity in strains. I like to think that it is more like parvovirus, which is also a very small, non-enveloped DNA virus, where the vaccines have been successfully employed for over 25 years.