Updating on the epidemiology of PCV2 and implications

Is the PCV2 a "new" virus in the swine population?

We have knowledge about the existence of the PCV2 since 1998 as a result of the search for the cause of clinical outbreaks described as of 1991. These outbreaks caused mainly a poor growth rate in the growing stage and an increased mortality in the pigs at the end of the weaner stage and at the beginning of the fattening stage, and the name given to this pathological condition was postweaning multisystemic wasting syndrome or PMWS (currently it has been suggested to call it PCV2-associated systemic disease, or PCV2-SD). The main epidemic outbreaks took place in Europe and Asia between 1998 and 2004, whilst in the American continent they happened between 2004 and 2007. Nevertheless, we have proof, through retrospective studies, of the existence of animals infected with the PCV2 since 1962 at least, and of animals with PCV2-SD since 1985 at least.

Is the PCV2 a frequent virus?

Since the first description of the PCV2 in 1998, the presence of the virus in all the countries in which it has been looked for has been shown, demonstrating that it is a ubiquitous virus at a worldwide level. In the same way, almost the 100% of the commercial farms are infected with PCV2, and almost all the pigs are PCV2-seropositive at the end of the fattening period. The worldwide distribution of the PCV2-SD has been described, just as it is shown in Figure 1.

Figure 1. Countries in which the PCV2-SD has been diagnosed (yellow-coloured).

How is the PCV2 transmitted?

The animals infected with PCV2 spread the virus through all the examined excretion routes, and the virus has been detected in the nasal cavity, the oral-tonsil secretion, the bronchial secretion, saliva, the eye secretion, faeces, urine, milk and semen. The main transmission route is the oronasal route, although the PCV2 has a high resistance in the environment, and even the airborne transmission is possible.

In a farm, the breeding animals are the ones that maintain the infection and transmit it to their offspring, normally via the horizontal route during the lactation. Nevertheless, the vertical transmission in this group of animals has also been described.

The information about the PCV2 infection dynamics in a farm can be looked up in a previous article: Effect of the viraemia due to the porcine circovirus type 2 (PCV2) on production parameters.

The potential infective ability of semen has only been demonstrated under experimental conditions, happening after the intraperitoneal inoculation of infected semen in piglets or reproducing the PCV2-associated reproductive disease after inseminating sows with experimentally-infected semen. Until now the transmission of the infection to the sow or the foetuses after the insemination with naturally-infected semen has not been described. So, these experiences suggest that the infection due to semen is not a frequent nor easy fact, because the usual viral load may not be sufficiently high to be infective.

What is its relatively recent pathogenic behaviour due to?

There is not a simple explanation for the fact that the PCV2, an ubiquitous virus, was associated with the epidemic appearance of a disease in a relatively sudden and global way. It is very possible that there are different aspects related to pig production and the international trade that can explain it partially. Nevertheless, what we know today is that this change in the clinical presentation from sporadic to epidemic is associated with a change in the prevalence from genotype PCV2a to genotype PCV2b. An example of this situation is shown in the data taken in Spain in Figure 2. On the other hand, there are some studies that show a higher probability of reproducing the disease using PCV2b rather than PCV2a inocula.

Figure 2. Detection frequency of PCV2a and PCV2b in Spain (adapted from Cortey et al., 2011 Vet J)

In this sense, a curious datum is the existence of a cross protection that genotype "a" confers against genotype "b", because the commercial vaccines that exist currently are based on virus with the first genotype.

Which factors can have an influence on the expression of the PCVDs¹?

The clinical profile that the animals can develop depends on multiple factors, as for example their age, their active or passive immune protection, the infection pressure, the individual viral load, the transmission route, the physiological situation (moment during the gestation), as well as the presence of concomitant infections and environmental factors. So, many epidemiological studies have described a series of risk factors associated with the development of the PCV2-SD that are described in Table 1 (we must clarify that it is a compilation of the results obtained in different studies, generally with an exploratory objective, where on occasions the biological association is not evident a priori in some of the cases, and they can be spurious effects).

Table 1. Factors related to the increase or the decrease of the risk of developing PCV2-SD.

¹PCVDs: Porcine Circovirus Diseases.