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Post-weaning multisystemic wasting syndrome (PMWS) and other porcine circovirus type 2 (PCV2)-related diseases have been reported throughout the world for about 10 years. The present paper reviews the knowledge acquired in different fields and is largely based on the authors' experience. The horizontal transmission of PCV2 is widely documented. Contact between pigs is the main route of transmission for both PCV2 and PMWS. However, experimental inoculation of PCV2 to pigs does not give consistent results and severe clinical signs as encountered in the field are rarely obtained. It is thus acknowledged that additional conditions are required for the disease to be severe in growing pigs. These are not all known but co-infections are thought to act as triggers. The spread of such triggers/enhancers, which may or may not be infectious, could have played a role in PMWS dissemination via normal national and international trade, in some cases conferring an epidemic pattern to this spread. Most of the risk factors identified in surveys relate to poor biosecurity and inadequate hygiene/husbandry/herd management. The good correlation between viral burden in the tissues and disease severity emphasized the role of infection pressure. Genomic analysis showed great similarities between PCV2 isolates. However, although two main genotypes (genogroups) could be distinguished from the phylogenic trees, and changes with time, no clear relationship with strain virulence was apparent. Isolates detected in PMWS-positive pigs could also be detected in healthy pigs from healthy farms. A strong sow effect was observed in disease expression in the offspring. Colostrum composition and colostrum intake are supposed to be key components of disease expression. Medication is relatively inefficient as a control measure. Commercial PCV2 vaccines are now becoming available. However, losses as a result of PMWS and PCV2-related diseases are greatly reduced by applying appropriate hygiene and husbandry practices.

The effect of different Parvovirus+Erysipelas vaccination schemes in PCV2-infected sows on PMWS outcome in the offspring was investigated under experimental conditions. Six PCV2-free sows were first infected oro-nasally with PCV2 two months before insemination (D0; "Day 0") and then by the intra-uterine route at insemination (D62). On D21 and D42, vaccinated sows received either the two commercial monovalent vaccines, A1(PPV) and A2(Erysipelas), or the bivalent vaccine B (PPV+Erysipelas). In addition, three SPF sows (foster-sows) were synchronized for farrowing dates to enable them to foster piglets born to infected sows and removed at birth before colostrum intake. A significantly higher proportion of mummified fetuses was obtained from PCV2-infected non-vaccinated sows than from vaccinated sows. Acute myocarditis lesions were found in their piglets, together with a high PCV2 genome load. The latter was significantly higher than in those born to PCV2-infected vaccinated sows. Sentinel PCV2-negative piglets, born to SPF foster-sows, seroconverted at almost the same time as piglets without PCV2 passive immunity and born to infected sows. Sixteen of the 84 liveborn piglets born to infected sows and foster-sows were affected by a syndrome possibly related to PMWS, as judged by clinical signs and histological lesions. Most were born to PCV2-infected non-vaccinated sows and 12/16 did not receive PCV2 passive immunity. The probability of PCV2 infection and the number of PCV2 genome copies per gram of tissue were significantly increased in piglets that did not receive PCV2 passive immunity.

Abstract: We assessed, using a modelling approach, the influence of several management practices within a farrow-to-finish farm on the age of PCV-2 infection. The impact of PCV-2 vaccination with different vaccination schemes on infection dynamics, was also tested. A stochastic individual-based model describing the population dynamics in a typical French farrow-to-finish pig farm was built and coupled with an epidemiological model of PCV-2 infection. The parameters of the infectious model were mainly obtained from previous transmission experiments. Results were subjected to a survival analysis of time-to-infection. For each comparison, the reference situation was no vaccination followed by random mixing of piglets after birth and after weaning. The risk of early infection was significantly reduced when mixing of piglets was reduced at different stages (avoiding cross-fostering and grouping piglets by litters in small pens after weaning, hazard ratio (HR) =0.52 [0.46; 0.59]). Sow-targeted vaccination delayed the infectious process until the waning of passive immunity and piglet-targeted vaccination considerably decreased the force of infection leading to a dramatic decrease of the total number of infections (HR=0.44 [0.37; 0.54]). The effect was even more pronounced when strict management measures were applied (HR=0.24 [0.19; 0.31]). Changing from a low (3%) prevalence of PCV-2-infected semen to a higher one (18%) significantly increased the risk of early infections (HR=1.36 [1.2; 1.53]), whereas reducing replacement rate or changing sow housing from individual crates to group housing had a limited impact on PCV-2 dynamics. [Copyright &y& Elsevier]

Transmission characteristics of PCV2 have been compared between vaccinated and non-vaccinated pigs in experimental conditions. Twenty-four Specific Pathogen Free (SPF) piglets, vaccinated against PCV2 at 3 weeks of age (PCV2a recombinant CAP protein-based vaccine), were inoculated at 15 days post-vaccination with a PCV2b inoculum (6 ⋅ 10 5 TCID 50 ), and put in contact with 24 vaccinated SPF piglets during 42 days post-inoculation. Those piglets were shared in six replicates of a contact trial involving 4 inoculated piglets mingled with 4 susceptible SPF piglets. Two replicates of a similar contact trial were made with non-vaccinated pigs. Non vaccinated animals received a placebo at vaccination time and were inoculated the same way and at the same time as the vaccinated group. All the animals were monitored twice weekly using quantitative real-time PCR and ELISA for serology until 42 days post-inoculation. The frequency of infection and the PCV2 genome load in sera of the vaccinated pigs were significantly reduced compared to the non-vaccinated animals. The duration of infectiousness was significantly different between vaccinated and non-vaccinated groups (16.6 days [14.7;18.4] and 26.6 days [22.9;30.4] respectively). The transmission rate was also considerably decreased in vaccinated pigs ( β = 0.09 [0.05–0.14] compared to β = 0.19 [0.11–0.32] in non-vaccinated pigs). This led to an estimated reproduction ratio of 1.5 [95% CI 0.8 – 2.2] in vaccinated animals versus 5.1 [95% CI 2.5 – 8.2] in non-vaccinated pigs when merging data of this experiment with previous trials carried out in same conditions. [ABSTRACT FROM AUTHOR]