Experimental reproduction of postweaning multisystemic wasting syndrome (PMWS) in pigs in Sweden and Denmark with a Swedish isolate of porcine circovirus type 2.

An experimental model using 3-day-old snatch-farrowed colostrum-deprived piglets co-infected with porcine circovirus type 2 (PCV2) and porcine parvovirus (PPV) is at present one of the best methods to study factors affecting development of postweaning multisystemic wasting syndrome (PMWS). A Swedish isolate of PCV2 (S-PCV2) retrieved in 1993 from a healthy pig has been used in this model to reproduce PMWS in pigs from Northern Ireland. This virus has been present in the Swedish pig population for at least a decade without causing any known PMWS disease problems, despite its potential pathogenicity. The reasons for this are unknown, but could be related to genetics, absence of triggers for PCV2 upregulation (infectious agent and/or management forms) within Swedish pig husbandry. In order to confirm the pathogenicity of S-PCV2, Swedish and Danish pigs were experimentally infected with this isolate according to the established model. Swedish pigs were also infected with a reference isolate of PCV2 (PCV2-1010) to compare the severity of disease caused by the two isolates in Swedish pigs. Both Danish and Swedish pigs developed PMWS after the experimental infection with S-PCV2. Antibodies to PCV2 developed later and reached lower levels in serum from pigs infected with S-PCV2 than in pigs inoculated with PCV2-1010. In general, pigs infected with S-PCV2 showed more severe clinical signs of disease than pigs infected with PCV2-1010, but pigs from all PCV2-inoculated groups displayed gross and histological lesions consistent with PMWS. All pigs inoculated with PPV, alone or in combination with PCV2, displayed interleukin-10 responses in serum while only pigs infected with PPV in combination with PCV2 showed interferon-alpha in serum on repeated occasions. Thus, the pathogenicity of S-PCV2 was confirmed and a role for cytokines in the etiology of PMWS was indicated.

Postweaning multisystemic wasting syndrome--PMWS. the first year with the disease in Sweden.

Postweaning multisystemic wasting syndrome (PMWS) is causally associated with porcine circovirus type 2 (PCV2) infection of pigs. PCV2 has been present in the Swedish pig population for at least ten years. Despite this, no signs of PMWS were observed in pigs of Sweden until 2003. Since then the disease has spread slowly in Sweden. The pig population of Sweden is geographically isolated, the density of pigs and the pathogen load in the country is low and the trade of animals is organised in a restricted way. To date, there has been little information placed in the peer-reviewed literature on the study of the spread of PMWS in a country during the early phase of the disease outbreak, mainly because diagnosis of PMWS has only occurred after the disease has been recognised on a number of farms. This manuscript documents the studies to date on the PMWS outbreak in Sweden which has been closely monitored since the initial outbreak of diseases on a single farm in 2003 was diagnosed. In Sweden PMWS was officially reported for the first time at a progeny test station during December 2003. One year later sixteen herds have been diagnosed and reported to the authorities: one progeny test station, one nucleus herd, thirteen piglet producers or integrated herds and one specialised fattening herd. Fifteen suspected cases have been deemed negative for PMWS with disease scenarios associated with Lawsonia intracellularis, Brachyspira pilosicoli, Mycoplasma hyopneumoniae, shortcomings in feed composition etc. To date, one year after the index case was reported ten other herds suspected for PMWS are under observation. The PMWS cases are concentrated into the southern part of Sweden. However, the disease is spreading slowly, and in general there are no obvious physical links between affected herds. The data generated to date in Sweden suggest that introduction of a new contagious microbe into the country that is responsible for the PMWS outbreaks appears unlikely, as does the spread of PMWS via semen.