The index herd with PMWS in Sweden: Presence of serum amyloid A, circovirus 2 viral load and antibody levels in healthy and PMWS-affected pigs
© Wallgren et al; licensee BioMed Central Ltd. 2009
Received: 22 October 2008
Accepted: 27 March 2009
Published: 27 March 2009
Postweaning Multisystemic Wasting Syndrome (PMWS) is an emerging disease in pigs of multifactorial origin, but associated to porcine circovirus type 2 (PCV2) infection. PMWS was first diagnosed in Sweden at a progeny test station that received pigs aged five weeks from 19 different nucleus herds on the day after weaning. The objective of this study was to examine, for the first time in an index outbreak of PMWS, the relationship between PCV2 virus, antibodies to PCV2 and serum amyloid a (SAA) in sequentially collected serum samples from pigs with and without signs of PMWS.
Forty pigs of the last batch that entered the station at a mean age of 37.5 days were monitored for signs of PMWS during the first 55 days after arrival. Serum was collected on six occasions and analysed for presence of PCV2 DNA and antibodies to PCV2, as well as for levels of SAA.
Four of the pigs (10%) were concluded to have developed PMWS, with necropsy confirmation in three of them. These pigs displayed low levels of maternal antibodies to PCV2, more than 107 PCV2 viral DNA copies per ml serum and failed to mount a serological response to the virus. Starting between day 23 and 34 after arrival, an increase in PCV2 viral load was seen in all pigs, but PCV2 did not induce any SAA-response. Pigs that remained healthy seroconverted to PCV2 as the viral load was increased, regardless of initially having low or high levels of PCV2-antibodies.
In this index case of PMWS in Sweden, pigs affected by PMWS were not able to mount a relevant serum antibody response which contributed to the disease progression. The maximal PCV2 virus load was significantly higher and was also detected at an earlier stage in PMWS-affected pigs than in healthy pigs. However, a viral load above 107 PCV2 DNA copies per ml serum was also recorded in 18 out of 34 pigs without any clinical signs of PMWS, suggesting that these pigs were able to initiate a protective immune response to PCV2.
Postweaning multisystemic wasting syndrome (PMWS) is a disease of pigs first recognised in Canada in 1991 that now is a global epizootic [1–3]. PMWS is regarded as a multifactorial disease although infection of pigs with porcine circovirus 2 (PCV2) is recognised as an essential component of the disease process. A difference in pathogenecity between various isolates of PCV2 has been suggested [4–8], but it is also generally accepted that the presence of other infectious or non-infectious factors is required for the development of the full clinical disease [9–12]. Experimental studies in colostrum deprived piglets have demonstrated that such factors can include co-infection with other microbes such as porcine parvovirus [9, 10, 13], porcine reproductive and respiratory syndrome virus [14, 15] or Mycoplasma hyopneumoniae , but PMWS could also be induced by PCV2 in combinations with either immunsostimulators  or immunosuppressors . Experimental infections in both conventional and specific pathogen-free (SPF) pigs with tissue homogenates from PMWS-affected weaners have also induced mild PMWS [19, 20]. In these experiments, all inoculated pigs seroconverted to PCV2, but not to any other known virus or bacteria. Transmission of PMWS has also been demonstrated by mixing healthy weaners with PMWS-affected pigs in previously emptied and cleaned facilities . However, the reasons why some pigs develop PMWS while other pen mates remain healthy is still not clear [12, 22].
PMWS was diagnosed for the first time in Sweden at a progeny test station in December 2003 . As a consequence the station was closed down, but all pigs present at the station were reared to the weight of 100 kg before closure. To date there have been no reports in the literature on the investigation of the health status related to the load of PCV2 in blood, the level of antibodies to PCV2 virus and serum amyloid A (SAA) determined in sequentially collected serum samples from an on-going index case of PMWS. Within the last batch of pigs reared at the test station, this was determined in 40 pigs that also were monitored closely for clinical signs of PMWS.
Initial health status of the animals
Pigs in Sweden are free from all diseases listed by the Office International des Epizooties (OIE), including Aujeszky's disease (AD), porcine reproductive and respiratory syndrome (PRRS), and also from porcine endemic diarrhoea (PED) and transmissible gastro-enteritis (TGE). The animals in this study emanated from purebred nucleus herds also declared free from atrophic rhinitis (toxin producing strains of Pasteurella multocida), Salmonella spp, swine dysentery (Brachyspira hyodysenteriae) and mange (Sarcoptes scabiei). Infections with Mycoplasma hyopneumoniae and Actinobacillus pleuropneumoniae are widespread in the conventional pig population in Sweden, but the influence of these diseases has decreased since the 1990s due to the commonly performed age segregated production from birth to slaughter .
Herd, animals and experimental design
The present study that was conducted at a progeny test station was approved by the ethical committee in Uppsala, Sweden (C38/4). The test station was established in March 2002, and introduced intensified rearing strategies previously not used in the country with the aim of improving genetic selection. Briefly, boars from 19 nucleus herds (pure bred Landrace, Yorkshire or Hampshire) were allocated to the test station on the day after weaning at the age of approximately five weeks. On arrival they were mixed with boars of the same age from other herds, and the animals were remixed according to weight every fortnight four times before entering the pen for individual testing. During the individual test period the boars were still group housed, but individually fed via transponders.
In December 2003 PMWS was diagnosed in this herd as the index case of Sweden  by employing the internationally accepted criterias for diagnosing PMWS at individual and herd levels [25, 26], As a consequence, the station was closed down, but animals already at the station were reared to echo-sounding at market weight before being slaughtered.
Herd of origin, breed, mean weight and age of the 40 pigs examined.
Herd of origin
PCV2 antibodies Range
Not PMWS – PMWS
41.3 ± 1.2
11.9 ± 10.6
2.2 – 2.8
1 – 0
36.5 ± 1.3
10.8 ± 0.9
2.2 – 3.1
1 – 1
39.0 ± 0.8
10.1 ± 1.6
2.2 – 3.1
0 – 1
39.5 ± 1.3
13.3 ± 2.0
2.2 – 2.8
36.8 ± 2.2
10.8 ± 0.7
2.5 – 3.4
33.3 ± 3.3
11.5 ± 1.0
2.2 – 3.1
33.5 ± 5.7
10.7 ± 1.9
2.2 – 2.8
0 – 1
39.8 ± 4.9
11.3 ± 2.1
2.2 – 3.1
40.3 ± 2.9
12.1 ± 2.0
2.2 – 3.7
35.3 ± 3.7
11.9 ± 1.4
2.5 – 3.1
0 – 1
2.2 – 3.7
2 – 4
37.5 ± 4.0
11.4 ± 1.6
Collection of blood and analyses performed
Blood samples without additives were collected by jugular vein punctures on days 9, 17, 23, 34, 43 and 55 after arrival. The sera were separated and stored at -20°C until analysed.
Presence of PCV2 in individual serum samples was measured using a quantitative real time PCR assay previously described ., with a detection limit of 1,100 DNA copies per ml (Log 3.04). In brief, nucleic acids were extracted from 200 μl serum using an EasyMag nucleic acid extractor (Biomerieux, Durha, USA) and eluted in 55 μl elution buffer. For the quantitative PCR, 2.5 μl of each elute was run in a 25 μl reaction with primers and probe previously described  on an MxPro 3005 PCR machine (Stratagene, La Jolla, USA). The detection limit of the PCR was 1.1 × 103 (10 Log 3.04) genome copies per ml serum, and results are presented as 10-logaritms.
Antibodies specific to PCV2 in serum were measured using an immuno-peroxidase-monolayer-assay (IPMA) method previously described. . In brief, freshly trypsinized cells of the PCV-free continuous cell line PK15 A were inoculated with PCV 2 (Stoon-1010) . The inoculated cell-suspension was seeded in 96-well cell culture plates and incubated for 5 days at 37°C (5% CO2). The culture medium was removed and the cells were washed with physiological saline. The plates were then fixed in 99.5% ethanol for one hour. The ethanol was removed and glycerol (87%) diluted 1:1 in PBS was added and the plates were kept at -20°C until further use. The glycerol was removed and the plates were washed with PBS containing 0.05% Tween (PBS-T). The serum samples were diluted in PBS-T with 5% fat-free milk powder in a total volume of 100 μl and the plates were incubated for 1 hour at 20°C. After washing with PBS-T the plates were incubated with HRP-conjugated rabbit anti-swine immunoglobulins (DakoCytomation, Glostrup, Denmark) diluted in PBS-T with 5% fat free milk for 1 hour at 20°C. The plates were washed with PBS-T and 50 μl of a substrate solution of 3-amino-9-ethylcarbazole with 0.05% H2O2 in 0.05 M Na-acetate buffer, pH 5, was added to the wells and the plates were incubated at 20°C for 15 minutes. The reaction was stopped by replacing the substrate with sodium acetate buffer and the results were examined with a microscope.
The antibodies specific to PCV2 were measured in individual serum samples diluted in twofold dilutions from 1:10 to 1:20,480 (Log 1.0 to Log 4.3), The results are presented as Log 10 levels of the antibody titres and seroconversion between two consecutive samplings was defined as an increase with at least two titre steps, corresponding to an increase with at least Log 0.6.
The serum levels of the acute phase protein Serum Amyloid A (SAA) were analysed using a commercial kit (Serum Amyloid A Assay TP-802, Tridelta, Maynooth, Ireland) according to the instructions of the manufacturer. The results are presented as mg SAA per L serum.
All results in the text are given as mean values ± standard deviations. Groups of pigs were compared using Student's t-tests in pair wise comparisons between groups. For comparisons within groups over time, consecutive recordings were compared with each other using paired t-tests.
The six pigs denoted as "thin" within the first 55 days after arrival to the test station.
Denoted as thin
DWG (from birth)
Day after arrival
Status Day 55 after arrival
Diagnose at necropsy
In four of the six pigs diagnosed as having PMWS (Table 2), the wasting coincided in time with serum levels of PCV2 exceeding 107 per ml. None of these pigs showed a clear seroconversion to PCV2 in relation to this increased serum load of PCV2 (Figure 1). As outlined above the remaining two "thin pigs in this group showed an active seroconversion to PCV2. A serum antibody titer of Log 4 was recorded in pig 1037 on day 43, but this pig had been attended as "thin" on day 32, preceded by PCV2 viral loads of 107.7 and 108.5 per ml serum on day 17 and 23, respectively, without seroconverting at that time (antibody levels Log 2.2 and Log 2.5, respectively). Pig 1037 was diagnosed with PMWS by necropsy on day 46, but the load of PCV2 had decreased to below 107 per ml serum at day 43. Thus it cannot be excluded that this pig was in an early phase of recovery from PMWS at the time for necropsy.
Increasing (p < 0.01) amounts of antibodies to PCV2 was observed from day 17 after arrival in the group with low amounts of maternal antibodies that remained healthy, and a clear seroconversion (p < 0.001) to PCV2 was observed in both the healthy groups between day 34 and 43 after arrival (Figure 2). In contrast, antibody levels in the four pigs diagnosed with PMWS did not increase (p = 0.22) between days 34 and 43, and all four pigs that developed PMWS were dead on day 55. As seen in figure 1, the two "thin" pigs that survived until slaughter showed a clear seroconversion to PCV2 in relation to increased PCV2 virus levels in serum.
Time point and magnitude for the maximal PCV2 loads in serum
Day after arrival
33.5 ± 8.2
8.9 ± 0.4
P < 0.001
p < 0.001
Healthy, low level of maternal antibodies
36.7 ± 5.7
7.3 ± 1.0
p < 0.05
Healthy, high level of maternal antibodies
39.8 ± 9.1
6.5 ± 0.9
p < 0.05
Mean levels of Serum amyloid A (SAA) in serum (mg per L).
Day after arrival
Healthy pigs, low level of maternal antibodies
Healthy pigs, high level of maternal antibodies
(n = 4)
(n = 17)
(n = 17)
424 ± 475
148 ± 306
115 ± 250
24 ± 17
27 ± 33
57 ± 76
111 ± 114
134 ± 304
94 ± 134
39 ± 26
57 ± 62 *
17 ± 8 *
92 ± 120
71 ± 109
31 ± 41
38 ± 75
42 ± 87
The close examination of 40 randomly selected pigs suggests that four pigs denoted as "thin" actually developed PMWS. This was confirmed by necropsies in three of them, and necropsy still is the golden standard for diagnosing PMWS in individual pigs [1–3, 26]. It is notable that all PMWS-affected pigs had low levels of maternal antibodies to PCV2, and that none out of the 17 pigs with high levels of maternal antibodies to PCV2 developed clinical signs resembling PMWS. This concurs well with suggestions that antibodies to PCV2 can hinder the development of PMWS [30–33]. The IPMA-method used in this study does not measure truly neutralising antibodies, but a positive correlation between neutralising antibodies and total amount of antibodies has previously been reported [34, 35].
Results from the present study support the important role of the maternal immunity in preventing development of PMWS, as also suggested by others [31, 36]. However, Table 1 shows that every nucleus herd sending pigs to the station had delivered individual pigs with low levels of maternally derived antibodies to PCV2, i.e. pigs that potentially could develop PMWS but did not. This is consistent with an earlier report showing that some farm pigs with low levels of PCV2 antibodies in serum did not develop PMWS whereas some pigs with higher levels did . The present study confirms this finding and suggests that low levels of maternal antibodies to PCV2 in piglets do not necessarily lead to development of PMWS. Indeed, 17 pigs with low levels of antibodies to PCV2 on arrival remained free from PMWS. These pigs responded better to the PCV2 exposure than pigs developing PMWS in terms of a rapid development of antibodies to PCV2. Pigs that developed PMWS basically did not seroconvert to PCV2 as they became diseased. The absence of a proper immune response to PCV2 in these pigs undoubtedly contributed to the excessive proliferation of PCV2 which is commonly seen in pigs affected by PMWS [25, 1–3].
As stated above, every nucleus herd had sent pigs that potentially could develop PMWS to the test station. Accordingly PMWS had been diagnosed by necropsies in pigs from every nucleus herd that had delivered pigs to the test station as previously reported . As clinical signs resembling PMWS significantly less often had been attended in pure bred conventional Hampshire boars (2.8%; n = 497) than in pure bred conventional Yorkshire (8.8%; n = 509) or Landrace boars (11.3; n = 655) , a genetic difference in resistance to development of the disease between breeds may be indicated. This has also been indicated by others, suggesting a lower resistance towards development PCV2-associated lesions of Landrace pigs [38, 39]. However, the station mixed pigs from different sources and also the effect of stressors and pathogen load at the herds of origin should be taken into account. Indeed, there was a variation in the incidence of pigs with clinical signs resembling PMWS within breeds depending on the herd of origin .
A higher level of PCV2 genome copies in serum was recorded in pigs that developed PMWS than in pigs that remained healthy. All four PMWS-affected pigs had expressed levels well above log 7 of PCV2 per ml serum. However, serum concentrations above log 7 of PCV2 per ml were also recorded in several pigs that were not denoted as "thin" (11 out of 17 pigs with low, and in 7 out of 17 pigs with high levels of maternal antibodies), which makes detection of PCV2 virus in serum unsuitable as a single diagnostic tool to diagnose PMWS. However, as significantly lower peak levels of PCV2 were recorded in pigs with high levels of maternal antibodies, an important role of antibodies to PCV2 in preventing an excessive proliferation of the virus was again indicated [30–33, 35].
It has been reported that an unrestrained growth of PCV2 in pigs with low levels of serum antibodies with concurrent infections and/or another stressor are required for development of PMWS [1–3, 40]. Production of high levels of SAA in pigs can be indicative of acute bacterial infections , and SAA has also been reported to be increased in pigs diseased with PCV2 . However, these authors compared the serum levels of several acute phase proteins in pigs of different sources and ages affected by different diseases with that of SPF pigs aged ten weeks, and it cannot be ruled out that the levels of acute phase proteins they reported could have been partly age and herd dependent . Such an effect of age has previously been shown with respect to the acute phase protein haptoglobin . Furthermore, individual serum levels of both pig-MAP and haptoglobin in PCV2 negative pigs could exceed that of equally aged PCV2-positive pigs in the same herd . In the present study, no association between SAA levels and PCV2 viral load was detected. Instead, the concentrations of SAA peaked on day nine after arrival, mirroring the effect of mixing pigs of different origin and thereby exposing them to an unfamiliar flora of microorganisms [45, 46]. Accordingly, this peak in SAA concentrations is likely to decay over time due to an adaption of the immune system to the new environmental flora , and acute phase proteins appears to be less valuable as indicators for PMWS.
In conclusion, the higher PVC2 viral load observed in pigs that developed PMWS agrees with suggestions of the importance of a rapid and relevant immune response in preventing PMWS [30–33]. The peak viral load was also seen earlier in pigs that developed PMWS, possibly indicating an impaired immune function in pigs developing PMWS. However, it is also of interest that a majority of the pigs with low maternally derived antibodies to PCV2 did not develop PMWS. This study was carried out in a progeny test station allocating and mixing recently weaned piglets at an early age. Thus, both the age of the pigs in relation to stressors, as well as their age at weaning, may be of importance for the development of PMWS.
We wish to thank the staff at the test station for collecting the samples and for their good book keeping, which they shared with us. We also would like to thank Maria Persson for skilful technical assistance. This work was supported by grants from EU, Project No: 513928 within the Sixth Framework Programme, from Formas, from the Swedish Farmers Foundation for Agricultural Research and from the Norwegian Research Council Project No. 14328601.
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