Postweaning multisystemic wasting syndrome (PMWS) in Sweden from an exotic to an endemic disease

Postweaning multisystemic wasting syndrome (PMWS) is causally associated with porcine circovirus type 2 (PCV2) infection of pigs. PCV2 was first demonstrated in Swedish pigs in 1993, although the virus was almost certainly present in pigs in the country before that. Despite this, no signs of PMWS were observed in pigs of Sweden until the first outbreak was reported in 2003. The accumulated number of PMWS-affected herds have increased via 16 (2004) and 41 (2005) to 123 in December 2006. Of these herds, 30 (25%) have now been declared free from PMWS. However, a number of other herds have had individual pigs that have fulfilled the demands for PMWS at necropsy and 52 of these herds have been declared negative on herd basis after treatment for intestinal or respiratory diseases, and/or by correcting shortcomings in management of the herd including feed. Thus, individual cases of the disease have been observed in around 200 herds by the end of 2006 and PMWS is now regarded as an endemic disease 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 use of growth promoters (low dose antibiotics in feed) was prohibited in 1986. Additionally, the trade of animals in Sweden is organised in a restricted way. Because of these factors it is possible to conduct meaningful real-time studies on the transformation of PMWS in Sweden from being an exotic to an endemic disease in a three year time scale. Initially the PMWS cases were concentrated in the southern part of Sweden, but have gradually spread north. The PMWS-positive herds have, in general, had an effective production, but some management errors have constantly been observed in affected herds. Physical links between affected herds are often missing, and the data generated to date on the PMWS outbreaks in Sweden do not suggest an introduction of a new contagious microbe into the country that is responsible for the PMWS outbreaks, nor does PMWS appear to be spread via semen. In Sweden, intensity in rearing, disease preventing measures and immaturity of the piglets appear to be important as predisposing factors to PMWS and, as such, are discussed in this article.     

Reproduction of postweaning multisystemic wasting syndrome in pigs experimentally inoculated with a Swedish porcine circovirus 2 isolate.

In recent years, porcine circovirus type 2 (PCV2)-associated postweaning multisystemic wasting syndrome (PMWS) has been reported worldwide. However, to date, PMWS has not been reported in Sweden despite the demonstration of serum antibodies to a PCV2-like virus in Swedish pigs. This communication reports the experimental reproduction of clinical PMWS after inoculation of colostrum-deprived (CD) pigs, derived from a Northern Ireland herd, with an isolate of PCV2 virus recovered from a clinically normal Swedish pig that was necropsied in 1993. The clinical disease and histological lesions observed in CD pigs inoculated with this virus were indistinguishable from those observed in previous studies on CD pigs inoculated with a PCV2 virus isolate recovered from pigs with PMWS. These results highlight the disease potential of PCV2 isolated from regions apparently free of PMWS and suggest that the status of the host and its environment is an important factor in the development of clinical PMWS.     

The presence of co-infections in pigs with clinical signs of PMWS in The Netherlands: a case-control study

In this study, 60 pigs with clinical signs of post-weaning multisystemic wasting syndrome (PMWS) from 20 different pig herds and 180 control pigs (without clinical signs of PMWS) were examined to get more insights into the frequencies of porcine circovirus 2 infections and the presence of co-infections in pigs with and without clinical signs of PMWS in the Netherlands. Porcine circovirus type 2 was detected in 100% of the pigs with clinical signs of PMWS by virus isolation and/or PCR and in 50% of the pigs from PMWS-free herds. There was an association between the levels of infectious PCV2 and/or PCV2 DNA load and the severity of clinical signs as described for PMWS. A high variation in PCV2 antibody titres was found in the clinically affected pigs, and 27% of these pigs did not mount PCV2 antibody titres higher than 1:200. A concurrent infection of PCV2 and porcine reproductive and respiratory syndrome virus (PRRSV) was found in at least 83% of the pigs with clinical signs of PMWS and in 35% of the pigs from PMWS-free herds. Co-infections of European- and American-type PRRSV were detected only in PMWS herds and in one control herd with a history of PMWS clinical signs.     

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

Background

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.

Methods

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.

Results

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.

Conclusion

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.     

Dynamics of serum antibodies to and load of porcine circovirus type 2 (PCV2) in pigs in three finishing herds,affected or not by postweaning multisystemic wasting syndrome

Background

Despite that PMWS commonly affects pigs aged eight to sixteen weeks; most studies of PMWS have been conducted during the period before transfer to finishing herds. This study focused on PCV2 load and antibody dynamics in finishing herds with different PMWS status.

Methods

Sequentially collected blood samples from 40 pigs in each of two Swedish (A and B) and one Norwegian (C) finishing herds were analysed for serum PCV2-load and -antibodies and saliva cortisol. The two Swedish herds differed in PMWS status, despite receiving animals from the same sow pool (multi-site production). However, the PMWS-deemed herd (A) had previously also received pigs from the spot market. ResultsThe initial serum PCV2 load was similar in the two Swedish herds. In herd A, it peaked after two weeks in the finishing herd and a high number of the pigs had serum PCV2 levels above 10⁷ per ml. The antibody titres increased continually with exception for the pigs that developed PMWS, that had initially low and then declining antibody levels. Pigs in the healthy herd B also expressed high titres of antibodies to PCV2 on arrival but remained at that level throughout the study whereas the viral load steadily decreased. No PCV2 antibodies and only low amounts of PCV2 DNA were detected in serum collected during the first five weeks in the PMWS-free herd C. Thereafter a peak in serum PCV2 load accompanied by an antibody response was recorded. PCV2 from the two Swedish herds grouped into genotype PCV2b whereas the Norwegian isolate grouped into PCV2a. Cortisol levels were lower in herd C than in herds A and B.

Conclusions

The most obvious difference between the Swedish finishing herds and the Norwegian herd was the time of infection with PCV2 in relation to the time of allocation, as well as the genotype of PCV2. Clinical PMWS was preceded by low levels of serum antibodies and a high load of PCV2 but did not develop in all such animals. It is notable that herd A became affected by PMWS after errors in management routine, emphasising the importance of proper hygiene and general disease-preventing measures.     

Comparative serologic and virologic study of commercial swine herds with and without postweaning multisystemic wasting syndrome

A comparative serologic and virologic study was performed in pigs from 5 herds with postweaning multisystemic wasting syndrome (PMWS) and 2 herds without PMWS in Quebec. In each herd, 60 blood samples were collected at 4-wk intervals from pigs from 3 to 23 wk of age. The serum was evaluated for the presence of antibodies to porcine circovirus type 2 (PCV2) and porcine reproductive and respiratory syndrome virus (PRRSV), as well as for the presence of nucleic acid of PCV2, PRRSV, and porcine parvovirus (PPV), by means of the polymerase chain reaction (PCR). Serologic profiles for PCV2 were very similar in 6 of the 7 herds, including the 2 without PMWS, and were characterized by a gradual decrease in antibody titres from 3 until 11 wk of age, followed by seroconversion at 15 wk, and high PCV2 antibody titres thereafter in all pigs. Only starting at 11 to 15 wk of age could PCV2 viremia be detected, except in 1 herd, in which clinical signs were observed at 6 to 7 wk of age. A PCV2 viremia could be detected within the same pigs for a minimum of 8 wk, and the virus could still be detected in 41% of the serum samples obtained at 23 wk of age. The antibody level did not appear to influence the occurrence of disease, since titres were similar in pigs in the herds with or without PMWS. Infection with PRRSV, as demonstrated by PCR and seroconversion, preceded that of PCV2 by at least 1 mo in both types of herd. Both PRRSV and PCV2 were detected in some pigs in 5 of the 7 herds, including 1 herd without PMWS. Porcine parvovirus could be detected in serum by PCR in 2 herds with PMWS after the onset of clinical signs and also in 1 herd without PMWS. Genomic analysis of PCV2 strains identified in the herds without PMWS indicated complete or very high homology (99.4% to 100%) with the PCV2 strains identified in 4 herds with PMWS. In our field study, the triggering of PMWS in the herds could not be linked to coinfection with either PRRSV or PPV or to the use of a specific immunostimulant, such as vaccines, or to particular genomic differences between the PCV2 strains identified.     

Genomic analysis of PCV2 isolates from Danish archives and a current PMWS case-control study supports a shift in genotypes with time

Porcine circovirus type 2 (PCV2) is the primary cause of Postweaning Multisystemic Wasting Syndrome (PMWS) in pigs. PCV2, however, is found in both PMWS-affected herds and non-affected herds. The objective of this study was to clarify if PCV2 genome nucleotide sequences isolated from pigs from PMWS-affected herds and non-affected herds cluster phylogenetically in two separate groups. All isolates (45) belonged to PCV2 group 1 and shared a nucleotide sequence identity of 99.4-100% indicating a very homogeneous PCV2 population in Denmark. Phylogenetic analysis of the PCV2 isolates revealed no distinctive clustering of case- and control-herds suggesting that there is no link between PCV2 sequences and herd disease status. The appearance of only PCV2 group 1 isolates in this study (isolates from 2003/2004) led us to determine if PCV2 nucleotide sequences had changed in Denmark over time. Interestingly, all PCV2 isolates from before the first outbreak of PMWS (2001) belonged either to a new PCV2 group identified for the first time in this study and named group 3 (isolates from 1980, 1987 and 1990) or PCV2 group 2 (isolates from 1993 and 1996). The shift from PCV2 group 2 to 1 was confirmed on a more global scale by placing all full genome PCV2 sequences submitted to GenBank from 1997 to 2006 in either of the groups by phylogenetic analysis. The analysis showed that the shift happened in 2003 or even earlier. This may indicate that PCV2 group 1 is a more adapted form of PCV2 and possibly could be more pathogenic.     

Spatial and temporal patterns of pig herds diagnosed with Postweaning Multisystemic Wasting Syndrome (PMWS) during the first two years of its occurrence in Denmark

The clinical syndrome Postweaning Multisystemic Wasting Syndrome (PMWS) in pigs has emerged globally during the last decade. In October 2001, the first pig herd diagnosed with PMWS was reported in Denmark, and since then the number of herds diagnosed with PMWS has increased markedly. The etiology of PMWS is not well understood, but increased knowledge of the causal factors is prerequisite for applying preventive interventions. In this study we described the temporal (time of diagnosis), spatial (location of herds) and spatio-temporal pattern of Danish pig herds diagnosed with PMWS during the first two years after the first herd was diagnosed, and we tested for spatial and spatio-temporal clustering using scan statistics. The study population consisted of pig herds that during the study period (October 2001-September 2003) performed diagnostic submissions to the two major veterinary diagnostic laboratories in Denmark (6724 herds). Of these, 277 herds were diagnosed with PMWS. Two statistically significant spatial clusters of herds diagnosed with PMWS were identified. These clusters included 11% and 8% of the study herds, respectively. Within these two clusters the relative risk for a herd to be diagnosed with PMWS was twice as high as expected. One statistically significant spatio-temporal cluster was identified between February and May 2002. We discuss different hypotheses that could explain why pig herds diagnosed with PMWS were clustered both spatially and spatio-temporally, and conclude that the results support the hypothesis that PMWS is caused by introduction of a new, unidentified, pathogen into the Danish pig production.     

Use of register data to assess the association between use of antimicrobials and outbreak of Postweaning Multisystemic Wasting Syndrome (PMWS) in Danish pig herds

In 2001, the first case of Postweaning Multisystemic Wasting Syndrome (PMWS) was reported in the Danish pig population. During subsequent years, the number of affected farms increased exponentially. The aim of this study was to determine how this increase influenced the use of antimicrobials between 2002 and 2004. We used national register data of herd characteristics, antimicrobial usage and disease occurrence. The analysis included data on antimicrobial usage in 3371 pig herds with weaners and 7434 pig herds with finishers, which accounted for 56 and 82% of the national amount of antimicrobials prescribed to weaners (prescribed by 347 practitioners) and finishers (prescribed by 522 practitioners), respectively.The estimation of the effect of PMWS was done by comparing the amount of antimicrobials (measured as Animal Defined Daily Doses (ADDkg) used per pig-day at risk each month in each herd) used in herds before and after an outbreak of PMWS, and by comparing the amount of antimicrobials used in herds experiencing PMWS with the amount of antimicrobials used in herds not experiencing PMWS. The effects were estimated in a three-level (veterinarian/herd/study-month) linear mixed regression model with an autoregressive correlation of order 1 (AR1).We found that after a herd had experienced an outbreak of PMWS, the antimicrobial usage in weaners was increased for a year. During the first 3 months post outbreak the usage increased by 22%, followed by an increase of 7% during the next 4th to 12th month when compared to the pre-outbreak usage. There was a significant variation between herds in this effect. Additionally, in herds experiencing an outbreak of PMWS, the usage of antimicrobials before the outbreak was 37 and 19% higher in herds with weaners and finishers, respectively, compared to herds not experiencing PMWS.Generalisation of the results to the entire Danish pig population indicated that the increase of PMWS infected herds from almost zero to about 20% during a 4-year period resulted in a national increase of 4–5% in antimicrobials usage in weaners. The effect of PMWS on usage of antimicrobials in finishers was unclear.     

Transmission of different variants of PCV2 and viral dynamics in a research facility with pigs mingled from PMWS-affected herds and non-affected herds

Post-weaning Multisystemic Wasting Syndrome (PMWS) has been identified in most swine-producing countries worldwide. The disease has resulted in significant health challenges and economic damage to the swine industry. The aim of this study was to determine horizontal transmission of porcine circovirus type 2 (PCV2) and to examine viral dynamics in pigs in a controlled PMWS transmission study. In the study pigs from PMWS-affected herds and non-affected herds were permitted to have close contact (same pen), nose-to-nose contact (to pigs in neighbouring pens) or no physical contact (pen across the aisle and pens in other compartments). By DNA sequence analysis, eight variants of genotype PCV-2b were identified in the research facility. From the spread of these PCV2-variants it was concluded that PCV2 primarily infects through close contact and nose-to-nose contact. PCV2 genome sequences were obtained from selected pigs at arrival to the research facility and again when the same pigs developed PMWS. This analysis showed that pigs from PMWS-affected herds developed PMWS caused by the same variant of PCV2 as they carried when entering the research facility. In contrast, pigs from non-affected herds developed PMWS with PCV2-variants identified in pigs from PMWS-affected herds. This was probably connected to at least 10³ higher mean serum-titer of PCV2 in pigs from PMWS-affected herds as compared to pigs from non-affected herds at the beginning of the transmission study. The study further showed that pigs able to control the PCV2 infection, as measured by the PCV2-titer in serum, recovered clinically (pigs from PMWS-affected herds) or stayed healthy (pigs from non-affected herds). Like this, pigs with a PCV2 titer below 5 × 10⁸ copies/ml serum during the study period had a chance of recover from the PCV2 infection whereas pigs with PCV2 titers above 5 × 10⁸ copies/ml serum at any time point generally died from PMWS.     

Examination for a viral co-factor in postweaning multisystemic wasting syndrome (PMWS)

In order to test the hypothesis that a putative co-factor for the development of postweaning multisystemic wasting syndrome (PMWS) in pigs could be of viral origin, we performed extensive virological examinations on organ material from pigs diagnosed with PMWS originating from within a Danish PMWS-transmission study. Virus isolation attempts were carried out on a large panel of different cell types including primary pig kidney cells and lung macrophages, primary rabbit kidney cells and seven established cell lines (MARC-145, ST117, PK15, BHK21, HeLa, Vero, and MDCK). Although these represent cells with susceptibility to a wide range of known viruses, the results did not provide evidence for a specific virus other than PCV2 contributing to the development of PMWS. Furthermore, in order to test whether specific genotypes of PCV2 may trigger the switch from PCV2 infection to clinical disease, we compared complete DNA genome sequences of PCV2 derived from PMWS-positive as well as PMWS-negative pigs. On the basis of the DNA sequences, the PCV2 isolates were divided into two groups. Group 1 consisting of one isolate originating from a herd unaffected by PMWS, with group 2 consisting of nine isolates originating from four PMWS-affected herds, four PMWS-positive pigs plus one unaffected herd. The PCV2 genomes from the two groups showed 95.5% identity. Alignment analyses of the sequences encoding the replicase and capsid protein from group 1 and group 2 PCV2 isolates showed two amino acid differences encoded in the replicase protein, while 19 amino acid differences were predicted among the capsid protein sequences. The PCV2 DNA sequence analysis supports recent observations from studies in USA as well as Europe, which suggest that strain variations may influence the clinical outcome of PCV2 infection.     

Spatiotemporal patterns and risks of herd breakdowns in pigs with postweaning multisystemic wasting syndrome

A retrospective cohort study of 116 British pig farms was undertaken to investigate the epidemiological risk factors associated with herd breakdowns with postweaning multisystemic wasting syndrome (PMWS). Farmers reported the PMWS status of their herd (case definition 1) and, where applicable, when the disease was first suspected and what they observed; they described a prolonged increase in mortality in six to 16-week-old pigs that was not attributable to any disease known to be on their farm. There was over 90 per cent agreement on the farmers' PMWS status between the farmers and their veterinarians. Approximately 70 per cent of the breakdowns were confirmed at the laboratory (case definition 2) except during the outbreak of foot-and-mouth disease (FMD) in 2001 when it was reduced to 30 per cent. Porcine circovirus type 2 antigen was detected in pigs examined postmortem (case definition 3) in approximately 90 per cent of the farms with increased mortality. The breakdowns occurred initially in the south of England and spread west and north, as well as locally in a radial pattern from the affected farms, and there was strong statistical evidence that there was non-random space-time clustering. The risk of herd breakdowns with PMWS was not constant; therefore, for each case definition, three survival models were developed with outcome variable time to breakdown of between January 2000 and January 2001, February 2001 to September 2001 (during FMD) or October 2001 to December 2003. Exposures with a bivariable significance of P<0.20 were tested in three multivariable Cox proportional hazard models. From January 2000 to January 2001 the risk of a herd breakdown with PMWS for definitions 1, 2 and 3 was greater for farms with 600 or more breeding sows, and for definitions 1 and 3 there was an increased risk associated with the purchase of replacement gilts rather than using homebred replacements. For definitions 1 and 3 the farms where the nearest pig farm had no breeding pigs were at greater risk of a breakdown than those where the nearest farm had breeding stock, as were the farms where visitors were not requested to avoid pigs for more than three days before visiting the farm during the FMD outbreak. From October 2001, the associated risks were identical for all three case definitions; farms were at greater risk when they had 600 or more breeding sows, if visitors had not avoided contact with pigs for more than three days before visiting the farm, and when there was a farm with PMWS less than five miles away. The affected farms were more likely to have disease associated with porcine parvovirus, porcine reproduction and respiratory syndrome virus, erysipelas, Escherichia coli and salmonella. These exposures were positively associated with large herds and the farm being close to other pig farms, but did not remain in the final models for breakdown with PMWS, indicating that such farms may be at greater risk of many infectious diseases.     

The detection of porcine circovirus in the Australian pig herd

OBJECTIVE: To determine if porcine circovirus (PCV) type 1 (PCV1) or type 2 (PCV2) is present in the Australian pig herd, to conduct preliminary genetic characterisation of any viruses detected, and to determine if there is any obvious virological reason why post-weaning multisystemic wasting disease (PMWS), associated with PCV infection in other countries, has not been detected in Australia. DESIGN: Serum samples were collected from 14 randomly selected pig farms in Western Australia and used for detection of PCV antibody. Additional samples from one farm were obtained at 2-week intervals from pigs between 2 and 12 weeks of age to detect any age-associated variations in prevalence of infection. Veterinary practitioners from four Australian states submitted tissues of dead or unthrifty weaned pigs, and these were examined for evidence of PCV1 and PCV2 infection. PROCEDURE: Sera were tested for antibody to PCV using an indirect immunofluorescence assay (IFA). Tissues were tested for PCV1 and PCV2 genomic material using a multiplex PCR. RESULTS: PCV antibody was detected in approximately 30% of Western Australian pigs tested. PCV1 DNA was detected in tissue samples from Western Australia, South Australia and New South Wales and PCV2 DNA was detected in tissue samples from Western Australia, New South Wales and Queensland. Sequence analysis of the PCR products indicated the PCV1 and PCV2 present in Australia were very similar to strains in other countries where PMWS is endemic. CONCLUSION: Both PCV1 and PCV2 are present in Australia and the viruses present appear similar to those in countries with PMWS. The absence of PCV2-associated PMWS in Australia may be due to absence of essential secondary factors required for PCV2 to produce PMWS.     

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.     

Descriptive summary of an outbreak of porcine post-weaning multisystemic wasting syndrome (PMWS ) in New Zealand

CASE HISTORY: Investigations were conducted to determine the cause of an acute, multi-farm outbreak of porcine respiratory disease that included diarrhoea and subsequent loss of body condition in affected pigs. A definition for post-weaning multisystemic wasting syndrome (PMWS) including both clinical and pathological features, previously developed for the pig industry in New Zealand, was applied to the current outbreak. In addition to self-reporting by owners of affected farms, local veterinarians, disease and epidemiology consultants, and animal health officials from the Ministry of Agriculture and Forestry (MAF) were involved in conducting farm visits and submission of diagnostic specimens. CLINICAL FINDINGS AND DIAGNOSIS: Pathogens known to be endemic in the pig industry in New Zealand as well as likely exotic diseases were excluded as causative agents of the outbreak. Clinical signs including dyspnoea, diarrhoea, and rapid loss of body condition were consistent with the New Zealand case definition for PMWS. Interstitial pneumonia, pulmonary oedema, generalised lymph-node enlargement, and presence of porcine circovirus type 2 (PCV2) inclusion bodies were consistently identified in affected pigs. Classical swine fever virus (CSFv), Porcine reproductive and respiratory syndrome virus (PRRSv), and Influenza virus were ruled out, using molecular and traditional virological techniques. Spread of the disease between farms was hypothesised to be facilitated by locally migrating flocks of black-backed seagulls. The original source of the disease incursion was not identified. DIAGNOSIS: Based on the consistent presence of circovirus-associated lesions in lymphoid tissues in combination with generalised enlargement of lymph nodes, histiocytic interstitial pneumonia, clinical wasting, and poor response to antibiotic therapy, a diagnosis of PMWS was made. CLINICAL RELEVANCE: PMWS should be considered in the differential diagnoses of sudden onset of respiratory dyspnoea, diarrhoea, and rapid loss of body condition in young pigs in New Zealand pig herds.     

Induction of porcine post-weaning multisystemic wasting syndrome (PMWS) in pigs from PMWS unaffected herds following mingling with pigs from PMWS-affected herds

In this paper we present the results from two experimental studies (I and II) investigating whether post-weaning multisystemic wasting syndrome (PMWS) can be induced in pigs from PMWS unaffected herds by mingling with pigs from PMWS-affected herds and to observe whether transportation and/or mingling of healthy pigs from unaffected herds could induce PMWS.The studies comprised pigs from 12 different herds. Eight herds had PMWS while four were unaffected. All 12 herds were found to be infected with PCV2. Pigs from PMWS-affected herds were mingled with pigs from unaffected herds in four separate compartments in both study I and study II. In addition, in study II, four groups of pigs from unaffected herds were included. Two groups with pigs transported and mingled from unaffected herds and two groups with pigs which were only transported. The PMWS diagnoses on the individual pigs were based on lymphoid depletion, histiocytic proliferation and the presence of giant cells or inclusion bodies together with the demonstration of PCV2 in lymphoid tissue.Healthy pigs, in both studies, developed PMWS 4–5 weeks after mingling with pigs clinically affected with PMWS. None of the pigs from unaffected herds which had no contact with pigs from PMWS-affected herds developed clinical signs of PMWS. Transportation and mingling of pigs from PMWS unaffected herds in combination or alone was insufficient to provoke PMWS.     

Temporal distribution of porcine circovirus 2 genogroups recovered from postweaning multisystemic wasting syndrome affected and nonaffected farms in Ireland and Northern Ireland.

Porcine circovirus type 2 (PCV2) is now recognized as the essential infectious component of porcine postweaning multisystemic wasting syndrome (PMWS). PMWS was first recognized in high-status, specific pathogen-free pigs in Canada in 1991 and is now an economically important disease that affects the swine industry around the world. Recently, reports of genomic studies on PCV2 viruses indicated that 2 distinctive genogroups of PCV2 exist.4,10 This report involves the results of a study on the distribution of predominant PCV2 genogroups recovered from samples taken from PMWS-affected and PMWS-nonaffected farms on the island of Ireland over a 9-year period and the results of a study on PCV2 genogroup recovery from fecal samples taken from a farm in Northern Ireland from 2003 to 2005 that was first diagnosed as PMWS positive in August 2005. The results indicate that, although at least 2 distinct genogroups of PCV2 have been circulating on pig farms on the island of Ireland, there does not appear to be a direct relationship between infection with these different genogroups of PCV2 and the development of PMWS.     

Muco-cutaneous candidiasis in two pigs with postweaning multisystemic wasting syndrome

In two distinct commercial swine herds, poor weight gain and an increased number of animals showing wasting were observed among nursery and growing pigs. Cases of postweaning multisystemic wasting syndrome (PMWS) and infection with Haemophilus parasuis had been previously diagnosed in these herds. One growing wasted pig from each herd was necropsied and showed enlarged lymph nodes. Pseudomembranous material adhered to the dorsum of the tongue, soft and hard palate in case 1, and in case 2, fibrinous material was seen as whitish plaques on the oesophageal surface with hyperkeratosis of the non-glandular stomach. The main histological lesions in both cases were found in lymphoid tissues with a multifocal accentuated lymphohistiocytic infiltrate, areas of lymphoid depletion and intracytoplasmic inclusions in histiocytic cells in lymph nodes and Payer's patches. Focally, extensive ulceration was found in the stratified pavement epithelium of the tongue with necrosis and necrosuppurative infiltrate in case 1; in case 2, there was ulceration in the stomach with lymphohistiocytic infiltrate in the submucosa and ulceration in the mucosa of the oesophagus associated with yeast cells and pseudo-hyphae. Candida albicans was isolated from the oral cavity lesions. Immunohistochemistry of the lymph nodes was positive for porcine circovirus 2 (PCV2). The association between PMWS and mucocutaneous candidiasis reported here supports the potential immunosuppressive state of PMWS infected pigs.     

Descriptive summary of an outbreak of porcine post-weaning multisystemic wasting syndrome (PMWS) in New Zealand

CASE HISTORY: Investigations were conducted to determine the cause of an acute, multi-farm outbreak of porcine respiratory disease that included diarrhoea and subsequent loss of body condition in affected pigs. A definition for post-weaning multisystemic wasting syndrome (PMWS) including both clinical and pathological features, previously developed for the pig industry in New Zealand, was applied to the current outbreak. In addition to self-reporting by owners of affected farms, local veterinarians, disease and epidemiology consultants, and animal health officials from the Ministry of Agriculture and Forestry (MAF) were involved in conducting farm visits and submission of diagnostic specimens.

CLINICAL FINDINGS AND DIAGNOSIS: Pathogens known to be endemic in the pig industry in New Zealand as well as likely exotic diseases were excluded as causative agents of the outbreak. Clinical signs including dyspnoea, diarrhoea, and rapid loss of body condition were consistent with the New Zealand case definition for PMWS. Interstitial pneumonia, pulmonary oedema, generalised lymph-node enlargement, and presence of porcine circovirus type 2 (PCV2) inclusion bodies were consistently identified in affected pigs. Classical swine fever virus (CSFv), Porcine reproductive and respiratory syndrome virus (PRRSv), and Influenza virus were ruled out, using molecular and traditional virological techniques. Spread of the disease between farms was hypothesised to be facilitated by locally migrating flocks of black-backed seagulls. The original source of the disease incursion was not identified.

DIAGNOSIS: Based on the consistent presence of circovirusassociated lesions in lymphoid tissues in combination with generalised enlargement of lymph nodes, histiocytic interstitial pneumonia, clinical wasting, and poor response to antibiotic therapy, a diagnosis of PMWS was made.

CLINICAL RELEVANCE: PMWS should be considered in the differential diagnoses of sudden onset of respiratory dyspnoea, diarrhoea, and rapid loss of body condition in young pigs in New Zealand pig herds.     

Infection of pigs in Ireland with lymphotropic gamma-herpesviruses and relationship to postweaning multisystemic wasting syndrome

Three species of porcine lymphotropic herpesviruses (PLHVs) have been described but there are few reports on the distribution and prevalence of these viruses in domestic pigs. We aimed to determine the PLHV status of Irish commercial pig herds, and to this end spleens taken from 110 healthy adult pigs sourced from 22 geographically distributed farms in Ireland were analysed for PLHV DNA using novel species-specific polymerase chain reaction assays. We now report that PLHV infection is widespread in the Irish domestic pig population and that PLHV-1 infections are most common (74% of all animals tested), followed by PLHV-3 and PLHV-2 (45% and 21%, respectively) and that infections with multiple PLHV species were frequently detected. As the PLHVs are lymphotrophic agents, we also investigated if co-infection with PLHVs was linked to the development of porcine circovirus-2 (PCV2)-associated postweaning mutlisystemic wasting syndrome (PMWS), a disease characterised in part by histopathological lesions in lymphoid tissues. We examined the PLHV infection status of young animals on two farms that were experiencing outbreaks of PMWS. Overall the findings are further evidence of the widespread prevalence of PLHVs in domestic pigs and are a first indication that co-infection with PCV2 and PLHVs does not lead to the development of PMWS in the absence of other cofactors.