A cohort study of post-weaning multisystemic wasting syndrome and PCV2 in 178 pigs from birth to 14 weeks on a single farm in England.

Our hypothesis was that pigs that develop post-weaning multisystemic wasting syndrome (PMWS) are detectable from an early age with signs of weight loss and other clinical and serological abnormalities. Therefore, the objective of this study was to investigate the temporally varying and fixed events linked with the clinical incidence of PMWS by comparing affected and unaffected pigs in a cohort of 178 male piglets. Piglets were enrolled at birth and examined each week. Samples of blood were collected at regular intervals. The exposures measured were porcine circovirus type 2 (PCV2) antibody titres in all 178 and PCV2 antigen in a subset of 75 piglets. We also observed piglet health and measured their weight, and a post-mortem examination was performed by an external laboratory on all pigs between 6 and 14 weeks of age that died. From the cohort, 14 (8%) pigs died from PMWS and 4% from other causes. A further 37 pigs between 6 and 14 weeks of age died from PMWS (30) and ileitis and other causes (7). PMWS was only apparent in pigs from 1 to 2 weeks before death when they wasted rapidly. There were no other characteristic clinical signs and no obvious gross clinical lesions post-mortem. There was no strong link with PCV2 antibody throughout life but PCV2 antigen level was higher from 4 to 6 weeks of age in pigs that died from PMWS compared with pigs that died from other causes.

The relationship between porcine circovirus 2 antigen score and antibody titre and histology of lymph nodes in 375 euthanased sick and healthy pigs from 113 British pig farms with and without postweaning multisystemic wasting syndrome.

Data from a cross-sectional study of 113 British pig herds carried out in 2004 were used to investigate the associations between postweaning multisystemic wasting (PMWS) in pigs and herds and porcine circovirus 2 (PCV2) antigen score and antibody titre, and associated histological signs in lymph nodes. The sensitivity and specificity of published herd definitions for PMWS were tested on the study farms to consider the role of PCV2 in PMWS. Herds were defined as PMWS-affected, -unaffected or -recovered based on current and past postweaning mortality (PWM), grower pigs with clinical signs of rapid wasting, hairiness and pallor and no other known cause of death on the farm. PCV2 antigen and antibody were not used in the definition of PMWS. In each PMWS-affected herd, up to three sick pigs with the clinical signs above and one healthy pig of a similar age were taken for postmortem examination (PME). In all other herds at least one healthy pig was taken for PME. Lymph nodes were analysed for PCV2 antigen and histological changes, and serum samples were analysed for PCV2 antibody. PCV2 antibody was present in all the herds sampled. There was a non-linear association between PCV2 antigen and antibody. There was no association between the presence of high scores of PCV2 antigen in pigs and the presence of high PWM in herds. PCV2 antigen score was significantly higher in sick than healthy pigs within farms, and high PCV2 score was associated with giant cells, coalescence and absence of germinal centres in lymph nodes. These results did not vary by PMWS-affected, -unaffected or -recovered farms. PCV2 antigen was present at high scores in approximately 10% of healthy pigs on all farms. All three herd definitions of PMWS were highly sensitive, defining PMWS-affected herds as affected, but had a specificity ranging from 23% to 43%. We conclude that the current diagnostic tests for PCV2 indicated higher scores of virus in sick pigs but were not useful to define pigs or herds with PMWS. The ubiquity of PCV2 and the lack of specificity of the PCV2 tests indicate that PCV2 may be a necessary but not sufficient cause of PMWS disease. Linking this with the knowledge that the herd breakdowns occurred in a space time epidemic indicates that another infectious co-factor may be necessary for disease to occur.

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.