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Vaccination
Management
Disease Information
A PMWS update (Jake Waddilove)
ABOUT PMWS & PDNS
National Pork Board PMWS Fact Sheet
About PDNS (Jake Waddilive)
CEI Emerging Disease Notices: PMWS / PDNS
Conference and meetings archive
Case Histories
Yorkshire Farm, UK - Mike Muirhead - Final Update, June 2002
Mike Muirhead's case history of a Yorkshire farm with PMWS and PDNS.
 
East Anglia Farm, UK - Philip Richardson
This paper charts the course and effects of the disease on a single herd as well as highlighting the economic impact.
Photographs
Clinical signs
Photos of the clinical signs that are seen generally in pigs with PMWS and PDNS. Includes skin lesions, enlarged lymph glands, wasting and dead pigs.
 
Post mortem (1)
Photos of the signs that are seen in post-mortem samples of pigs with PMWS and PDNS. Includes interstitial pneumonia, secondary bacterial infection, enlarged lymph nodes, oedema and intra cytoplasmic inclusions
 
Post mortem (2)
More Photos of the signs that are seen in post-mortem samples of pigs with PMWS and PDNS.


PMWS Research Archives

Published Friday, June 15, 2007: Vet Immunol Immunopathol. 2007 Jun 15
Ontogeny of systemic cellular immunity in the neonatal pig: Correlation with the development of post-weaning multisystemic wasting syndrome.
Grierson SS, King DP, Tucker AW, Donadeu M, Mellencamp MA, Haverson K, Banks M, Bailey M.
The aetiology of porcine post-weaning multisystemic wasting syndrome (PMWS) is poorly understood. Porcine circovirus type 2 (PCV-2) is an essential component of the experimental disease model for PMWS: however, evidence from experimental and field studies indicates that additional factors play a critical role in the aetiopathogenesis of PMWS. Current candidates include (1) immune stimulation (for example, via co-infection or vaccination), and (2) a novel infectious agent. A prospective, longitudinal case-control study was designed to investigate molecular triggers in leucocytes of neonatal piglets that may predispose to the development of PMWS. Blood samples were collected weekly from pigs (n=125) within five farms, from 1 week to 8 weeks of age: that is, before the appearance of clinical signs. Four colour flow cytometry was used to investigate changes in subsets of peripheral blood mononuclear cells, using monoclonal antibodies against the following cell associated markers; sIgG, CD3, MHCII dR, CD14, CD4a, CD8a, CD45RC, CD25, SWC3a, SWC8, CD163 and CD45. Sampling and laboratory analysis was supported by monitoring of clinical signs from 1 week to 20 weeks of age, or until disease supervened. At the conclusion of the study, 68 pigs (54%) were classified in Group 1 (no signs of clinical disease), 34 pigs (27%) in Group 2 (signs of clinical disease but not characteristic of PMWS), 17 pigs (14%) in Group 3 (suspect PMWS case) and 5 pigs (4%) in Group 4 (PMWS case). A single case of Porcine Dermatitis and Nephropathy syndrome (PDNS) was also diagnosed. Significant changes with age were demonstrated in clinically normal, neonatal pigs (Group 1), including an increase in B-cells and T-cells, and an increase in the proportion of total T-cells expressing MHCII. Within the T-cell subset, the proportion of CD8(+high) CD4(-) T-cells increased, in addition to the proportion of CD4(+) T-cells co-expressing CD8. Of the factors recorded, farm was found to have a highly significant effect on immune system development in the neonate. Comparison of Groups 1 and 4 cases identified significant differences between pigs which remained normal and those which subsequently developed PMWS. Pigs which went on to develop PMWS had a greater proportion of T-cells expressing MHCII in early life, higher mean intensity of expression of MHCII on T-cells, higher mean intensity of expression of MHCII on B cells and higher expression of CD25 on CD45RC(-) T-cells. These findings suggest that lymphocyte activation may be a key early event in the aetiology of PMWS.

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