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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 Tuesday, December 22, 2009: BMC Vet Res. 2009 Dec 22;5:45.
Cellular Adaptive Immune Response against Porcine Circovirus Type 2 in Subclinically Infected Pigs.
Steiner E, Balmelli C, Gerber H, Summerfield A, McCullough K.
BACKGROUND: Porcine circovirus type 2 (PCV2) is a dominant causative agent of postweaning multisystemic wasting syndrome (PMWS), a multifactorial disease complex with putative immunosuppressive characteristics. Little is known about adaptive PCV2-specific immune responses in infected pigs. Therefore, the T and B cell responses following PCV2 infection in 3-week old SPF piglets infected with PCV2 or PCV2 plus porcine parvovirus (PPV) were studied.

RESULTS: All animals were asymptomatically infected. At 7 days post infection (d p.i.), B lymphocyte and T lymphocyte numbers decreased in the dual infected, but not in the single infected piglets. At this time point a transient PCV2 viraemia was noted in the PCV2 infected groups. Antibodies against the infecting virus were detectable at day 24-28 p.i. for anti-PCV2 antibodies and at day 10 p.i. for anti-PPV antibodies, with no apparent influence of PCV2 on the early PPV antibody development. In the animals infected with PPV alone, IFN-gamma secreting cells (SC) that were not specific for PCV2 were detected by ELISPOT assay at day 7 p.i. Interestingly, this response was absent in the PCV2/PPV dual infected animals. PCV2-specific IFN-gamma SC were observed in the PCV2/PPV infected group at 7 d p.i. and in the PCV2 single infected group at 21 d p.i. A reduction in the numbers of IFN-gamma SC was observed following anti-CD4 and anti-CD8 antibody treatment, suggesting roles for both CD4+ and CD8+ T cells in the response against PCV2 infection. This was supported by an observed increase in the percentage of IFN-gamma positive CD8hi cytotoxic T cells as well as IFN-gamma positive CD8-/low helper T cells after PCV2 in vitro re-stimulation.

CONCLUSIONS: Infection of weaned SPF piglets with PCV2 alone or combined with PPV does not induce disease and in both cases a relatively slow anti-PCV2 antibody response and weak T lymphocyte responses were found. Knowledge on such immunological characteristics is important for both PCV2 pathogenesis and vaccination.

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