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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.
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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 Wednesday, February 24, 2010: Veterinary Microbiology, Volume 141, Issues 1-2, 24 February 2010, Pages 22-30
Porcine Circovirus 2 (PCV2) Induces a Procoagulant State in Naturally Infected Swine and in Cultured Endothelial Cells
Fernanda S. Marks, José Reck Jr., Laura L. Almeida, Markus Berger, André M.R. Corrêa, David Driemeier, David E.S.N. Barcellos, Jorge A. Guimarães, Carlos Termignoni, Cláudio W. Canal
Porcine circovirus 2 (PCV2) is the primary causative agent of porcine circovirus disease (PCVD). PCVD is an emerging disease that has been reported worldwide, associated with wasting, lymphoid depletion, enteritis, pneumonia, vasculitis, ischemic lesions, and necrotizing dermatitis. Although PCVD causes considerable economic losses, the pathogenesis of PCV2 has not been fully understood. The aim of the present work was to study the participation of hemostatic system and of vascular endothelium in PCV2 infection, as well as their possible role in PCVD pathogenesis. Our results showed that naturally PCV2-infected swine displayed a prothrombotic state in vivo, since a diminished coagulation time (recalcification time, activated partial thromboplastin time and prothrombin time), a higher platelet aggregation ability (despite a diminished platelet blood count), and an increased thrombin plasma activity (associated with a reduced fibrinogen level) were observed. The PCV2-infected animals showed vasculitis and positive staining for PCV2 antigen in capillary vessels. Furthermore, PCV2-infected endothelial cells displayed an activated phenotype, characterized by an increase in cell surface procoagulant activity. Moreover, the PCV2-infected endothelial cells pre-treated with exogenous thrombin displayed an increased viral load. This work reports, for the first time, the role of the hemostatic system and of endothelium in the pathogenesis and infectivity of PCV2. The study reinforces the importance of the phenomena which occur during PCV2 infection, and affords a better knowledge of the mechanisms behind the pathophysiology of PCVD.


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