Post-weaning multi-systemic wasting syndrome in swine

Preferred citation: Anipedia, www.anipedia.org: JAW Coetzer and P Oberem (Directors) In: Infectious Diseases of Livestock, JAW Coetzer, GR Thomson,
NJ Maclachlan and M-L Penrith (Editors). JA Ellis, EG Clark, GM Allan and GS Krakowka, Post-weaning multi-systemic wasting syndrome in swine, 2018.
Post-weaning multi-systemic wasting syndrome in swine

Post-weaning multi-systemic wasting syndrome in swine

Previous authors: E G CLARK, J A ELLIS, G M ALLAN AND S KRAKOWKA

Current authors:
J A ELLIS - Professor, DVM, PhD, Diplomate ACVP, Diplomate ACVM, Department of Veterinary Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, 52 Campus Drive,  Saskatchewan, S7N5B4, Canada
E G CLARK - Prairie Diagnostic Services, Western College of Veterinary Medicine, University of Saskatchewan, 52 Campus Drive, Saskatoon, Saskatchewan, Canada
G M ALLAN - Personal Chair of Porcine Virology, Queen’s University, 51 Cabin Hill Gardens, Belfast, Northern Ireland, BT5 7AQ, United Kingdom
G S KRAKOWKA - Department of Veterinary Biosciences, College of Veterinary Medicine, Ohio State University, Columbus, OH, USA

Introduction

In 1974 a small circular, non-enveloped DNA virus was first observed as a “contaminant” in a pig kidney cell line (PK-15).85, 87 When this agent was used to experimentally infect pigs in the mid-1980s,  and again in the mid-1990s, no disease was produced9, 86  and so it was considered to be avirulent.  In 1994, an outbreak of subacute to chronic, progressive, systemic, inflammatory disease with a high mortality rate, restricted primarily to young weaned pigs, was first identified in several minimal disease herds of pigs in western Canada.14, 35, 37 A viral aetiology was suspected, largely on the basis of the presence of basophilic inclusion bodies within cells in the granulomatous inflammatory foci. These lesions had been recognized as distinctive among swine in Saskatchewan as long ago as 1991 but the cause was not determined.14  The disease presentation in its epidemic form in affected herds was so distinctive that the term ‘post-weaning multi-systemic wasting syndrome’ (PMWS) was coined in 1996 to emphasize its most important features, namely the occurrence in pigs eight to 12 weeks of age of a disease with multiple organ system involvement whose chief clinical manifestations were progressive wasting and failure to thrive.14, 35 During the investigation of this outbreak, and on the basis of the morphologic similarities between the ‘inclusion bodies’ in PMWS cases and similar inclusions characteristic of a circovirus disease of birds, psittacine beak and feather disease, tissue sections from paraffin-embedded formalin-fixed PMWS tissues were stained with rabbit antisera prepared against the original porcine circovirus (PCV) and strong reactivity of the inclusions with this reagent was seen. A circovirus was first isolated from diseased porcine tissues in Canada,22 and then in Europe.7, 8 Since it was shown to be similar to known PCV, but sufficiently different, the original circovirus was named PCV-1, and the new, apparently pathogenic virus was designated PCV-2.4

In addition to classical PMWS, the constellation of porcine circovirus-associated diseases (PCVAD) include: the porcine respiratory disease complex (PRDC), enteric disease, reproductive disorders and abortion, and porcine dermatitis and nephropathy (nephritis) syndrome (PDNS).12, 17, 19, 33, 40, 74, 76, 79, 80, 83, 84, 90  Porcine circovirus 2 and PCVADs are found  in domestic and wild pig populations worldwide.1, 12, 17, 40, 47, 49, 63 Over the last two decades much has been learned  about the epidemiology, pathogenesis and modes of transmission of this small virus, and  many excellent reviews have been published.1, 4, 18, 22, 29, 41, 43, 52, 62, 76, 77  These findings and their implications for the production of pigs are summarized in this chapter, with a focus on PMWS.

Aetiology

The porcine circoviruses, PCV-1, a common avirulent contaminant of the PK-15 (ATCC-CCL 33) porcine cell line,21 and the pathogenic PCV-2 are in the genus Circovirus within the family Circoviridae.   The Circoviridae 51 comprises a group of small DNA virus pathogens of plants, birds and pigs.7, 8  The viruses are unique in that they are the smallest known autonomously replicating viruses. The form of their viral DNA, as a single-stranded (ss) circularized DNA molecule, is also distinct.2, 5, 7, 66, 88  The Circoviridae family contains two genera: the Gyrovirus genus is represented by chick anaemia virus, which is the type virus for this group,1, 51, 66  and the Circovirus genus which contains both porcine circoviruses (PCV-1 and PCV-2) and several avian circiviruses including psittacine beak and feather disease virus.66 The avian members of the Circoviridae are well-known viral pathogens. Similarities between PCV-1 and plant nanoviruses have been identified and these similarities have led to the suggestion that PCV-1 may represent the most ancient mammalian DNA replicon. The circoviruses probably originated by recombination of a plant nanovirus with a vertebrate virus.61 In plants, circoviruses have long been associated with disease and the plant nanoviruses are an important group of viral pathogens in their respective host plant species.

In vitro, both porcine circoviruses (PCVs) replicate in subconfluent monolayers of porcine kidney cells (PK15 cells) without producing obvious viral cytopathic effects;1, 87 cellular foci of virus production in monolayers are monitored by immunohistochemistry with monoclonal antibodies2, 61  to the PCV proteins.  Porcine circovirus-2  replicates in human monocytes1 and human transformed cell lines;39   PCV-1 does not replicate in human cells.5, 63

The...

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