Post-weaning multi-systemic wasting syndrome in swine

Post-weaning multi-systemic wasting syndrome in swine



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 in 1994.15, 34, 35 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 in Saskatchewan as long ago as 1991 but the cause was not determined.15 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.15, 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 avians, psittacine beak and feather disease, tissue sections from paraffin-embedded formal infixed PMWS tissues were stained with rabbit antisera prepared against porcine circovirus (PCV) (now PCV-1) and strong reactivity of the inclusions with this reagent was seen. Shortly thereafter, a circovirus was isolated from diseased porcine tissues in Canada24 and Europe9, 10 and shown to be similar to known PCV-1 but sufficiently different to be given the designation, PCV-2.2

At present, PMWS is recognized as a sporadic but economically important disease in Canada, the USA, France, Spain, the UK (including Northern Ireland), Republic of Ireland, the Netherlands, Denmark, Republic of Korea, Taiwan, Germany, Belgium and Italy.2, 13, 18, 27, 40, 47, 49, 60 In addition to PMWS, other porcine disease syndromes are now associated with PCV-2 infection namely porcine dermatitis and nephropathy (nephritis) syndrome (PDNS),14, 19, 32, 40, 66, 70, 71, 74 and abortion and reproductive disorders.79The virus is, in addition, increasingly being implicated as an important pathogen in the porcine respiratory disease complex (PRDC). While much remains to be learned about the epidemiology, pathogenesis and modes of transmission of this unusual viral disease, substantial progress has been made; these findings and their implications for the production of pigs are summarized in this chapter. Two excellent reviews on porcine circoviruses have recently been published,2, 68 and an indexed bibliography on circoviruses and their diseases is now available.27


Various techniques, including viral isolation,direct immunofluorescence, in situ hybridization (ISH) and polymerase chain reaction (PCR) have consistently shown a close association between PCV-2 and the lesions of PMWS.2, 13, 33, 49, 55, 62 In contrast, PCV-1, a common contaminant of the PK-15 (ATCC-CCL 33) porcine cell line,21 has not been associated with PMWS and there is general consensus that it is avirulent for pigs.44, 75, 76 The Circoviridae family50 comprises a group of small DNA virus pathogens of plants, birds and pigs.9, 10 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.3, 6, 9, 63, 77 The Circoviridae family contains two genera: The Gyrovirus genus is represented by chick anaemia virus, which is the type virus for this group,2, 50, 63 and the Circovirus genus which contains both porcine circoviruses (PCV-1 and PCV-2) and psittacine beak and feather disease virus.63 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.58 Recent work has re-enforced this belief and indicates that this virus (PCV-1), and presumably also PCV-2, may have originated by recombination of a plant nanovirus with a vertebrate virus.58In 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) and possibly in a subpopulation of G-CSF-responsive porcine pro-monocytes30 without producing obvious viral cytopathic effects;2, 75 cellular foci of virus production in monolayers are monitored by immuno histochemistry with monoclonal antibodies3, 56 to the PCV proteins. Porcine circovirus 2 will replicate in human monocytes1 and human transformed cell lines;39 PCV-1 will not replicate in human cells.6, 60

The PCVs are icosahedral, non-enveloped virions with a buoyant density of 1,37 gm/cm3 in cesium gradients,2, 68 and are non-haemagglutinating agents resistant to inactivation following exposure to pH 3,0, chloroform and heating to 56 and 70 °C. The entire sequence of PCV-2 has been published33, 58 and the kinetics of its replication in vitro have been determined.12 Cell-free infectious virus is detected at 30...

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