Porcine reproductive and respiratory syndrome

Porcine reproductive and respiratory syndrome

T W DREW AND D J PATON

Introduction

Porcine reproductive and respiratory syndrome (PRRS) — as its name suggests — manifests as both reproductive failure and respiratory disease,55, 63 and is caused by a virus of the genus Arterivirus (family Arteriviridae). Pigs of any age and any parity are affected. A rare but overt clinical sign is the appearance of cyanotic lesions in the extremities, particularly the ears. In uncomplicated infections, a characteristic interstitial pneumonia may be seen microscopically.

The disease was first described in pigs in North Carolina, Minnesota and Iowa, USA, in 1987,43, 47 although retrospective serological studies have revealed evidence of infection since the late 1970s to early 1980s in Canada and the USA,14, 19, 26 and also in countries which had imported pigs from the USA at that time.83, 84 This condition has now been reported in many parts of the world, although some countries are still purportedly free.63 In May 1992, the disease was included in List B (annual reporting) of the Organization International des Epizooties (OIE).8 There is little doubt that countries reporting the disease have subsequently suffered in terms of trade in pigs and semen.

Aetiology

In July 1991, workers at the Central Veterinary Institute at Lelystad, the Netherlands, announced the isolation of a hitherto unknown virus, which they called ‘Lelystad virus’. 102 The virus was isolated using cell cultures of pig alveolar macrophages (PAMs) obtained from a six-week-old specific pathogen-free (SPF) piglet. The virus was highly cytopathic and was noted to be sensitive to chloroform. It did not agglutinate the red blood cells of chickens, guinea pigs, sheep, pigs or humans. The virus had a buoyant density of 1,18g/cm3 in CsCl.

In the USA, another isolate of procine reproductive and respiratory syndrome virus (PRRSV) was also described and designated the ATCC VR 2332 isolate.11, 23 Unlike the European strain, the USA isolation was made in an established monkey kidney cell line CL 2621 (a clone of MA 104).10

A sub-clone of MA 104, called MARC 145, has been prepared, which has enhanced susceptibility to PRRSV and this line is routinely used for isolation of American isolates.48 European isolates of PRRSV do not grow so readily in this cell line, but can be successfully adapted by multiple passage.

Porcine reproductive and respiratory syndrome virus is classified as a member of the genus Arterivirus within the family Arteriviridae, order Nidovirales, whose members have been grouped according to their morphology, genome organization, physicochemical properties and host cell specificity.64, 64, 65 Other members of the family are lactate dehydrogenase elevating virus (LDV) of mice, equine arteritis virus and simian haemorrhagic fever virus. They all have positive sense, single strand ribonucleic acid (RNA) genomes and transcribe multiple subgenomic mRNAs. Although the genomes of the arteriviruses are shorter than those of coronaviruses and their virions differ morphologically, being smaller and having icosahedral rather than helical nucleocapsids, they all possess similar replicative strategies.

Morphologically, the PRRSV virion is round, enveloped and somewhat variable in size, being 45 to 65 nm in diameter, with an icosahedral nucleocapsid of 25 to 35 nm.101 The Arterivirus genome is approximately 15kB and has eight open reading frames (ORFs), arranged as a 3’ co-terminal nested set. The first two ORFs, 1a and 1b, are linked by a ‘slippery knot’ frameshift junction sequence and encode the enzymes involved in replication. Open reading frames 2 to 7 encode structural proteins. Further details of the genome organization of PRRSV can be found in a definitive review by Meulenberg et al.64

Detailed analyses of isolates of PRRSV from America and Europe show them to be genetically and antigenically distinct.70, 99 To a lesser extent, diversity is also seen among isolates from Europe31, 89 and America,7, 12, 56 leading to the conclusion that they represent two distinct genetic groups, with divergent evolution of the two genotypes from some unknown ancestor.70 Emerging evidence indicates that greater diversity than was hitherto expected, may exist among isolates of PRRSV from Eastern Europe and Northern Asia.6 It is likely that the distinction between genotypes may become less straightforward, since evidence of recombination between the two genotypes has recently been reported.107 Such events may have profound effects on the pathogenesis of strains and on the efficacy of vaccines.

Epidemiology

The spread of PRRS suggested an infectious aetiology, yet it was some time before the causative agent was discovered. Many pathogens, both viral and bacterial, were implicated by virtue of their isolation from a high percentage of clinical cases, yet no pathogen was able to reproduce the disease experimentally, either alone or in combination.39, 48, 72 Whilst there was little doubt that these pathogens often contributed to the clinical picture seen in the respiratory form of field cases of PRRS, the lack of consistent isolation of any single agent from cases of the disease suggested that, rather than being the primary agents, their presence was opportunistic, causing secondary infections leading to multifactorial disease. Serological studies failed to identify any single known viral...

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