The PRRS virus is an enveloped RNA virus in the genus Arterivirus, classified in the virus family, Arteriviridae. There is considerable heterogeneity in the genome of the PRRS virus because of inherent errors common in transcription of RNA. The prototype US virus is related to but distinct from the first European isolate (referred to as Lelystad virus) identified in the Netherlands. There are significant genetic and antigenic differences between these initial isolates. Genetic and antigenic variability between isolates, even within a country, remains a continuous challenge to control of the disease.
PRRS is probably the most important swine disease of the last half-century. Serological testing has revealed there are many infected herds in which signs are not apparent. Where signs are apparent, they vary and are influenced by (1) virulence of the virus, (2) whether it is an initial infection or ongoing (endemic with herd immunity), (3) the age group affected, (4) other disease causing agents present in the population, and (5) herd size and management practices.
Clinical signs and history often suggest PRRS, especially in acute outbreaks. Characteristic microscopic lesions in lungs and several other tissues also are suggestive but not pathognomonic. PRRS infection is widespread in US herds so care must be taken to both confirm an active infection and to rule out other infectious diseases. Any tentative clinical diagnosis should be confirmed by detection of the PRRS virus. This can be by virus isolation (VI), detection of PRRS antigen by fluorescent antibody tests (FAT) or immunohistochemistry (IHC), or detection of PRRS virus genome by polymerase chain reaction (PCR) and be coupled with presence of typical lesions. Serology provides indirect evidence of infection but does not determine if there is actual disease caused by PRRS virus.
There is no single successful strategy for control of PRRS, largely because of virus variation, large swine populations, and unresolved issues of transmission. In some smaller herds, immunity may be sufficient so that infection is not causing significant economic losses, in which case no intervention is necessary. Often, there are sufficient losses to consider some or all of the following points for control. A control program should be tailored to fit the individual farm situation.
An accurate diagnosis is essential to confirm the disease and epidemiology on a particular farm. This requires both disease characterization (demonstrate disease agents and lesions) and a serologic profile of pigs in the various stages of production. Serologic testing of a significant sample of animals from each stage of production should indicate the stage (acute or chronic) of infection in the herd as well where and how the virus is being spread in the herd. Once the disease is defined, a strategy can be developed to achieve one of two general goals, either to eliminate PRRS or to control (“live with”) PRRS.
The goal of many herds is to “stabilize” the infection in the sow herd by assuring immunity in all breeding stock. This “herd immunity” prevents the reproductive failure and can decrease the likelihood of transmission of virus from dams to fetuses and offspring. When coupled with segregated rearing of offspring, clinical effects of infection can be minimized. Breeding herd stabilization can sometimes be accomplished by vaccination, intentional whole-herd infection, aggressive acclimatization of replacement breeding stock, or combinations of these strategies.