Porcine Reproductive and Respiratory Syndrome (PRRS) was first recognized in the United States in North Carolina in 1987. From there it quickly spread throughout the United States. It next appeared in Germany in 1990, and it has since continued to spread worldwide. Today PRRS is believed to be present in most areas of the world where large numbers of swine are raised, and to be one of the most economically important diseases faced by the swine industry.

Many infections with the causative virus (PRRS virus) are subclinical, however, infection sometimes results in reproductive failure (i.e. the virus crosses the placental barrier to infect and adversely affect the conceptus), or respiratory tract illness, or both. Mainly on the basis of field observations, it also has been speculated that infection with PRRS virus can potentiate the effects of other pathogens.

Because of the economic importance of PRRS for the swine producers (and consumers) in the United States, a research project was started at the National Animal Disease Center (NADC) several years ago. As a result of the combined efforts of scientists throughout the world, a great deal has been learned about PRRS since its sudden appearance almost a decade ago. But there still is no clear strategy for its prevention and control, and PRRS continues to have a major negative impact on the swine industry.

Nevertheless, the future looks promising in that a vaccine has recently been developed and is available commercially. Moreover, we are gradually beginning to understand the nature of PRRS and its causative virus.

Our research at the NADC has addressed a number of different topics relative to PRRS. Despite a variable degree of overlap these can, in a general sense, be thought of as studies on pathogenesis, clinical effects of infection, diagnosis, immunity, vaccine development, the ability of PRRS virus to potentiate the effects of other pathogens, and epidemiology. In the following paragraphs we briefly summarize some of the types of studies that have been pursued during the last several years and a few comments about some of what has been learned.

Pathogenesis: We have found that transplacental infection (and consequently reproductive failure) is more likely to follow maternal infection late in gestation than maternal infection early in gestation. This probably explains why PRRS virus-induced reproductive failure is most often a disease of late gestation, i.e. late-term dead fetuses, stillborn pigs, and weak and unthrifty neonates than of early gestation, i.e. embryonic death and resorption and fetal death and mummification. The possibility that early gestation fetuses are somehow resistant to infection (which might also explain why PRRS virus-induced reproductive failure is more often a problem of late gestation) was precluded by injecting PRRS virus directly into fetal fluid and finding that early gestation fetuses were apparently just as susceptible to infection as were late gestation fetuses. The cause of death of fetuses in utero is still in question, however, the finding of a severe vasculitis affecting both fetuses and extra fetal membranes suggests fetal nutrition may be compromised during the late stages of infection.

Clinical effects: In addition to the clinical effects of PRRS virus relative to reproduction, the virus has the ability to cause extensive consolidation of the lungs and a marked enlargement of lymph nodes. Under the best of conditions, i.e. when young pigs farrowed by SPF gilts and kept in a clean, isolated environment are exposed to virulent PRRS virus, lung lesions appear between 1 and 2 weeks after exposure. However, in the absence of other pathogens the lesions are resolved, at least grossly, and by 4 weeks after exposure may be almost absent. On the other hand lymph adenopathy seems to increase from 2 to 4 weeks. Therefore lungs of pigs necropsied 4 weeks after exposure may appear almost normal, whereas lymph nodes may be 4-5 times normal size.

Diagnosis: The disease is best diagnosed by isolation and identification of the causative virus. Limitations are selection of the most suitable cell type for replication of the virus in vitro, and selection of the most suitable diagnostic sample from which to isolate the virus. In the experience of the National Veterinary Services Laboratories (USDA, APHIS), Ames, Iowa, MARC-145 cells appear to be useful for isolating at least most strains of PRRS virus present in the United States (personal communication, Dr. Merwin L. Frey). In our experience blood (serum) is an excellent sample from which to isolate PRRS virus if the sample is collected from a young pig during acute infection. Under other conditions we have had more success in isolating PRRS virus from alveolar macrophages collected by pulmonary lavage, either from pigs at necropsy or from anesthetized live pigs.

Immunity: In several studies females exposed to PRRS virus prior to conception (with attenuated or virulent strains) have developed protective immunity as evidenced by their resistance to subsequent challenge with virulent virus during gestation. In most cases immunity has been complete, i.e. there was no transplacental infection with virulent challenge virus. However, in a few cases 1 or a few fetuses were infected. Ingestion of colostrum containing antibody for PRRS virus may provide some immunity to neonates, but the degree of cross protection among strains of the virus is still in question.

Vaccines: Several strains of PRRS virus have been attenuated for use as vaccines. Testing completed to date indicates they are safe, i.e. do not cause reproductive failure even if administered oronasally during late gestation and are effective. They are currently being tested for their ability to protect against the respiratory facet of PRRS in young pigs.

Potential for other infections: In a single study completed to date we have not been able to demonstrate the suspected role of PRRS virus in potentiating the effects of other pathogens; namely, the effect of transmissible gastroenteritis virus in 4-week-old pigs exposed 2 weeks before to PRRS virus was not clearly different than that in litter and age-matched pigs not previously exposed to PRRS virus. However, additional studies are planned to further investigate this topic.

Epidemiology: In general we have found that PRRS virus can be transmitted from young pigs to other young pigs and from a dam to her piglets for a long period of time (for at least 8 weeks). Transmission among adults appears to be less common and in several experiments in which adults infected at least 3 weeks before with PRRS virus were placed in contact with susceptible adults we found no evidence of virus transmission. The recent development in our laboratory of a test to differentiate among strains of PRRS virus should assist in epidemiologic studies in which the source of virus is in question.

Despite major progress in the last few years relative to our understanding of PRRS and PRRS virus there are still a number of questions to be answered before we can feel confident that the disease is under control and we can turn our attention to its possible eradication.