Porcine Reproductive and Respiratory Syndrome (PRRS)

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PRRS is an acronym (porcine reproductive and respiratory syndrome) for a viral disease characterized by two overlapping clinical presentations, reproductive impairment or failure in breeding animals, and respiratory disease in pigs of any age. PRRS is the most economically significant disease to affect US swine production since the eradication of classical swine fever (CSF).


Porcine reproductive and respiratory syndrome virus (PRRSV) occurs in all age groups. Reproductive impairment or failure, more obvious in sows or gilts, also affects some boars. The respiratory syndrome is seen more often in young growing pigs but also occurs in naïve finishing pigs and breeding stock.

Although reported initially in only a few countries in the late 1980s, PRRS now occurs worldwide in most major swine-raising countries. PRRS is prevalent in the United States and exists both in epidemic and endemic forms.

Historical information

In the US, the clinical disease was first described in 1987-88 in North Carolina, Iowa and Minnesota. Several outbreaks in Indiana were reported in 1989-90. During the subsequent decade, PRRS spread rapidly, both in Europe and North America. By the end of 1992 the disease was reported in Canada, Great Britain and several European countries. Two distinct strains of virus, one in Europe and one in the United States, were characterized as genetically different but are clinically similar in most respects. Both are now in the United States, along with a multitude of viral variants.

The disease was first described as a syndrome and confused initially with several other diseases. It was referred to as swine mystery disease (SMD) or swine infertility and respiratory syndrome (SIRS) before porcine reproductive and respiratory syndrome (PRRS) became the generally agreed-upon name.

During the past 20 years, there has been much research on the PRRS virus. Although much now is known about the virus, details on control of the disease for all types of swine-raising operations are far from complete. PRRS is the most economically important disease now affecting producers. Swine industry consolidation of the past 15 years has led to entire production systems being designed around strategies for controlling or eliminating this disease.


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.

The PRRS virus is only moderately resistant to environmental degradation. The virus is easily inactivated by phenol, formaldehyde, and most common disinfectants. The virus has a predilection for cells of the immune system, including pulmonary intravascular macrophages (PIM) and pulmonary alveolar macrophages (PAM); in the latter it replicates extensively. Primary PAMs and a limited number of continuous cell culture systems are used in isolating and maintaining virus. Strains of PRRS virus vary markedly in virulence. The basis for virulence differences is not yet known. Protective epitopes are not described nor can they be predicted from genomic analysis. The virus often appears to interact with other pathogenic viruses, bacteria and Mycoplasma hyopneumoniae to magnify severity of diseases.


An important feature of the virus is its ability to persist in long-term carrier pigs (greater than 200 days). However, field observation suggests that most infected pigs eventually become immune, then cease to shed virus by 60 days post-infection. This is accompanied by a steady decline in antibody titers over a period of four to eight months after infection. Shedding carriers probably are the most common means of virus introduction to a herd or population of pigs. The virus is highly infectious (infectious dose is as little as 10 virions) but not highly contagious. It is present in nasal secretions, urine, semen, mammary secretions and feces. With the advent of artificial insemination, semen became a major source of viral introduction. The virus spreads readily by direct contact. There is limited experimental evidence of aerosol spread between farms but anecdotal opinions suggest it occurs at least sporadically. In some cases, infection is manifested as an epidemic of respiratory disease or reproductive failure but in other outbreaks, infection may spread slowly. Overall, virus transmission between groups of pigs is poorly understood. Debate continues as to roles of both vertical and/or lateral sources of infection in new outbreaks.

Sows infected while pregnant may deliver viremic, persistently infected piglets as a congenital PRRS virus infection. Virus can transmit from infected piglets or dams to other piglets. The cycle of shedding and infection can continue well into the nursery phase in situations where the sow herd is actively infected. Older infected pigs held back in nurseries or cross-fostered in the farrowing house often are a source of virus for younger pigs. Likewise, older pigs and their secretions can be a source of infection to younger pigs on premises where biosecurity between groups is lacking.

Boars are known to shed PRRS virus in semen for up to 92 days post-infection and can infect dams during breeding. Infection of sows occurs through natural breeding or artificial insemination. The advent of artificial insemination and boar studs has created a need for strict biosecurity and monitoring of PRRS virus in these facilities. Research suggests that the virus is unlikely to be spread to pigs by birds or rodents. There are no known replication-competent insect vectors but mosquitoes and house flies are capable of acting as fomites with the potential to spread the virus mechanically.


Once transmission of virus to the tonsil or upper respiratory system has occurred, primary replication occurs in lymphoid tissues. Viremia follows and may persist for several weeks. The virus has a predilection for lymphoid tissues (spleen, thymus, tonsils, lymph nodes, Peyer’s patches). It infects and compromises the function of pulmonary alveolar and intravascular macrophages resulting in interstitial pneumonia. PRRS appears to increase susceptibility of the lungs to other pathogens.

PRRS virus is known to cross the placenta in late gestation (after the 72nd day) and may reach a high titer in fetuses. It may kill all, part or none of the fetuses. It is suggested that fetuses are killed by hypoxia that occurs as a result of the arteritis that may develop in umbilical vessels. Abortions are common, the result of either the effects of acute disease and fever in sows or infection and death of fetuses. Recovered sows are resistant to re-infection when exposed to a homologous strain of the virus but are likely to show clinical signs if a heterologous strain is encountered.

Clinical signs

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.

Breeding age gilts, sows, and boars: Clinical signs may include a period of anorexia, fever, lethargy, depression, and perhaps respiratory distress or vomiting. Mild cyanosis of the ears, abdomen and vulva has been reported in some outbreaks. Reproductive problems, often the most obvious signs, include a decrease in the number of dams that conceive or farrow. There is usually an increase in premature farrowings, late term abortions, stillborn or weak piglets and mummified fetuses. Preweaning mortality is high. Nursing pigs may have dyspnea (“thumping”). The period for reproductive signs varies with herd size but is usually two to three months in duration. A slow improvement in reproductive performance then begins. In larger operations, signs may be cyclical, especially if naïve gilts or sows continue to be introduced into the herd. There is evidence that subpopulations within large breeding herds escape initial infection but are infected when exposed later and serve as sources of continued virus shedding. Also, herds may be infected with multiple, heterologous strains of PRRS virus that are not completely cross-protective. In boars, clinical signs are similar to sows and are accompanied by a decrease in semen quality.

Young, growing and finishing pigs: Primary clinical signs among young pigs are fever, depression, lethargy, stunting due to systemic disease, and pneumonia. Sneezing, fever and lethargy are followed by expiratory dyspnea and stunting. Peak age for respiratory disease is four to ten weeks. Postweaning mortality often is markedly increased, especially with more virulent strains and the occurrence of ever-present concurrent and secondary infections. Older pigs, especially naïve, high-health swine, have similar respiratory signs. Heterologous infections may lead to prolonged or repeated outbreaks of respiratory disease.


PRRS virus infection generally results in mild to severe lesions in lungs and lymph nodes. The interstitial pneumonia varies from multifocal to lobular to diffuse in distribution. Lungs appear mottled and tan but are highly variable in extent. Lymph nodes are generally swollen, tan and edematous or cystic. Microscopic lesions may include nonsuppurative interstitial pneumonia, mild nonsuppurative encephalitis, myocarditis, rhinitis, and perhaps depletion of germinal centers of lymph nodes.

Most fetuses and stillborn pigs with uncomplicated PRRS have no discernible lesions but some may have umbilical cord arteritis and hemorrhage; patchy distribution of slightly firm lungs (interstitial pneumonia); enlargement of lymph nodes; hemorrhages in the skin; edema of the eyelids, periorbital tissues, colonic mesentery and various body cavities; and dehydration with prominence of the vertebral column. Sows with acute PRRS virus infection have typical lung and systemic lesions. Endometritis, myometritis and placental lesions have been reported.

Other infections are common in pigs with PRRS. Differential diagnosis for respiratory disease includes lesions or co-infections caused by influenza virus, Streptococcus suisMycoplasma hyopneumoniaeSalmonella choleraesuisHaemophilus parasuisPasteurella multocida, porcine circovirus, porcine respiratory coronavirus, and Actinobacillus pleuropneumoniae.


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.

Detection of PRRS virus is best performed in affected pigs during the early stages of PRRS infection. Suitable specimens are obtained from weak-born neonates that have not nursed, or clinically affected (thumping, febrile) nursing pigs, and from febrile, anorectic postweaned pigs and sows. Probably the best tissues for virus detection methods include bronchoalveolar lavage (BAL), serum, lung, lymph nodes, tonsil and spleen.

Aborted, mummified, or stillborn pigs are sometimes (50% positive) useful for diagnosis by performing PCR on fluids and also for ruling out other infections. Sows that are not sick at the time of abortion are usually not viremic but should have high antibody levels in serum. Sows that are acutely ill should have virus in serum that can be detected by PCR or virus isolation.

Viral antigen can be identified in infected fresh tissue, preferably lung, by direct fluorescent antibody test but is more commonly identified in formalin fixed tonsil or lung by IHC. Using IHC, the virus can be visualized within typical lesions. PCR or in situ hybridization can be used to demonstrate viral RNA.

Serology may be helpful in confirming the presence (seropositivity) and stage (high levels of antibody in recent infections) of PRRS infection in the herd. A series of blood samples from various stages of production is useful to determine the age that PRRSV is most commonly infecting pigs. Several different tests for PRRS antibody have been used. In the United States, indirect immunofluorescent antibody (IFA), serum neutralization, and enzyme-linked immunosorbent assay (ELISA) tests often are used. ELISA has many advantages, including automation, an approximate quantification of antibody, and the ability to identify both European and American strains of virus. Finding PRRS virus antibodies in a few serum samples may not be evidence of active disease; many “normal” herds have animals with antibodies and maternally derived antibody may be detectable up to six weeks of age.

Techniques for differentiating viral isolates are sometimes available, including the use of restriction enzymes and RNA fragment analysis (RFLP) or actual sequencing of portions of the viral genome. Thus far, sequencing has been a valuable epidemiology tool but neither it nor RFLP predict antigenicity or the presence of cross-protective epitopes. The value of sequencing is determining the relatedness (homology) of two or more PRRS virus isolates to determine source of infection or whether more than one “strain” is present in a population.


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.

Two major, generally recognized as essential, components are to limit the frequency of seed stock introductions to the sow herd and to assure that the replacement gilts be well-acclimatized to the PRRS virus present in the sow herd. Seed stock introductions to sow herds should not be more frequent than monthly, with quarterly or semiannual introductions preferred. Assuring infection of replacement gilts, followed by at least 60 days recovery (cool-down) before they enter the sow herd is strongly recommended. Ideally, replacement gilts should originate from a single, PRRS-negative source and be infected only with the PRRS strain(s) present in a particular sow herd.

Boars introduced into negative herds should be quarantined for 60-90 days after purchase and confirmed negative serologically. Those entering PRRS-positive herds require acclimatization to resident PRRS virus in a fashion similar to gilts. Many organizations that provide semen for artificial insemination now use PCR to assure that semen is free of PRRS virus.

Sow herds and offspring that remain positive for PRRS may prefer to strive for minimizing clinical effect rather than trying to eradicate it and prevent re-infection. Acclimatization of breeding animals and management of pig flow allows for some success in “living with” PRRS. There are both killed and live commercial vaccines for control of reproductive and/or respiratory forms of PRRS that may be useful; experience suggests they are inconsistently efficacious. Autogenous killed PRRS vaccines have also been used with very limited success.

Herds successfully “stabilized” for PRRS virus may produce PRRS-negative offspring. Once the breeding herd is producing PRRS-negative offspring, it is necessary to evaluate the nursery, grower and finisher phases. Initial testing should indicate whether it would be necessary to depopulate, clean and disinfect these stages. Nursery depopulation often improves production. All phases of production should use all in/all out management.

Some sow herds that consistently produce negative offspring may attempt to eliminate PRRS from the sow herd. At that point, all subsequent replacement seed stock should be naïve for PRRS infection and any residual infected sows in the herd should be eliminated. The latter has been accomplished by testing (serology, PCR) and removal, or in some cases, by normal attrition.

In some operations, it may be economically feasible to depopulate, clean and disinfect the facilities and, after a few weeks, repopulate with stock free of PRRS and other major diseases. Herd closure for at least 200 days has also been used as another means to stabilize a breeding herd without having to depopulate. Most breeding stock companies today provide PRRS-free seed stock which was once a major limitation. Before embarking on this strategy, one should honestly assess risk factors for re-infection of the herd as well as the level of biosecurity that can be maintained by the producer. Herds located in swine-dense areas are at great risk for re-infection.

There is no specific treatment for PRRS. Broad-spectrum antibiotics may be useful in controlling secondary infections. Anti-inflammatory products (e.g. aspirin) are commonly administered during acute disease. Other helpful techniques include early weaning and isolation of piglets, various PRRS vaccination protocols, regular serologic monitoring, testing (ELISA, PCR and IFA) and removal of persistent carriers in herds with <10% infection, and improving biosecurity.

Since the PRRS virus, the control strategies, and the specific farm situations are so variable, it is imperative that experienced practitioners, diagnosticians and research workers continue to objectively expand their knowledge to better control and eventually eliminate this financially devastating disease.