Porcine reproductive and respiratory syndrome (PRRS) is a viral disease that was first reported in 1987 in the US and is now found throughout North, Central, and South America; Asia; Africa; and Europe. PRRS is characterized by reproductive failure in boars and sows and systemic infection in growing-finishing pigs, and it is marked by respiratory disease, slow growth, and impact on survivability. Commonly used diagnostic tests include serological testing and PCR assay. There are no effective treatments; however, modified live vaccines provide partial protection against infection.
Porcine reproductive and respiratory syndrome (PRRS) was first reported in the US in 1987. Since then, outbreaks of PRRS and successful isolation of the virus that causes it have been confirmed throughout North, Central, and South America; Asia; Africa; and Europe.
Etiology and Epidemiology of Porcine Reproductive and Respiratory Syndrome
The etiological agent of porcine reproductive and respiratory syndrome is a virus in the family Arteriviridae. The virus is enveloped and ranges in size from 45 to 80 nm. PRRS virus (PRRSV) can be inactivated by treatment with ether, chloroform, or other disinfectants; however, the virus is very stable under freezing conditions, retaining its infectivity for several years at freezing temperatures, for months at 4°C (39°F), for weeks at room temperature, and for just a few minutes at ≥ 50°C (122°F).
There are two distinct PRRSV species—PRRSV-1 and PRRSV-2—both with widespread global distribution. Each species can be further classified into different lineages, and subsequently into different variants. The pathogenicity differs widely within and between species; in general, PRRSV-2 has strains that have a more clinically severe impact. One hallmark of PRRSV is its ever-evolving capability, through mutation and recombination, making it a moving target for vaccine development.
After a naive herd is infected by PRRSV, exposure of all members of the breeding population is inconsistent, such that naive, exposed, and infected subpopulations of sows develop. This complicated situation is exacerbated over time by the addition of improperly acclimated replacement gilts and leads to shedding of the virus from carrier animals to animals not previously exposed, perpetuating the PRRSV infection cycle.
The primary route for PRRSV transmission is the infected pig and contaminated semen. Controlled studies have indicated that infected swine can be long-term carriers; adults are able to shed PRRSV for up to 86 days after infection, and weaned pigs can harbor virus for 157 days. Experimentally infected boars can shed virus in the semen up to 93 days after infection (1, 2).
Aerosol transmission of PRRSV out to 9.1 km has been reported. Environmental factors that favor PRRSV transmission include favorable wind direction, low sunlight, and air temperature close to 0°C (32°F). PRRSV can also be transmitted by fomites such as contaminated needles, boots, coveralls, transport vehicles, and shipping containers. Humans can also indirectly transmit the virus after recent contact with infected pig populations. Finally, experimental transmission via certain species of insects (Aedes vexansmosquitoes and house flies [Musca domestica]) has been reported.
Clinical Findings of Porcine Reproductive and Respiratory Syndrome
Porcine reproductive and respiratory syndrome can cause reproductive failure and postweaning respiratory or systemic disease. The reproductive phase of the disease includes increases in the number of stillborn piglets, mummified fetuses, premature farrowings, and weak-born pigs. The rates of stillbirths and mummies can increase by up to 25–35%, and the rate of abortion can be > 10%.
Lactating sows show anorexia and agalactia, which result in an increase (by 30–50%) in the preweaning mortality rate in piglets. Suckling piglets develop a characteristic thumping respiratory pattern, and histological examination of lung tissue reveals severe, necrotizing, interstitial pneumonia.
PRRSV is capable of crossing the placenta in the third and possibly second trimester of gestation. Piglets can also be born viremic and transmit the virus for 112 days after infection (3). PRRS also affects performance after weaning. Because PRRSV replicates in macrophages, the immunological system of infected pigs becomes impaired, predisposing affected pigs to exacerbation of clinical consequences upon coinfection with other pathogens.
Clinical outbreaks of the reproductive form of PRRS have been reported to last 1–4 months, depending on the biosecurity and management practices of the affected facility and on the initial health status of the pigs. After this initial phase, herd immunity usually decreases clinical signs in the breeding herd, transitioning the disease to a nearly subclinical infection in that stage. In the absence of immunization, PRRSV will continue to cause problems in the nursery or at finishing, when maternal immunity wanes and the virus replicates without constraints.
In contrast, the postweaning pneumonic phase of PRRS can become chronic, decreasing daily weight gain by 85% and increasing the mortality rate to 10–80%. Numerous other pathogens are commonly identified along with PRRSV in affected nursery or finishing pigs.
Other bacteria, including Streptococcus suis, Escherichia coli, Salmonella enterica serotype Choleraesuis, Glaesserella parasuis, Pasteurella multocida, and Mycoplasma hyopneumoniae, have been reported, as well as viruses such as porcine circovirus type 2 and influenza A virus.
Diagnosis of Porcine Reproductive and Respiratory Syndrome
Serological testing via ELISA
PCR assay
Virus genome sequencing
The most commonly used serological assay to determine whether a herd has been exposed to porcine reproductive and respiratory syndrome virus is ELISA. It measures IgG antibodies against PRRSV's nucleocapsid protein. The test cannot measure the level of protective immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7–10 days after infection and can persist for several months.
Direct tests for PRRSV include PCR assay, virus isolation, and immunohistochemistry. Nucleic acid sequencing of the open reading frame (ORF) 5 region of the virus (approximately 600 base pairs) is an excellent tool for epidemiological investigations in the field to confirm similarity between isolates recovered from different sites. Whole genome virus sequencing (approximately 15,000 base pairs) is another option for characterizing the virus for epidemiological purposes, including the ability to identify recombinations or multiple strains in a sample. Sampling of processing fluids, postmortem tongue fluids, or oral fluids also has been widely applied as a means to sample a population of pigs.
For diagnostic monitoring of PRRSV, population-based samples have been increasingly used, because they are practical and cost-efficient, and they offer much greater coverage of the animals, compared with individual samples. Examples of population-based samples include postmortem tongue fluids (ie, pieces of tongue collected from dead piglets), tissues collected after castration and tail docking, and oral fluids (eg, from rope chewed by pigs in a pen).
Treatment and Control of Porcine Reproductive and Respiratory Syndrome
Modified live vaccines (partial protection)
Biosecurity
Herd closure
At the time of this writing, there is no cure for acute porcine reproductive and respiratory syndrome. Attempts to decrease fever by administering NSAIDs (eg, aspirin) or appetite stimulants (eg, B vitamins) appear to have minimal effect on PRRSV replication; however, these drugs should help to restore appetite and promote recovery. The use of antimicrobials or autogenous bacterins to decrease the effects of opportunistic bacterial pathogens has also been reported; however, results have been mixed, depending on the coinfection scenario and herd immunity status.
Prevention of infection appears to be the primary means of controlling PRRS. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimation of incoming stock, is critical to preventing introduction of the virus. Pigs should be retested on arrival at the isolation facility and 14 days later, before entry to the herd.
Pearls & Pitfalls
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Commercial modified live virus (MLV) vaccines against PRRSV have been licensed, and even though they do not prevent infection with heterologous wild-type strains, they have been effective in controlling PRRS outbreaks, decreasing viral shedding and lesions, mitigating clinical consequences, and decreasing economic losses. Because MLVs replicate in pigs, causing viremia and shedding, molecular diagnostic tests (PCR-based assays) have been developed to help differentiate wild-type strains from vaccine-derived strains.
In cases of PRRS outbreaks in breeding herds, veterinarians help producers determine the goal of a response plan: either to eliminate the virus from the herd or to control the clinical consequences of infection by maintaining strong herd immunity.
A goal of PRRSV elimination makes sense when there is confidence that the herd can be kept PRRSV-negative for at least 2–3 years (ie, biosecurity is high) and that an elimination plan can be implemented (ie, compliance is high). When MLV vaccines are used for PRRSV control, herds are typically vaccinated 2–4 times per year, depending on the regional pressure of lateral infection with other strains. In such cases, viremia is short-lived (lasting only a few days), and the impact on productivity (abortions, preweaning deaths) is low.
Herd Closure to Control PRRS
Elimination of PRRSV has been demonstrated to be possible on individual farms through use of the herd closure technique. Briefly, herd closure consists of temporarily interrupting the introduction of replacement females (gilts) into the breeding herd, ideally until diagnostic evidence supports the consistent production of PRRSV-negative piglet production.
In many instances, herd closure is associated with whole herd immunization, a practice often referred to as "load-close-expose": load the breeding herd with extra gilts, close by halting new animal introduction until the herd is stable, and expose the whole herd by immunizing all sows and gilts to homogenize the PRRSV infection stage of the whole herd. This practice minimizes the development of subpopulations of sows with variable PRRSV exposure and shedding.
Successful elimination of PRRSV should be followed by strict quarantine and testing programs, the purchase of PRRSV-naive breeding stock and semen, sanitation of transport vehicles, and strict protocols of fomite and personnel movement between farms to prevent reintroduction of the virus. In addition, monitoring the status of artificial insemination centers by PCR analysis of blood samples collected from the auricular or femoral vein (blood swab), as well as applying air filtration to artificial insemination centers and breeding herds, is very effective at decreasing entry of the virus via contaminated semen and aerosols.
Genetic Selection for Resistance to PRRS
Another way of controlling PRRSV is to genetically engineer pigs resistant to PRRSV infection. Research has shown that pigs with altered CD163 (receptor in macrophages for PRRSV infection) are resistant to infection of most known PRRSV lineages (4, 5). Although "PRRSV-resistant pigs" are not yet commercially available, they provide proof of concept of applied use of genetic engineering for livestock health.
Key Points
Porcine reproductive and respiratory syndrome is the one of the most costly diseases of the global swine industry.
PRRSV-1 and PRRSV-2 have global epidemiology. Both species have a relatively high evolution rate by mutations and recombination events.
PRRS virus can be eliminated from infected breeding herds through herd closure.
Commercially available modified live virus vaccines do not prevent infection; however, they have been shown to substantially decrease viremia, lesions, and clinical signs after wild-type PRRSV infection.
A comprehensive program of biosecurity, targeting both mechanical and airborne risk factors, is essential to maintaining naive herd status.
For More Information
Neumann EJ, Ramirez AJ, Schwartz KJ. Swine Disease Manual. 4th ed. American Association of Swine Veterinarians; 2009.
Swine Disease Reporting System. Iowa State University of Science and Technology, Field Epidemiology.
Sample Size Calculators (PRRSV surveillance tab). Iowa State University of Science and Technology, Field Epidemiology.
Holtkamp DJ, Torremorell M, Corzo CA, et al. Proposed modifications to porcine reproductive and respiratory syndrome virus herd classification. J Swine Health Prod. 2021;29(5):261-270.
References
Wills RW, Doster AR, Galeota JA, Sur JH, Osorio FA. Duration of infection and proportion of pigs persistently infected with porcine reproductive and respiratory syndrome virus. J Clin Microbiol. 2003;41(1):58-62. doi:10.1128/JCM.41.1.58-62.2003
Wills RW, Zimmerman JJ, Yoon KJ, et al. Porcine reproductive and respiratory syndrome virus: a persistent infection. Vet Microbiol. 1997;55(1-4):231-240. doi:10.1016/s0378-1135(96)01337-5
Rowland RRR, Lawson S, Rossow KD, Benfield DA. Lymphoid tissue tropism of porcine reproductive and respiratory syndrome virus replication during persistent infection of pigs originally exposed to virus in utero. Vet Microbiol. 2003;96:219–235. doi:10.1016/j.vetmic.2003.07.006
Nesbitt C, Galina Pantoja L, Beaton B, et al. Pigs lacking the SRCR5 domain of CD163 protein demonstrate heritable resistance to the PRRS virus and no changes in animal performance from birth to maturity. Front Genome Ed. 2024;6:1322012. doi:10.3389/fgeed.2024.1322012
Whitworth KM, Prather RS. Gene editing as applied to prevention of reproductive porcine reproductive and respiratory syndrome. Mol Reprod Dev. 2017;84(9):926-933. doi:10.1002/mrd.22811
