Key Takeaways for Vets & Producers 

  • Preventing PRRS pays twice: productivity + lower antibiotic use.  
  • Audit biosecurity by route and benchmark; filtration matters in pig‑dense areas.  
  • Layer surveillance (processing fluids, OF, TF) to move herds through status phases faster.  
  • Sequence routinely; watch for vaccine/wild recombinants.  
  • Track regulatory moves: gene‑edited resistance is coming, but timelines vary by market. 

Why PRRS Still Matters in 2025 

Porcine Reproductive and Respiratory Syndrome (PRRS) remains the most economically damaging endemic disease of swine globally. Fresh modelling from Iowa State University (ISU) places US annual losses at roughly US$1.2 billion, about 80% higher than estimates a decade ago – driven by productivity drag, mortality, treatment costs and market disruptions. Growing genetic intensity, multi‑site flows, and high herd density in pig‑dense regions continue to amplify risk.  

At the same time, antimicrobial stewardship targets across the EU, UK and North America are under pressure: new field work shows antibiotic use (ABU) rises sharply following PRRS outbreaks, underscoring the disease’s indirect cost to sustainability metrics.  

Regulators are moving: in April 2025 the US FDA approved the gene edit underlying the PIC PRRS‑resistant pig, a development linking genetics, biotech regulation and transboundary disease control.  

Bottom line: controlling PRRS is now a three‑way play – productivity, stewardship and market access. 

Aetiology & virus diversity of PRRS

PRRS is caused by the PRRS virus (PRRSv), an enveloped, positive‑sense RNA arterivirus (family Arteriviridae) with 2 species/lineages of primary concern: PRRSV‑1 (formerly European type) and PRRSV‑2 (formerly North American type). Both circulate globally; regional dominance varies, and co‑circulation is common in Asia and parts of Europe.  

The ~15 kb genome encodes at least 11 ORFs; high mutation and recombination rates – exacerbated by the error‑prone RNA‑dependent RNA polymerase – drive antigenic diversity and immune escape. ORF5 (GP5) is especially variable and widely sequenced for molecular epidemiology, lineage tracking and vaccine decision‑making.  

Implication: Continuous sequencing and strain benchmarking are no longer optional where PRRS is endemic. 

Pathogenesis & clinical presentation by production phase of PRRS

PRRSv displays tropism for macrophages (esp. pulmonary & reproductive tract) leading to immune modulation, reduced innate responses (incl. interferon suppression), and prolonged viraemia. Clinical expression ranges from subclinical to severe, influenced by strain virulence, immune status, co‑pathogens and environment.  

Breeding females – late‑gestation exposure yields abortions, early farrowing, weak‑borns, stillbirths, mummies; variable return‑to‑oestrus.  

Neonates & suckling pigs – high pre‑weaning mortality, dyspnoea, lethargy, poor growth; can seed downstream flows.  

Nursery/ grow‑finish – respiratory disease, fever, uneven weights; potentiates Porcine Respiratory Disease Complex (PRDC) with bacterial agents; linked to increased antimicrobial interventions.  

Blue to reddish ear discolouration is transient and not a reliable field marker.  

Economic burden of PRRS  

Updated modelling across US production systems estimates about US$1.2 billion annual PRRS cost, about 80% higher than 2010‑era values; productivity losses extend across reproductive and growing pig phases. Global modelling remains fragmented, but national and regional datasets (Japan review; EU case series) confirm material impacts on weaned pig output and mortality.  

Transmission pathways & survival of PRRS

PRRSv spreads horizontally (pig‑to‑pig), vertically (in utero), via semen, aerosols, contaminated transport, people, equipment and biological materials. Research emphasises categorising risks into direct (live animals, semen) and indirect (fomites, aerosols, feed, manure, vectors) to target interventions.  

Recent field investigations of vaccine‑derived outbreaks reaffirm aerosol drift potential between adjacent sites under certain conditions. While long‑distance airborne spread scales with virus load and meteorology, area air‑filtration programmes have measurably reduced breeding‑herd breaks in dense US regions.  

Environmental stability is moderate; the virus is fragile outside hosts but can persist in organic matrices (manure, tissues) long enough to enable mechanical spread without proper sanitation.  

Biosecurity: From basics to next generation biosecurity (NGB) of PRRS

Biosecurity remains the linchpin of PRRS prevention. The NGB framework operationalises risk‑based controls across routes—live animal introduction, semen, people flow, transport sanitation, aerosol mitigation (air filtration), feed mitigants, mortality & manure handling, and perimeter management – backed by auditing and benchmarking.  

Practical priorities for field teams: 

  • Structured gilt isolation, testing & acclimation.  
  • Semen source controls; PCR prior to shipment; closed‑loop AI centres.  
  • Transport biosecurity: thermal/chemical trailer disinfection; clean–dirty line enforcement.  
  • Air filtration / positive‑pressure barns in high‑density pig areas.  
  • Feed ingredient mitigation (holding times, additives) where risk documented.  
  • People & equipment entry protocols; downtime; showers‑in/out.  

Return on investment is realised not only in fewer breaks but in lower antimicrobial spend and improved sow KPIs when herds remain stable.  

Vaccination Landscape of PRRS: What Works, What Doesn’t & What’s Next 

Commercial modified‑live virus (MLV) and killed (inactivated) vaccines remain the primary licensed tools. MLVs generally provide better homologous protection and reduction in clinical signs; cross‑lineage (heterologous) protection is inconsistent. Killed products favour safety but limited efficacy as stand‑alone primaries; often used in booster strategies.  

Field Efficacy & Limitations:

Recent challenge studies show that even under heterologous exposure, MLV vaccination can reduce viraemia and lung pathology but rarely prevent infection.  

Experimental consensus‑sequence PRRSV‑1 (EU‑PRRSV‑Con) candidate delivered broader heterologous reduction in RNAemia vs benchmark MLV in controlled trials—proof that rational antigen design may extend protection breadth. [^17] 

Control, stabilisation & eradication strategies of PRRS

Strategic goals vary: minimise clinical impacts; produce PRRS‑negative weaned pigs (stabilisation); regional elimination; national freedom. Toolkits combine herd closure & rollover, live‑virus exposure / controlled acclimation, MLV programmes, test‑and‑remove, and depopulation‑repopulation in severe or high‑value settings.  

Timelines: Achieving stable negative piglet flow frequently requires 120–240 days post‑intervention; variability reflects compliance, sow immunity, and regional pressure.  

Metrics: Routine RT‑qPCR of processing fluids, family oral fluids, or stillborn TF plus periodic serology support movement through AASV status phases; sequencing confirms freedom from prior strains.  

Area / Regional Control: Coordinated regional biosecurity & air‑filtration networks (e.g., multi‑system initiatives in US Midwest) have lowered breeding‑herd break rates; opportunities exist to link with national AMU reduction targets.  

Co‑infections & production impacts (PRDC & enteric interactions) 

PRRSV’s immunomodulatory effects predispose pigs to Porcine Respiratory Disease Complex pathogens (e.g., Streptococcus suis, Glaesserella parasuis, Actinobacillus pleuropneumoniae) and can interact with enteric pathogens.  

A 36‑batch US wean‑to‑finish field study found that flows with higher PRRSv detection often exhibited elevated Lawsonia intracellularis and PCV2 genomic copies and higher mortality (about 15.7%) in low‑performing groups, highlighting the need for integrated health analytics.  

These pathogen stacks likely drive some of the post‑PRRS antibiotic surges observed in production datasets.  

Global occurrence of PRRS & PRRS‑free zones  

Endemic regions: Most pig‑producing areas of North & South America, the EU (except designated free countries/regions), UK, and wide areas of Asia including China, Japan (regional variation), Vietnam, Philippines, Malaysia, Korea.  

Recognised or self‑declared free / free with surveillance: 

Australia & New Zealand (never reported; stringent import controls).  

Scandinavian cluster: Norway, Sweden, Finland—long‑standing freedom maintained via strict biosecurity; periodic risk reviews confirm status (see epi syntheses).  

Switzerland (no domestic PRRS; strong border controls).  

Chile – self‑declared PRRS‑free April 2024 after surveillance; pending international acknowledgement steps; critical for export chains to Asia.  

Dynamic / partial status: Subnational zones or compartmentalised flows in high‑density regions use surveillance plus movement controls to reduce risk; check latest national reports.  

Always verify current status with WOAH disease information and national veterinary authorities before moving pigs, semen, or embryos.  

FAQ on PRRS

Q1: What is PRRS and why is it called “blue ear disease”? 
A1: PRRS stands for Porcine Reproductive and Respiratory Syndrome, a viral disease of pigs. It causes two main problems – reproductive failure in breeding pigs and respiratory illness in young pigs. The nickname “blue ear disease” comes from one possible symptom: in some outbreaks, pigs’ ears can develop a bluish discoloration due to circulatory issues. However, this sign is not always present. PRRS was first recognised in the late 1980s and has since become one of the most important swine diseases worldwide. 

Q2: What are the symptoms of PRRS in pigs? 
A2: In breeding sows, PRRS causes reproductive issues – think abortions, premature farrowings, stillborn or mummified piglets, and weak newborn piglets that often die shortly after birth. In growing pigs and piglets, PRRS mainly causes respiratory symptoms: fever, lethargy, loss of appetite, and pneumonia with heavy, “thumping” breathing. You may see coughing and increased mortality in piglets. Young pigs fail to thrive, and there’s often a higher incidence of secondary infections (like pneumonia or scours) because PRRS weakens the immune system. Some pigs can be infected without obvious signs, but generally PRRS-positive herds suffer elevated piglet illness and death losses. 

Q3: How does PRRS spread between farms? 
A3: PRRS is highly infectious. The primary way it spreads is via movement of live pigs or semen from infected boars. The virus is present in blood, saliva, nasal secretions, feces, urine, and semen of infected pigs. So, if an infected pig (even one that seems healthy) is introduced to a herd, it can shed virus and infect others. PRRS can also hitchhike on contaminated objects – equipment, boots, transport trucks – if strict biosecurity isn’t observed. Airborne spread is possible too: the virus can travel on air currents over several kilometers, especially under the right wind conditions. Even insects like mosquitoes and flies have been shown to carry PRRS virus short distances. Therefore, to prevent spread, farms focus on isolating new stock, sanitising vehicles and equipment, filtering barn air, and controlling insects – all to stop the virus from entering. 

Q4: Is there a vaccine or treatment for PRRS? 
A4: There is no cure-all treatment for PRRS – because it’s a virus, antibiotics don’t kill it (though they may be used to control secondary bacterial infections). Once PRRS is in a pig, you can only provide supportive care and hope the pig’s immune system clears it over time. However, we do have vaccines for PRRS. Modified-live virus (MLV) vaccines are commonly used in breeding herds to boost immunity. Vaccination can reduce the severity of outbreaks – fewer abortions, less pneumonia – but vaccines are not 100% effective, especially if the farm gets a different PRRS strain than the vaccine strain. Inactivated (killed) vaccines also exist but are less commonly used alone. So in summary: no direct treatment to eliminate PRRS from an infected pig, but vaccination and good management can prevent or lessen outbreaks. Severely sick pigs are given supportive care (fluids, anti-inflammatories) and antibiotics for secondary infections, but the key is prevention. 

Q5: How can I prevent PRRS in my pig herd? 
A5: Preventing PRRS comes down to strict biosecurity and smart herd management. Key steps include: maintaining a closed herd or only buying replacements from PRRS-free sources; quarantining and testing any incoming pigs for at least 30–60 days before they join the herd; using only PRRS-free semen for AI; and ensuring trucks, equipment, and people coming onto the farm are clean and disinfected (the virus can survive in manure and blood). Many farms implement shower-in/shower-out protocols for staff and visitors. Air filtration systems in pig-dense regions can reduce virus blowing in from neighbors. You should also promptly vaccinate breeding stock with PRRS vaccine if recommended – it won’t stop all infections, but it can dampen an outbreak’s impact. Finally, having a PRRS monitoring programme (regular blood tests or oral fluid PCR samples) helps catch any incursion early, so you can respond before it spreads farm-wide. In short, keep the virus out with strong biosecurity – and be prepared with vaccination and monitoring in case it sneaks in. 

Q6: Can PRRS be eradicated, or will it always be a problem? 
A6: Eradicating PRRS from an individual farm is challenging but possible – many farms have succeeded in going PRRS-negative through techniques like herd closure and rollover (i.e. stop introducing new pigs for several months, stabilise herd immunity, and remove persistently infected animals). Once a herd clears PRRS, stringent biosecurity and only introducing PRRS-negative stock can keep it out. At a country level, eradication is difficult wherever PRRS is widespread, because the virus can hide in carrier pigs and keep circulating. However, a few countries have eliminated PRRS nationally (e.g. Sweden, Switzerland) by stamping-out outbreaks and controlling pig movements. There’s also new hope from PRRS-resistant pigs created by gene editing – these pigs can’t get PRRS at all. If adopted widely in the future, that could theoretically eradicate the disease. For now, most experts focus on regional control programs (coordination among farms in an area to break the infection cycle). So while PRRS isn’t gone yet, ongoing efforts in biosecurity, vaccination, and emerging technologies aim to eventually relegate PRRS to history.