How to most efficiently protect against PRRSV

A combination of different key choices and actions are to consider:

• Optimal targets: stable sow-herd with weaning and vaccination of PRRSV negative piglets
• Immune strategy: Vaccination (recommended) or live virus inoculation (LVI), while recognizing its inherent risks and emphasizing that LVI is not equivalent to vaccination (see LVI section).
• Vaccination: live (MLV) vaccines, inactivated dead (INV) vaccines, or complementary MLV + INV vaccination schemes (CVS)
• Monitoring strategy: frequency and diagnostic methodologies
• Supportive internal biosecurity management (biocontainment): Gilt introduction, All-in all-out, and hygienic procedures

The optimal strategy is to target a permanently stable sow-herd, giving birth to and weaning PRRSV negative piglets. Gilts are introduced via quarantine-like facilities, immunised by CVS and entered the mating compartment after cool-down (qPCR negative). The sows are boosted regularly, also in a CVS scheme. Whereas the PRRSV negative piglets are immunised by an MLV vaccine, and as close to 6 weeks-of-age, as possible and convenient. To further decrease viral infectious load and PRRS impact (and most other infectious diseases) on all animals in the herd, due diligence, strict age segregated production, hygienic procedures are key routines to be maintained. The herd productivity and PRRSV health status is monitored, for increase of losses, and by diagnostics optimal to animal group and herd status, weekly-monthly depending on how far away from stable the herd is.

Depending on the status and changes herein, the above procedures are adjusted accordingly to promote and permanently maintain s PRRSV stable status = virus negative, seropositive and protected, without losses.

PRRSV stable status with no evident PRRSV circulation should be the target for any PRRSV endemic sow herd. This way recurrent reproductive and production losses due to PRRS are avoided. Furthermore, the immune suppression induced by PRRSV is not facilitating secondary infections, increasing antimicrobial use (AMU), or reducing vaccine responses.

This way, outcome and stability of production is maximised towards PRRSV, secondary infections, and other diseases vaccinated for, together with animal health and welfare. Losses and AMU are minimised.

An optimal vaccination strategy is the recommended choice over LVI for immunisation, to get stability in production, viral circulation, and generation of new highly pathogenic PRRSV strains; and to avoid further increase shedding and disease risk of all other pathogens present.

LVI is theoretically favorable due to price, and strain similarity during immunization. Also, it may or may not decrease the time to baseline production; an inconsistent finding. However, several negative points are to be considered. Not only one but several different PRRSV strains are common in farms, and all transferred by LVI, together with other pathogens, like Salmonella, PPV, PCV2, Rota virus, Strep, E. coli and several others. This increases pathogen circulation and disease risk, and increasing time-to-stability = low prevalence status, by ≥12 weeks, and severely increasing the risk of generating new virulent strains on farm, by recombination.

The optimal vaccination strategy to control PRRSV circulation and protect against losses is the MLV + INV complementary vaccination scheme (CVS). A heterologous prime-boost vaccination concept.

The conventional PRRSV modified live virus (MLV) vaccines protects very well against the exacts same strain as the one in the vaccine. As soon as the field strain has a few percent genomic difference to the vaccine strain, efficacy in protection reduces rapidly and significantly. Today the field strain to vaccine strain difference is easily 12-15%, hence poor protection. Poor cross-protection and safety in shedding, reversion-to-virulence, and risk of recombination are common hallmarks of conventional PRRSV MLVs.

The killed inactivated (INV) vaccine given to animals never experienced PRRSV infection or MLV vaccination, does not produce a robust protection. However, given to an animal previously infected of MLV vaccinated, it produces a broader and better protection than the MLV-only. Also, it is safe, as it is not live. Post vaccination reaction and efficacy varies with vaccine design.

Complementary vaccination schemes (CVS) are a combination of priming with an MLV and boosting for stronger, broader protection and better viral clearance by an INV PRRSV vaccine. A heterologous prime-boost vaccination concept.

The next-generation CPD attenuated PRRSV2 MLV vaccine, providing significantly better cross-protection and safety than conventional MLVs can still benefit from CVS combination with INV, not the least in an PRRSV1+2 endemic herd.

Figure created by AI

The recommended optimal complementary vaccination scheme (CVS) is:

• 1^st MLV immediately after arrival (W0)
• 2^nd MLV 4 weeks later (W4)
• 1^st INV 4 weeks later (W8)
• 2^nd INV 3 weeks later (W11)

• MLV in 5-7^th week of gestation
• INV in the 3^rd week prior to farrowing

• In situations of highly virulent strains one dose of INV 2 weeks following MLV is commonly used with significantly better outcome.

Sow-herd PRRSV stability is best monitored by tung tip fluids (TTS) of stillborn and suckling piglets tested in two separate pools, to check both sow-stability and biosecurity of the farrowing compartment; grow finishers are monitored by several and pooled oral fluid (OF) samples every 1-4 weeks.

Weekly processing fluid (PF) investigation can be used in the sow herd, but sensitivity is lower, with the risk of anticipating stability on low level circulation, and with no ability to predict PRRSV status at weaning.

Combinations with familial-OF or serum sampling at weaning into processing fluids or TTF on stillborn-only are other options.

The frequency of sampling is every batch/week during outbreaks, ever 2^nd- 4^th batch/week at baseline production and stability.

The key internal biosecurity management routines are gilt introduction and immunisation to cool-down via quarantine like facilities over at least 12 weeks, strict age segregated production and hygienic procedures.

Gilt introduction via quarantine-like facilities for at least 12 weeks, in groups of batches of 4 consecutive weeks to optimally align vaccination age, heat induction and fit into farrowing batches

Strict age segregated production from birth and weaning till slaughter, all-in, all-out with no comingling between batches, and no moving back of older lesser performing pigs to younger.

Strict hygienic procedures: 1) Due diligence in monitoring, treatment ill and euthanasia of non-recovering piglets (McRebel-light), 2) Wash-soap-wash-disinfect-dry out-reheat, for visible cleanliness, removal of biofilm, thorough disinfection, and bringing the room up to pig(let) demands before entering.

The pen has the same infectious risk level: Needle change between pens, scalpel disinfected between piglets; teeth grinded only the very tip, tail cautery cutter sufficiently hot to disinfect and close wound.

Long-term PRRSV control depends on combining appropriate vaccination, consistent biosecurity, and. In endemic sow herds, producing PRRSV-negative piglets at weaning is an important measure of stability. Control programs should be reviewed regularly using herd performance, laboratory results, circulating viral strains, and veterinary assessment to adapt interventions as conditions change.

FAQs

1. What does PRRSV stand for?
   PRRSV stands for Porcine Reproductive and Respiratory Syndrome Virus, a pathogen that causes reproductive disorders in breeding pigs and respiratory disease in pigs of different ages. The virus is a major health and economic challenge for the global swine production.
2. What is the difference between PRRSV-1 and PRRSV-2?
   PRRSV-1 and PRRSV-2 are two distinct viral species associated with porcine reproductive and respiratory syndrome. They differ genetically and antigenically both between and inside the two PRRSV types,, which strongly influences the protection provided by different vaccines, and can influence diagnostic approaches.
3. What are the main economic consequences of PRRSV infection?
   PRRSV can cause reproductive losses, increased piglet mortality, respiratory disease, poorer production performance, and immunosuppression allowing for secondary infections and reduced response to vaccines given during PRRSV impact. Additional costs may arise from veterinary treatment, diagnostic testing, biosecurity measures, and disease-control interventions.
4. How can producers tell whether PRRSV control measures are working?
   Producers can evaluate PRRSV control through regular diagnostic surveillance and production indicators, including reproductive performance, piglet survival, and clinical disease. Trends over time help veterinarians assess whether a herd is maintaining or moving toward PRRSV stability.

References

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