Here we will focus the discussion on the practical applications and on lessons learned from recent field studies on response strategies for PRRSV management in affected breeding herds.

The PRRS virus (PRRSV) continues to evolve, resulting in new strains, from which some are ‘more of the same,’ and others are of relatively high virulence. Recent examples of high virulence strains include the Lineage 1C variant of RFLP 1-4-4 and the L1C of RFLP 1-2-4.

In response to the evolving virus, veterinarians and producers continue to join forces and mount resources to improve the capability to prevent, respond, and recover from infection. Recent developments include novelties in monitoring and surveillance strategies, new herd classification systems to document better the PRRSV activity & associated response strategies, and accumulation of field-based data on the effectiveness of different response strategies.

Epidemiological considerations: seasonality and the importance of grow-finish populations
The swine disease reporting system (SDRS) is a collaborative project that aggregates diagnostic data from multiple veterinary diagnostic laboratories. The SDRS reveals macro-epidemiological aspects associated with pathogen activity over time, geographical regions, age groups, farm types, and specimens. Specifically, about PRRSV, the SDRS project has repeatedly reported that:

The positivity of PCRs from grow-finish samples is consistently higher than that of sow farms.

The seasonal spikes in the positivity of breeding herds are preceded by spikes in the grow-finish population.
Altogether, these findings support the importance of grow-finish populations in the ecology of PRRSV in the swine industry.
We hypothesize that the grow-finish population is an important reservoir and a crucial amplification spot for PRRSV.

According to the SDRS advisory group, the higher positivity in grow-finish and the preceding spike in grow-finish related to breeding herd is partly explained by the relatively lower biosecurity and biocontainment measures in grow-finish sites. It is common in the US for producers to mix sources in grow-finish sites and to share labor, equipment, and mortality removal transport vehicles. These characteristics may help maintain and perhaps amplify PRRSV circulation in that production stage. Epidemiological links such as common labor, pig transportation, and feed delivery may explain how the virus gets transmitted from grow-finish sites to breeding herds.

There is, therefore, a great opportunity to ‘raise the bar’ on biosecurity & biocontainment of grow-finish sites, lowering the overall pressure of PRRSV infection in the industry. One could hypothesize that a lower infection pressure will lead to a significant reduction in the outbreak frequency of breeding herds, breaking the cycle of PRRSV infection and transmission. Coordinated regional disease control programs are needed to validate this concept. The existing monitoring & surveillance tools partnered with available cyber-infrastructure provide great foundation for such projects, as outlined by Magalhaes et al (2021) in his Frontiers in Veterinary Science publication entitled “Next Generation of Voluntary PRRS Virus Regional Control Programs”.

Another significant advancement in knowledge on the ecology of PRRSV in pig populations comes from case reports implementing whole PRRSV genome sequencing (WGS) in farms experiencing outbreaks. In one particular study, Dr. Trevisan et al. implemented WGS in 20 breeding herds and reported that in all but two farms (90%), there was evidence of multiple PRRSV co-circulating simultaneously. Some farms had evidence of 4+ strains present. They also reported that recombination between and within wild-type and attenuated virus vaccine viruses was a common finding. Those findings highlight that there is hardly ‘a’ virus circulating in breeding herds. Instead, there is a diverse ‘cloud’ of PRRSV co-circulating and ever-evolving. This may be one of the reasons why the virus is a moving target to existing immunologic solutions to build herd immunity. It is also known that the number of diverse strains co-circulating in the herd positively correlate with virulence. In other words, the more PRRSV variants are circulating in the herd, the greater clinical expression is expected in the pig population.

Several epidemiological studies following breeding herds after a PRRSV outbreak until recovery have been made in the past ten years. In these studies, the production impact is often reported as the magnitude of piglet losses from the outbreak until recovery. Time-to-stability is reported as the weeks it took from the outbreak until consistently producing PRRSV-negative at weaning following the American Association of Swine Veterinarians terminology. Overall, the factors associated with shorter time-to-stability and lower production impact include:

Naïve herds take much longer to recover productivity and to produce PRRSV-negative pigs than herds having herd immunity derived from a previous outbreak or modified-live virus vaccination.

Herd closure increases the success rate of achieving stability.

Herds intentionally targeting to reach a ‘negative’ status were twice more likely to achieve stability (80% versus 40%) compared to herds targeting to reach low prevalence but not necessarily clearing the virus.

Herds implementing a deliberate whole-herd exposure achieved stability and had a lower production impact than herds relying solely on natural exposure. The herds using a modified-live virus (MLV) vaccine had a lower productivity impact but longer time-to-stability compared to herds that used live-virus inoculation (LVI) as part of the whole-herd exposure program.
Farms implementing batch farrowing had a better recovery than farms operating on a standard continuous breeding & farrowing system.

Herds implementing stricter bio-management practices soon after the outbreak had a more expedited recovery than herds postponing the implementation of McRebel-like practices.

Herds infected with certain emerging PRRSV strains (e.g., RFLP 1-7-4 or 1-4-4) had a relatively more severe outbreak.
Farms having relatively higher genetic variability, i.e., ≥3 PRRSV, had a 12-week increase in the median time to achieve low prevalence compared with herds with ≤ 2 strains detected.

Farms with ≤ 2 PRRSV strains detected (n = 10) had 1,837 fewer piglet losses per 1,000 sows.

Farms with no recombination events detected (n = 8) had 1,827 fewer piglet losses per 1,000 sows compared to farms with ≥3 PRRSV strains (n = 8) or detected recombination events (n = 10), respectively.

Despite the lack of a silver bullet to fully prevent losses caused by wild-type PRRSV infections, the combination of existing strategies such as bio-management practices, gilt flow, and herd immunization results in significantly reducing the losses and bringing the breeding herd (and downstream flow) back to baseline productivity within 3-4 months from the outbreak, and producing PRRSV-negative pigs within 5-6 months.