When 1+1 is more than 2: interactions causing the Porcine respiratory disease complex (PRDC) (2/3)

5. What are the most useful tools for detecting PRDC in farms?

Once you’ve built your diagnostic strategy, the next step is surveillance and that’s where many farms fall short. As Cano put it, “If you’re waiting for pigs to cough, you’re already late.” The goal isn’t just to diagnose PRDC once it’s visible, but to spot the early signs that something’s brewing.

Segalés and Cano shared several practical tools and strategies to monitor PRDC proactively:

• Routine necropsy with lesion tracking: It’s not just about doing necropsies it’s about looking for changes over time. Tracking lesion severity and patterns can help identify emerging trends or shifts in pathogen pressure long before they become clinical outbreaks.
• Lung lesion scoring systems: Using a consistent scoring system across batches (whether done at slaughter or on-farm) provides measurable data. Segalés noted that lesion scoring isn’t just for research: “It’s one of the few field tools that gives you objective feedback on how your control program is working.”
• Growth curve monitoring and treatment rates: Subtle drops in average daily gain or increased use of injectables often precede clinical disease. If you're watching close enough, the numbers speak before the lungs do.
• Active surveillance programs: Oral fluid PCR, targeted nasal swabs, or pooled samples can provide early clues of pathogen activity. These tools are especially useful in large systems, where catching circulation early can prevent flow-wide spread.

Click here to watch the recorded webinar.

6. What are the factors that influence the development of PRDC?

PRDC doesn’t just appear out of nowhere. According to Cano, “Pathogens are everywhere, it’s the environment that decides who gets sick.” That’s why two farms with similar infections can have totally different outcomes.

Segalés and Cano emphasized that PRDC is fueled not only by pathogens, but by the conditions that allow them to cause damage. When the system is already under stress, even mild infections can turn into severe disease.

Here are the main highlighted causes:

• High-density production: Cano didn’t mince words: “If you pack pigs like sardines, don’t be surprised if disease spreads like wildfire.” High stocking density increases direct contact, aerosol transmission, and overall stress, all of which favor respiratory pathogens.
• Poor ventilation: a common culprit. When airflow is inadequate, gases like ammonia and CO₂ build up, damaging the respiratory tract and impairing local immune defenses. In winter, reduced ventilation to conserve heat often leads to unseen problems.
• Temperature fluctuations: sudden swings in temperature (especially between day and night) disrupt the pigs’ thermoregulation, weakening their ability to respond to pathogens. Segalés noted that young pigs in nurseries are especially vulnerable to these shifts, particularly when transitioning between barns or flows.
• Stress factors: transport, weaning, handling, mixing — all of these activate the hypothalamic-pituitary-adrenal axis, suppressing the immune system. Even heat stress in summer can increase respiratory disease severity.
• Commingling animals of different ages: when pigs of different sizes or immune backgrounds are mixed, older pigs may transmit pathogens asymptomatically, while younger pigs struggle to mount an effective response. Cano described it as “playing a football match where one team gets helmets and the other doesn’t.”
• Continuous flow systems: this was a big one. In continuous systems, new pigs enter before the environment has been cleaned and dried allowing pathogens to linger and re-infect incoming groups. Segalés reinforced that “if you never reset the system, you never break the cycle.”

Ultimately, the farm environment either amplifies or suppresses PRDC. That’s why managing ventilation, density, and flow design isn’t just a comfort issue, it’s a disease control strategy.

Click here to watch the recorded webinar.

7. Can vaccination prevent PRDC?

Yes, but not by itself. That was the clear message from both Cano and Segalés. As Cano put it, “Vaccination is a tool, not a magic trick.” You can’t vaccinate your way out of poor management or a broken production flow. They emphasized that vaccines are essential, particularly against primary viral agents like PRRSV, IAV, and Mycoplasma hyopneumoniae, but their effectiveness depends on three critical factors:

• Knowing what’s circulating: before designing a vaccination program, you need to know which pathogens are present, how they behave in your specific production flow, and what immunity already exists in the herd. Segalés warned against “blanket vaccine programs that haven’t seen a diagnostic report in three years.”
• Timing and strategy: it’s not just what you vaccinate against, it’s when. Vaccinating too early may be wasted on maternal antibodies; too late, and the virus is already circulating. Cano pointed out that mass vaccination of piglets without flow separation often ends up doing more harm than good by creating false security.
• Combining with management: This was perhaps their strongest point: vaccination must be paired with biosecurity, monitoring, and flow discipline. Cano was clear: “If you vaccinate and then mix pigs across ages and flows, you’re undoing your own work.” A good vaccine strategy means nothing if pigs are stressed, poorly ventilated, or constantly exposed to new infection sources.

And when it comes to bacterial vaccines (APP or Pasteurella) the speakers reminded us they should be used selectively, and only after confirming their relevance in the herd through lesion scoring and lab testing.

In short: Vaccination can absolutely reduce the impact of PRDC, but only when it’s diagnosis-based, well-timed, and part of a broader control strategy. As Segalés said: “Vaccines are part of the orchestra, but they don’t play solo.”