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Some time ago, we interviewed Jean-Paul Cano and Joaquim Segalés to explore the Porcine Respiratory Disease Complex (PRDC), as well as the interactions between immunosuppressive agents that contribute to this multifactorial disease. We invite you to read the interview summary we have prepared.
1. What makes PRDC more than a respiratory infection?
When veterinarians talk about PRDC, it’s easy to think of it as just another respiratory disease. But as Quim Segalés reminded us “PRDC isn’t one disease, it’s the perfect storm.” That’s what makes it so tricky. Unlike infections with a single pathogen, PRDC is a synergistic process. It involves multiple viruses and bacteria working together or rather, affecting the pig’s immune response together. Each pathogen weakens a different part of the immune system or lung structure, creating ideal conditions for the next invader to succeed.
Click here to watch the recorded webinar.
However, the problem doesn’t stop at the microbes. Environmental stress, poor ventilation, and production flow design all act as invisible co-pathogens. Cano put it bluntly: “If the barn design is broken, the vaccines won’t save you.” PRDC is as much a problem of management as it is of microbiology.
So yes, PRDC causes coughing and pneumonia. But the real danger is how silently it sets in building up across time and production stages until the losses are too big to be ignored.
2. Which pathogens are commonly involved in PRDC?
Segalés and Cano walked us through the “usual suspects,” but emphasized that knowing who’s involved isn’t enough, you have to know what they do together.
Let’s start with the primary pathogens:
- PRRSV doesn’t just infect pigs, it weakens them. By targeting alveolar macrophages, it cripples the innate immune response and opens the door to everything else.
- Swine Influenza A Virus (IAV) damages the epithelial lining of the airways, making it easier for bacteria to invade and harder for the pig to clear them.
- Mycoplasma hyopneumoniae takes its time, it damages the cilia in the trachea and bronchi, disrupting the mucociliary escalator and setting the stage for chronic infections.
Then come the secondary pathogens, opportunistic bacteria like Pasteurella multocida, Actinobacillus pleuropneumoniae (APP), and Bordetella bronchiseptica. They’re not usually the ones that start the complex, but they’re experts at mantaining it once the lungs are compromised.
Cano reminded us: “It’s not just about what pathogens are present, it’s about the order they arrive in, and the immune gaps they find along the way.”
Click here to watch the recorded webinar.
The takeaway? If you only look for the obvious, you’ll miss the real story. Understanding PRDC means understanding the pathogen dynamics, not just the list of names on the lab report.
3. How do these primary pathogens interact in the lung?
As Cano said, “They don’t just co-exist, they set each other up for success, at the pig’s expense.”
That’s the danger of PRDC. It’s not that PRRSV, Mycoplasma, or influenza are individually devastating (even though they can be). It’s that together, they become the perfect team. One weakens the immune system, another damages the airways, and a third stalls the lungs’ ability to clear infections. The result? A wide-open door for secondary bacteria, and a pig that can’t fight back.
As Segalés noted, “It’s not 1 + 1. It’s more than 2.” The immune suppression, structural damage, and inflammation create an environment where opportunistic bacteria can take over, and that’s when lesions turn severe and performance crashes.
This is why field diagnosis usually underestimates the problem. You might see Mycoplasma and think it’s a mild case, but if PRRS is circulating at the same time, you’re dealing with something far worse than it looks.
4. Why is field diagnosis challenging?
Both Cano and Segalés agreed: you can’t diagnose PRDC by looking at a coughing pig from across the pen. The challenge isn’t just that the symptoms are vague, it’s that the disease is complex, layered, and constantly evolving. “PRDC doesn’t wear a name tag,” Cano joked. Clinical signs like fever, coughing, or uneven growth are just the surface. Behind them, there might be one pathogen, or three, or a rotating cast depending on the flow, the season, and the immunity status of the herd.
That’s why they consider a multi-layered diagnostic approach, that combines:
- Farm history: Have there been recent introductions? Are pigs vaccinated? What’s the previous PRRS or influenza status of the flow?
- Necropsy and lung scoring: This is where Cano insisted: “If you’re not opening lungs regularly, you’re flying blind.” The distribution and character of lesions offer vital clues that the nasal swab won’t tell you.
- Laboratory testing:
- PCR is essential to confirm the presence of key pathogens.
- Histopathology helps distinguish the nature of lung damage, especially in complex or overlapping infections.
Still, even with these tools, timing matters. A sample taken too late might miss the peak viral load; too early, and the bacterial colonization hasn't started yet. As Segalés said, “If you don’t understand when and where to sample, even the best test won’t help.”
Diagnosis in PRDC isn’t about finding a cause. It’s about understanding the interplay and catching it before it spirals into a trainwreck.
333 staff
