When 1+1 is greater than 2: the interaction that causes CRP (1/3) - Article - , Pig Pages

Jean-Paul Cano and Joaquim Segals share practical and academic perspectives on the management and pathogenesis of CRP.

We interviewed Jean-Paul Cannon and Joaquim Segales to explore the relationship between porcine respiratory complications (PRC) and the immunological agents that contribute to this multifactorial disease.

1. What makes CRP more than just a respiratory infection?

When vets talk about CRP, it's easy to think it's just another respiratory disease.But as Quim Segales reminded us, "CRP is not a disease, it's a perfect storm."And that is exactly what makes it difficult to control.Unlike an infection caused by a single pathogen, CRP is a synergistic process involving several viruses and bacteria that work together, or rather, that the pig's immune system.Coordinated changes in response.Each pathogen weakens a different part of the immune system or lung structure, creating ideal conditions for the next agent to succeed.

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However, the problem is not limited to microbes.Environmental stress, poor ventilation and production flow design act as invisible co-pathogens.Cano puts it emphatically: "If the ship is poorly designed, the vaccine will not save you."CRP is as much a management problem as it is a microbiological problem.

Yes, CRP can cause coughs and pneumonia.But the real danger lies in its silent progress, accumulating over time and stages of production until the losses are too obvious to ignore.

2. What pathogens are commonly involved in CRP?

Segales and Cano studied the "usual suspects," but insisted that it is not enough to know which pathogens are present. But it is necessary to understand how they interact with each other.

Starting with the main pathogens:

- Prrs virus (PRRSV) not only infects pigs, but also dilutes them.By attacking alveolar macrophages, he paralyzes the inherent immune response and leaves the door open to other pathogens.

- Swine influenza A virus (IAV) damages the epithelium of the respiratory tract, making it easier for bacteria to enter and difficult to digest.

- Mycoplasma hyopneumoniae acts slowly, damaging the cilia of the trachea and bronchi, altering mucociliary elevation, and promoting chronic infection.

Added to this are secondary pathogens such as opportunistic bacteria Pasteurella multocida, Actinobacillus pleuropneumoniae (APP) or Bordetella bronchiseptica, which rarely initiate this complex but are experienced in maintaining it after the lungs are already compromised.

The rule summarizes as follows:"It's not just about which pathogens are there, but in what order they come and what immune deficiencies they encounter."

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Moral?If you're just looking for the obvious, you're missing the real focus of the problem.Understanding CRP means understanding pathogen dynamics, not just a list of names on a lab report.

3. How do these primary agents interact in the lung?

As Cano explains, "Not only do they coexist, they prepare the ground for each other's success at the expense of the pig."

This is the big threat of CRP. PRRSV, mycoplasma, or influenza are not destructive on their own (although they can be), but together they form a perfect team. One weakens the immune system, another damages the airways, and the third hinders the lungs' ability to clear the infection. The result? The door opens to opportunistic bacteria and pigs who are unable to defend themselves.

Segales trembled him perfectly: "It's not 1 + 1. It's more than 2."Immunization, structural damage, and inflammation creates an ideal breeding point for secondary bacteria, which is when injuries get worse and plumbing performance.

Therefore, field diagnostics tend to underestimate the problem.You may detect mycoplasma and think the situation is mild, but when PRRS is circulating at the same time, the situation is much more serious than it appears.

4. Why is CRP field testing a challenge?

Both experts agreed: CRP cannot be diagnosed by observing a coughing piglet from the other side of the pen.The challenge is not only that the clinical symptoms are non-specific, but also that the disease is complex, dynamic and evolutionary."CRP has no label," Cano joked.Clinical symptoms such as fever, cough and irregular growth are only the tip of the iceberg.There may be more to it.one pathogen, three or a changing combination depending on the state flow, season or immune status.

They therefore recommend a multi-step diagnostic approach that combines:

- Farm history: Have the animals been delivered recently? Have the pigs been vaccinated? What is the status of previous PRRS and flu infections?

- Necropsy and Lung Assessment: This is where Canon claims, "If you don't open your lungs regularly, you'll go blind."The distribution and type of lesions give clues that the nasal swab is not present.

- Laboratory test:

- PCR is necessary to confirm the presence of major pathogens.

- Histopathology helps distinguish the nature of lung injury, especially in complex or overlapping infections.

However, even with these tools, timing is important.A sample taken too late may not detect peak viral load;And if it's too early, bacterial colonization may not have started yet.As Segales put it: "If you don't know when and where to take the sample, even the best testing method won't work."

Diagnosing CRP is not about finding the cause.It's about understanding the interactions and taking action before a problem becomes a disaster.