Introduction
As the winter season sets in, low temperatures bring not just a chill to the air but also an increased risk of respiratory diseases in pigs. These colder conditions create an environment where common infectious agents like Swine Influenza Virus (SIV), Porcine Reproductive and Respiratory Syndrome Virus (PRRSV), and Mycoplasma hyopneumoniae (Mhp) thrive, putting pigs, most significantly post-weaning, at a heightened risk of illness and mortality. The previously mentioned pathogens trigger excessive production of reactive oxygen species (ROS), overwhelming the natural antioxidant defenses of pigs, disrupting the balance of pro-oxidants and antioxidants in the body. This oxidative stress damages cellular components, weakens the immune response, and contributes to systemic inflammation, complicating recovery. Understanding the challenges pigs face following infection enables the implementation of targeted interventions to mitigate and preserve health.
This TechTalk explores the mechanisms by which respiratory diseases trigger oxidative stress in pigs, the consequences on morbidity and mortality, and the efficacy of interventions, particularly water-soluble vitamin and micronutrients supplementation, in mitigating these effects.
Mechanisms of oxidative stress:
After infections occur, oxidative stress is indeed a consequence of the immune response. During inflammation, immune cells release reactive oxygen species (ROS), which can lead to oxidative stress by exceeding the body’s antioxidant defenses. This oxidative burst is crucial for pathogen elimination but can also damage surrounding tissues, creating a cycle of inflammation and further oxidative stress. Additionally, oxidative stress can activate signaling pathways that enhance inflammatory responses, linking the two processes tightly together. Thus, oxidative stress and immune response are interdependent mechanisms in various diseases. Research indicates that all of these agents significantly increase ROS levels in infected pigs, resulting in oxidative damage to lipids, proteins, and DNA.
Oxidative Stress Triggers:
- Reactive Oxygen Species (ROS) Production: after infections cells start producing NADPH oxidase (a critical enzyme complex whose main function is to produce ROS), contributing to oxidative stress and respiratory tissues injury.
- Innate Immune Response: The respiratory infectious agents stimulate a strong innate immune response, enhancing pro-oxidation processes and increasing the expression of cytokines and interferon-stimulated genes.
- Co-Infections: Co-infection with other pathogens like Mycoplasma hyopneumoniae can exacerbate oxidative stress, leading to more severe disease outcomes.
- Gene Regulation: Infection with SIV affects genetic pathways related to immune and inflammatory responses, further promoting oxidative stress (4). Mhp infection alters the expression of genes involved in redox homeostasis and antioxidant defense, such as those regulated by the transcription factor NRF2. This response is linked to the pathogen’s ability to produce hydrogen peroxide, a cytotoxic agent (5).
- Mitochondrial Dysfunction: PRRSv and Mhp enhance mitochondrial calcium uptake from the endoplasmic reticulum, resulting in mitochondrial ROS release, which exacerbates oxidative stress (6).
- Inflammatory Response: these agents induce a strong inflammatory response, further contributing to oxidative stress and tissue damage (10).
In a study at a large Midwest swine producer, weaned pigs, approximately 20 days old were given ImmuFend immediately 
In a study involving 141,045 pigs conducted by a large Midwest swine production system, ImmuFend demonstrated an overall reduction in nursery mortality from 4.96 to 4.19% — a 15.5% decrease (P < 0.0001)