This episode was recorded at the 2025 Florida Ruminant Nutrition Symposium.

Dr. Baumgard begins with an overview of his presentation, “Importance of gut health to drive animal performance and health.” He notes the metabolic and inflammatory fingerprint of all stressors is essentially the same, indicating they likely all emanate from the gut. Overall, we’re gaining a better understanding of how typical on-farm stressors negatively influence gut barrier function. He thinks the most likely mechanism of leaky gut is the immune cell known as a mast cell. When an animal or human is stressed, the enteric nervous system releases corticotropin-releasing factor, which binds to the mast cell, the mast cell degranulates, and the former contents of the mast cell (TNF-alpha, proteases, histamine, etc.) causes the gut to become leaky. (4:20)

Once the GI tract barrier becomes compromised, antigens like lipopolysaccharide (LPS) can infiltrate, stimulating the immune system. Immune activation causes loss of appetite much like any other infection. The gut heals fairly quickly upon removal of the stressor(s), and the gut can also acclimate to stress such that the early stages of a stress event are more severe than later stages. Strategies to combat leaky gut remain scarce, and there is no silver bullet. There are a variety of dietary strategies to target the gut permeability issue itself. Another approach would be to bind pathogens or curb their proliferation at the membrane of the small intestine. (7:06)

Dr. Neiehues asks if an antihistamine would work on gut mast cells the way it does in other body systems. Dr. Baumgard isn’t sure that’s ever been looked at, although there have been some studies in pigs using a product targeted to prevent mast cell degranulation. Dr. Nelson wonders if we should interfere in some of these processes because they’re obviously there for a reason. Panelists discuss stress events related to parturition and transition, particularly for first-calf heifers. Dr. Baumgard notes that stacking stressors on top of one another compromises an animal’s ability to tolerate stress. (9:28)

We know stress can cause ulcers in humans and horses - what about ruminants? Dr. Baumgard thinks it is likely that it’s happening, but we aren’t looking for it. Few animals who die on-farm do receive a thorough postmortem exam. It could also be that these types of insults to the gut are not visible to the naked eye. (19:11)

Dr. Nelson asks what makes some cows, despite all the challenges, able to be up and milking 150 pounds a day in no time after calving. What makes them unique? Dr. Baumgard lists some possibilities, including lower pathogenic inflammation than other cows, less tissue trauma damage to the uterus during calving, and lower sensitivity to immune activation. The panel disagrees with the notion that high-producing cows are stressed. (23:16)

Dr. Niehues and Dr. Baumgard trade stories of experiments where cows maintained production even with high stress and inflammatory markers. The panel goes on to discuss subclinical infections and their impact on transition cows. Dr. Nelson notes there are retrospective datasets where cows who had metritis showed decreased feed intake even before calving. Dr. Baumgard feels that the decrease in intake has been incorrectly assumed to be the cause of the metritis. He says the decrease in intake is often around two weeks before calving and he doesn’t think it’s a coincidence that at the same time, the mammary gland is initiating lactogenesis. He hypothesizes the mammary gland is causing an immune response, resulting in a decrease in intake. Dr. Nelson wonders if measuring somatic cell counts of colostrum would show any differences in mammary gland inflammation during this prepartum period. (29:18)

Panelists share their take-home thoughts. (42:02)

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