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  • Endotoxins: The Hidden Dairy Cow Performance Inhibitor

    About Endotoxins

    Endotoxins, also known as lipopolysaccharides (LPS), are essential components of the outer membrane of all the bacteria classified as Gram-negative. Among these bacteria are many pathogens such as Escherichia coli (E. coli), Salmonella and Campylobacter. Dairy cows are constantly in contact with Gram-negative bacteria through the feed, water, air, dust and faeces and consequently, they are always exposed to endotoxins from these bacteria. Endotoxins act as metabolic disruptors which contribute to ketosis and they activate the immune system to generate an inflammatory response in dairy cows (Kvidera et al., 2017). There is also a high endotoxin activity during subacute rumen acidosis (SARA), due to rapid growth of Gram-positive bacteria in the rumen and to the death and lysis of Gram-negative bacteria as a result of the decline in ruminal pH. In addition, recent in vitro studies have shown that endotoxins can stimulate the growth of starch fermenting bacteria contributing to the development of ruminal acidosis.

    Endotoxins may also originate from numerous sources within the cow, but the major sites in dairy cows include the uterus (metritis), mammary gland (mastitis) and the rumen. During the weeks surrounding calving, cows are exposed to a lot of stress which may allow endotoxins to get into the blood stream and thereby initiate an inflammatory response. Systemic postpartum inflammation is common and occurs even in cows which remain seemingly healthy throughout the transition period. The magnitude and persistency of the inflammatory response seems to influence transition cow performance as it has a substantial demand on metabolic energy (Kvidera et al., 2017).

    The cost of endotoxin-induced inflammation

    In the dairy cow endotoxin-induced inflammation uses feed energy and redirects nutrients away from the normal processes that support milk and muscle synthesis and this leads to reduced productivity. Approximately 1 kg of glucose is used by an intensely activated immune system during a 12-hour period in lactating dairy cows. This diversion of glucose during inflammation caused by endotoxins has particular consequences during lactation as it requires ~72 g of glucose for synthesizing 1 kg milk. Furthermore, increased utilization of glucose occurs simultaneously with infection-induced decreased feed intake. These two events: the coupling of enhanced nutrient requirement with reduced feed intake obviously decrease the amount of nutrients available for the synthesis of valuable products such as milk, meat, and the foetus (Horst et al., 2019).

    How Glycal Forte® can help

    There is a lot of research nowadays directed towards health maintenance and disease avoidance in dairy cows through nutritional strategies. The feed ingredient, Glycal Forte® has a very strong ability to help manage the rumen metabolism and contribute to enhanced dairy cow productivity. Glycal Forte® has also been found to have a potent effect against endotoxins as tested at an independent European laboratory. The activity of Glycal Forte® against endotoxins was tested in a Limulus Amebocyte Lysate (LAL) test with the Glycal Forte® included at 2% by weight. Glycal Forte® was found to reduce activity to below 0.05 Endotoxin Units (EU) /ml, which indicated a significant effect against endotoxins. The LAL test is recommended in all international pharmacopeias as the method for finding bacterial endotoxins (Lindsay et al., 1989).

    This in vitro study clearly indicated that Glycal Forte® has a strong inhibitory effect against endotoxins. It is possible that some of the beneficial responses seen with Glycal Forte® in dairy cows may be due in part to a reduction in endotoxin levels.



    K. Kvidera et al. (2017). Leaky gut’s contribution to inefficient nutrient utilization. WCDS Advances in Dairy Technology, 29: 137-143.

    K. Lindsay et al. (1989). Single-step, chromo genic Limulus Amebocyte Lysate assay for endotoxin. Journal of Clinical Microbiology, 27: 947-951.

    A. Horst, et al. (2019). Causes and metabolic consequences of leaky gut. https://ecommons.cornell.edu/bitstream/handle/1813/67035/P4%20Baumgard%20(manu).pdf?sequence=2.