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One Health In Animal Agriculture—Integrated Disease Prevention

One Health integrates human, animal, and ecosystem health to prevent diseases at their source. This integrated approach fosters collaboration across multiple sectors, disciplines and communities to optimize health outcomes, like diseases, antimicrobial resistance (AMR) and food safety, through evidence-based policies and practices. For Ecolex Animal Nutrition, this holistic approach not only fuels feed additive innovations for better gut health, immunity, and productivity—but is complemented by extensive knowledge transfer in biosecurity and hygiene, and AMR.


One Health Approach
One Health Approach

For animal health, the focus is on proactive measures—such as nutrition, biosecurity and hygiene, and farm management—instead of reactive interventions, such as antibiotic treatment.

One Health Approach to Animal Health
One Health Approach to Animal Health

Animal health is critical to One Health as estimates indicate that more than 70% of medically important antimicrobials are consumed in food-producing animals, amplifying resistance that threatens human medicine (such as resistance to colistin, the antibiotic of last resort for gram-negative infections, spreading from farms to communities and hospitals).


Applying One Health to Animal Health


Consider a broiler farm with a recurring problem with necrotic enteritis (NE), caused by the ubiquitous and opportunistic Gram-positive bacteria Clostridium perfringens (Cp)—also a common cause of food poisoning in humans—and treated with in-feed antibiotics. Due to the complexity and multifactorial aspects of NE, there is no single solution—it will depend on the most important challenges of each farm. Integrated control strategies mitigate multiple predisposing factors that result in the overgrowth of pathogenic Cp, and resulting toxin production, caused by types A and C, avoiding damage to the gut lining, that lead to decreased nutrient absorption, and significant mortality.


Examples of One Health interventions to reduce reliance on antibiotics and mitigate AMR include:


Feed and Nutrition


  • Least-cost diets, which prioritize minimizing feed costs, can increase the risk of NE if not managed carefully.

  • Cp lacks many genes required for amino acid biosynthesis, so it cannot grow in an environment where the supply of amino acids is limited. Avoid formulating diets with excess crude protein (over requirements) and poorly digestible proteins which reduces the undigested protein in the hindgut (where Cp normally lives as part of the gut microbiome without causing harm) that promotes overgrowth of Cp.

  • Animal proteins, in particular with high concentrations of poorly digested proteins are associated with higher incidences of NE.

  • Animal proteins like fishmeal and meat and bone meal provide highly digestible proteins that release undigested peptides and amino acids (e.g., glycine, arginine) and biogenic amines in the lower gut, fueling Cp growth compared to plant proteins.

  • Avoid high-viscosity small grains (like rye, wheat, oats and barley) that contain a lot of indigestible soluble fiber, especially during times of heavy coccidia cycling, without proper enzyme treatment helps prevent the thick, sticky gut conditions that promote Cp growth.

  • Protease supplementation to improves protein digestibility, while carbohydrases (e.g., xylanases) reduce the viscosity of digesta, making the environment less favorable for Cp proliferation.

  • Avoid abrupt feed changes in feed composition, or changes from starter to grower feed that can disrupt the microbiota and increase susceptibility.

  • Use of feed additives to enhance gut health. Probiotics, prebiotics, and organic acids can maintain a healthy gut microbiota. Essential oil compounds can control the proliferation of Cp in the intestine.

  • Finely ground diets, particularly when using small grains, is a risk factor. Coarse ground feed, or whole grains increases gizzard activity, which consequently triggers hydrochloric acid production and increases feed retention time in the gizzard and proventriculus.

  • Mycotoxins can reduce immune function, and also cause gut damage, resulting in proteins leaking from the plasma to the gut, increasing levels available for Cp growth.

  • Oxidized animal fats generate peroxides that damage gut mucosa, impair nutrient absorption, and create a pro-inflammatory environment favoring Cp. Saturated animal fats slow digesta transit, trapping substrates for bacterial growth.


Biosecurity and Hygiene

  • Cleaning and disinfection of houses between flocks decreases the bacterial load.

  • Biofilms in water systems protect Cp from disinfectants, contributing to bacterial persistence. Biofilms can also clog nipple drinkers, causing leaking, contributing to wet litter.

  • Dead birds rapidly decompose, releasing Cp toxins and increasing bacterial loads. Cannibalism by healthy flockmates spreads pathogens directly to the gastrointestinal tract.


Farm Management 

  • Intestinal damage from coccidiosis is the main predisposing factor for NE, anticoccidial programs are essential. However, intestinal damage can occur due increased resistance to ionophores, or chemical anticoccidials, or vaccination with live coccidiosis vaccines.

  • Immunosuppressive viral diseases (e.g., Marek’s disease, infectious bursal disease, and chicken infectious anemia) can reduce resistance to bacterial infections in the gut.

  • Chick quality affects immune and digestive system development, which in turn affects feed intake and nutrient absorption.

  • Wet litter (>30% moisture) becomes compacted, reducing oxygen penetration and creating anaerobic zones, providing an ideal opportunity for the strictly anaerobic Cp to proliferate.

  • High stocking density increases NE risk by increasing manure output, increasing litter compaction, reducing air exchange efficiency, trapping humidity, and competition from drinkers increases spillage. Furthermore, high stocking density elevates stress hormone levels (primarily corticosterone, the avian equivalent of cortisol), increasing necrotic NE risk through immune suppression and gut dysbiosis.

  • Lighting programs influence NE risk primarily through their effects on feeding behavior, gut pH, and stress resilience. For instance, continuous lighting promotes constant feed intake, leading to rapid crop emptying, higher foregut pH (>5.5), and faster digesta transit. This reduces acid secretion in the gizzard/proventriculus, creating a neutral environment that favors Cp proliferation.


Want To Know More?

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