Necrotic Enteritis Management: An Evidence-based Strategy

Necrotic enteritis (NE) is an economically important enteric disease of broilers and other poultry that typically presents as a spectrum ranging from subclinical performance loss to acute mortality. The condition is most often linked to intestinal overgrowth of pathogenic Clostridium perfringens and toxin-mediated epithelial injury, which reduces nutrient absorption and increases inflammation-associated inefficiency. 

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Pathogenesis: Why “Presence” Is Not the Same as “Disease”

Because C. perfringens is widespread in the environment, NE is best understood as a dysbiosis-driven event that occurs when intestinal conditions shift in favor of clostridial expansion and virulence expression. A major advance in NE biology was the identification of NetB (necrotic enteritis B-like toxin), a pore-forming toxin strongly associated with avian NE and demonstrated to be a critical virulence determinant in experimental disease.

However, toxin potential alone does not predict outbreaks. Contemporary reviews emphasize that NE commonly requires predisposing stressors that disturb the intestinal ecosystem—especially epithelial damage and changes in nutrient substrates available to bacteria.

Key Predisposing Factors To Target

Coccidial cycling and mucosal injury. Eimeria infection is repeatedly described as a major trigger because it compromises barrier function and increases luminal proteinaceous substrates that can support clostridial proliferation.

Diet composition and digestibility. Rations that increase undigested nutrients reaching the distal small intestine (e.g., abrupt formulation changes, poorly digested protein, certain cereals with higher non-starch polysaccharides) can increase fermentation pressure and alter microbial competition, raising NE susceptibility.

Exposure pressure from the production environment (including feed). Multiple surveys have documented C. perfringens in ingredients and finished feeds, particularly in animal protein–rich raw materials, supporting the concept that feed can contribute to continuous microbial “inputs” into the gut. 

A Multi-Hurdle Necrotic Enteritis Management Program

Because NE is multifactorial, best practice is “stacked controls” rather than reliance on a single intervention:

• Reduce epithelial damage events. Optimize coccidiosis control (vaccination or anticoccidials as appropriate), litter moisture management, and environmental stability to reduce inflammatory cycling and barrier disruption.

• Nutritional mitigation to limit clostridial substrates. Focus on digestible amino acid balance, control dietary protein excess, consider enzyme strategies (e.g., to reduce viscosity and improve nutrient capture), and avoid abrupt transitions that destabilize intake and digestion.

• Modulate microbiota and gut function. Peer-reviewed reviews describe the use of non-antibiotic tools (e.g., selected probiotics, organic acids, phytogenics) as part of broader gut health programs aimed at improving colonization resistance and reducing pathogen expansion opportunities.

• Feed hygiene as upstream risk control. By reducing the overall microbial load entering the bird each day through feed, sanitation and recontamination prevention across storage, augers, bins and transport interfaces can lower the microbial ‘pressure’ on the gastrointestinal tract and help reduce stress on gut function—especially during periods when the intestine is more vulnerable. 

Necrotic enteritis management is strongest when it is engineered as a systems program: protect the mucosa, reduce fermentable substrate overflow, support a resilient microbiome, and lower pathogen inputs—especially during predictable high-risk windows such as coccidial cycling and diet transitions. 

To learn more about feed as a fomite or learn how feed sanitation can enhance your necrotic enteritis prevention efforts download our Enteritis guide today.

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