Necrotic Enteritis in Broilers: Identifying the Farm-Level Risk Factors

A broiler flock showing wet litter, poor performance or rising mortality may have several problems operating at the same time. With necrotic enteritis (NE), identifying Clostridium perfringens is only one part of the investigation. The more useful question is what has altered the intestinal environment enough to favour disease. 

NE is influenced by multiple interacting factors. Damage to the intestinal epithelium, changes in mucus production, disruption of the gut microbiota, altered intestinal transit, and impaired immunity can create conditions that favour C. perfringens proliferation and toxin production^[1],[2]. 

Coccidiosis: Look for the intestinal trigger 

Coccidial infection is an important factor to investigate because Eimeria damages the intestinal epithelium and increases mucus production and the availability of protein-rich nutrients in the gut. When Eimeria infection occurs together with C. perfringens, intestinal lesions become more severe and mortality increases compared with unaffected birds^[3]. 

This makes coccidiosis control an important component of NE prevention. When investigating an NE problem, the veterinarian should therefore assess the flock's coccidial status rather than considering the bacterial component in isolation. 

Feed formulation can alter the intestinal environment^[3] 

What the birds are eating can influence conditions within the intestine. Diets containing high levels of animal protein and cereals rich in non-starch polysaccharides (NSPs) can favour C. perfringens proliferation. NSPs increase digesta viscosity and water intake, contributing to wetter litter and conditions that favour sporulation and environmental contamination. 

Protein sources can also influence the severity of intestinal disease. Fish meal and potato protein concentrate produce higher intestinal lesion scores than soybean meal. Increasing fish meal inclusion also increased ileal C. perfringens abundance in challenged birds. 

These findings make the feed history clinically relevant. A recent formulation change, a different protein source or a diet high in NSPs may become particularly important when other NE-promoting factors are present. 

Feed quality can further increase the risk 

Mycotoxin contamination can create additional intestinal pressure. Deoxynivalenol (DON), produced by Fusarium, is a common poultry-feed contaminant, and DON contamination at 3000–4000 μg/kg significantly increases the incidence of NE by increasing the total protein concentration of duodenal contents, thereby favouring C. perfringens growth and toxin production. DON can also reduce villus height and transepithelial electrical resistance while increasing intestinal permeability in the duodenum and jejunum^[3],[4],[5]. 

Fumonisin can produce a similar intestinal challenge. At a feed contamination level of 20 mg/kg, fumonisin exerts toxic effects on intestinal epithelial cells and alters the microbial profile, while reducing small-intestinal length, villus height, and crypt depth^[5]. Such disruption of intestinal structure and barrier function can further predispose birds to NE. 

For the veterinarian, feed quality should therefore be considered alongside feed formulation when investigating an NE problem. 

Assess immune status and stocking density^[3] 

The bird's ability to withstand intestinal challenge also matters. Immunosuppression and viral infections including Marek's disease, chicken infectious anaemia and infectious bursal disease can predispose birds to NE. 

Management conditions may add further pressure. Increasing stocking density can increase caecal C. perfringens, alter the intestinal microbiota, and lower intestinal pH . A flock showing signs of NE should therefore prompt assessment of stocking density as well as disease and feed history. 

Temperature stress can tip the balance^[2] 

Environmental temperature can also influence intestinal health. Heat stress impairs intestinal integrity and alters the gut microbiota, with increased NE lesion incidence and severity reported following heat stress. 

Cold stress can have a similar effect. At 15 °C, a greater proportion of birds developed NE and intestinal lesions were more severe. The finding highlights the importance of considering periods of cold exposure when investigating an NE problem, particularly when other predisposing factors are already present. 

Put the risk factors together 

Rather than looking for one isolated cause, assess the flock across the major pressure points: 

• Coccidiosis: Intestinal damage and concurrent coccidial challenge 
• Diet: Animal-protein sources, NSP-rich ingredients and formulation changes 
• Feed Quality: DON, fumonisin and other potential mycotoxin concerns 
• Immune Status: Immunosuppressive diseases and infections 
• Stocking Density: Crowding and its effects on the intestinal environment 
• Temperature: Periods of heat or cold stress 

Clinical Bottom Line 

NE develops in an intestinal environment shaped by more than C. perfringens alone. Coccidial damage, dietary composition, mycotoxin exposure, immunosuppression, stocking density and temperature stress can all contribute to conditions that favour disease. 

For the practicing veterinarian, the useful question is therefore not simply whether C. perfringens is present. It is which combination of intestinal, nutritional, immune, and management pressures is present in the flock, and which of these can be addressed to reduce the risk of NE.

References:

1. Moore RJ. Necrotic enteritis predisposing factors in broiler chickens. Avian pathology. 2016 May 3;45(3):275-81. https://www.tandfonline.com/doi/pdf/10.1080/03079457.2016.1150587
2. Rodgers NJ, Swick RA, Geier MS, Moore RJ, Choct M, Wu SB. A multifactorial analysis of the extent to which Eimeria and fishmeal predispose broiler chickens to necrotic enteritis. Avian Diseases. 2015 Mar 1;59(1):38-45. https://www.academia.edu/download/67681551/A_Multifactorial_Analysis_of_the_Extent_20210619-27641-1kwq578.pdf
3. Fathima S, Hakeem WG, Shanmugasundaram R, Selvaraj RK. Necrotic enteritis in broiler chickens: a review on the pathogen, pathogenesis, and prevention. Microorganisms. 2022 Sep 30;10(10):1958. https://www.mdpi.com/2076-2607/10/10/1958
4. Wu SB, Rodgers N, Choct M. Real-time PCR assay for Clostridium perfringens in broiler chickens in a challenge model of necrotic enteritis. Applied and environmental microbiology. 2011 Feb 1;77(3):1135-9. https://journals.asm.org/doi/pdf/10.1128/aem.01803-10
5. Antonissen G, Van Immerseel F, Pasmans F, Ducatelle R, Haesebrouck F, Timbermont L, Verlinden M, Janssens GP, Eeckhaut V, Eeckhout M, De Saeger S. The mycotoxin deoxynivalenol predisposes for the development of Clostridium perfringens-induced necrotic enteritis in broiler chickens. PLoS One. 2014 Sep 30;9(9):e108775. https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0108775&type=printable
6. Antonissen G, Croubels S, Pasmans F, Ducatelle R, Eeckhaut V, Devreese M, Verlinden M, Haesebrouck F, Eeckhout M, De Saeger S, Antlinger B. Fumonisins affect the intestinal microbial homeostasis in broiler chickens, predisposing to necrotic enteritis. Veterinary Research. 2015 Sep 23;46(1):98. https://link.springer.com/content/pdf/10.1186/s13567-015-0234-8.pdf