Overview of Necrotic Enteritis In Poultry

November 3, 2022
Gut Health

What is Necrotic enteritis?

Necrotic enteritis is one of the world’s most common poultry diseases affecting around 40% of commercial poultry. The disease is caused by the overgrowth of Clostridium perfringens type A and type C and its exotoxins in the small intestine. Clinical forms lead to a sudden increase in flock mortality and severe problems in a very short time. While in subclinical forms, it is characterized by impaired digestion. The economic impact of necrotic enteritis on global poultry production amounts to billions of dollars annually. 

Clostridium Perfringens

Clostridium Perfringens Bacteria

Clostridia are large, Gram-positive, rod-shaped, toxin-producing bacteria that are anaerobic and can produce endospores to survive. They are ubiquitous worldwide, being found in soil, dust, and animals. This organism can grow faster than most other pathogenic bacteria if the conditions are optimal. Clostridium perfringens is spore-forming and, therefore, can survive under variable environmental conditions for extended periods. It may be transmitted between facilities within an integrated broiler chicken operation. Spread within a flock kept on litter predominantly takes place via the fecal-oral route, and flies are also suspected to be important contributors to the spread. Another potential source of infection is feed, which may be contaminated despite pelleting and heat treatment. Fish meal is considered a particularly likely source of Clostridium perfringens contamination.

Incidence of Necrotic enteritis

Necrotic enteritis occurs in broiler chickens raised on litter at 2 to 5 weeks of age and at 7 to 12 weeks in turkeys. The disease will remain in the flock for 5 to 10 days, causing 2% to 50% mortality (Merck Veterinary Manual, 1998). Typically, necrotic enteritis occurs in broiler chickens; however, layers and turkeys can also be affected (Droual et al.,1995; Dhillon et al., 2004).


Economical significance

Necrotic enteritis has increased in occurrence and severity over the years. It impairs nutrient absorption, growth rate, feed conversion, and animal welfare. When it comes to the damage it causes, producers often adopt the figure of US$0.05 per chick derived from a US$2 billion loss on a worldwide scale estimated in 2000. Since then, parameters have changed, as have the actual costs of NE, which could come close to US$6 billion in 2015 (World Poultry, 2015).

Causes of necrotic enteritis

Necrotic enteritis is caused by toxins produced by Clostridium perfringens as it grows in the intestinal tract of birds. Clostridium perfringens is a bacterium that grows under anaerobic conditions (in the absence of oxygen) and produces spores that are highly resistant to drying, heat, acid and other harsh conditions. The spores produced by this organism are commonly found in water, soil, feed, manure and other environmental sources.

Although small numbers of Clostridium perfringens are commonly found in the intestinal tract of healthy broilers as normal inhabitants, they do not cause disease. Under normal conditions, the “good bacteria” in the intestinal tract keep the Clostridium perfringens population small in number. However, when conditions change in the intestinal tract, Clostridium perfringens numbers increase and toxins are produced. The toxins will induce cell damage known as Necrotic Enteritis (NE).

Symptoms and clinical signs

Necrotic enteritis - Confluent necrosis of the jejunum.

During necrotic enteritis outbreaks, birds do not present obvious external signs. There are two forms of Necrotic Enteritis, the acute clinical form and the subclinical form. Although it can be seen at any age, the acute clinical form is primarily a disease in young chickens, showing severe depression, reluctance to move, diarrhea, ruffled feathers, sudden death, and an increased mortality rate that can sometimes reach 50%.
The subclinical form produces no outward signs but has a significant impact on performance, in addition to increased condemnation rates at slaughter due to liver lesions. Chronic damage to the intestinal mucosa leads to impaired digestion and absorption of nutrients, weight loss and reduction in weight gain.
Lesions: necrosis of the mucosa of the small intestine. In the clinical form, the necrosis might progress into fibrinonectoric enteritis, forming a diphtheritic membrane. There is a lot of watery brown, blood-tinged fluid and a foul odour during post-mortem examination. The liver is dark, swollen, and firm, and the gall bladder is distended. In the mild form, focal areas of intestinal mucosal necrosis without further clinical signs can be found.

Predisposing factors for necrotic enteritis

The enterotoxemia that results in clinical disease most often occurs either following an alteration in the intestinal microflora or from a condition that results in damage to the intestinal mucosa, which increases the prevalence of the symptoms. The following factors influence the incidence of necrotic enteritis:

Management-related factors

Stress conditions - Animal housing - Poor water quality

Nutritional factors 

Viscous grains - Un-homogenous diet - Unbalanced diet - High protein diet - Variation in particle size - Reduced gut integrity

Pathogenic factors 

Coccidiosis - Mycotoxicosis - Enteric pathogens - Immune suppression


Necrotic enteritis incidence might be substantially reduced using actions taken at the farm level. The Farm variable comprises many factors (e.g. the quality of animal housing and other aspects of the physical environment, farm management quality, and biosecurity measures). Any factor that causes stress in broiler chicks could suppress the immune system and disturb the balance of the intestinal ecosystem in such a way that the risk of a necrotic enteritis outbreak increases. While stress can come from numerous sources, the proper set-up and management of the poultry house environment is the most obvious method of controlling stress.
Poultry management could significantly affect the pathogenesis of Necrotic enteritis. In particular, feed restriction and coccidiosis vaccination can protect against Necrotic enteritis, while extreme house temperature, feed mycotoxins and high stocking density predispose to Necrotic enteritis. It becomes really important to understand the pathogenesis of the disease, as well as to clarify the interactions between husbandry, nutritional and infectious factors and the outbreak of necrotic enteritis. This is necessary and extremely important in order to develop managerial strategies at the farm level to control the incidence and severity of the disease in the post-antibiotic era.


The nature of the diet is an important non-bacterial factor that influences the incidence of necrotic enteritis. Diets with high levels of indigestible, water-soluble non-starch polysaccharides (NSP) predispose to necrotic enteritis. Thus, grains: wheat, oats and barley are risk factors for necrotic enteritis. The high level of indigestible NSPs in these grains increases the viscosity of the intestinal contents, decreases the passage rate, reduces nutrient digestibility, and alters the digestive ecosystem. A highly viscous intestinal environment will increase the proliferation of facultative anaerobes like gram-positive enteric bacteria, e.g. Clostridium perfringens. Furthermore, a large amount of undigested material in the small intestine, together with a slow passage, increases the chances of rapid bacterial colonization of the intestine. 

Feeding high dietary concentrations of animal protein, such as meat and bone meal or fishmeal, creates a favourable condition in the intestine for the proliferation of pathogens and increases the incidence of necrotic enteritis (Truscott & Al-Sheikhly, 1977; Drew et al., 2004; Gholamiandehkordi et al., 2007). The poorly digestible protein cannot be digested and absorbed in the upper part of the intestinal tract; instead, it builds up in the lower portion and acts as a substrate for the bacteria. The result of protein fermentation produces unfavourable by-products such as amines and ammonia, increasing intestinal pH and encouraging the proliferation of pathogenic bacteria like Clostridium perfringens. The dietary fat source may also have an effect on the Clostridium perfringens population. Animal fat increases Clostridium perfringens counts compared with vegetable oil (Knarreborg et al., 2002). Even the physical form of the feed may influence the incidence of necrotic enteritis. Feed containing some large-sized and many small-sized particles predisposes more to necrotic enteritis than feed containing particles uniform in size (Branton et al., 1987; Engberg et al., 2002).

Increasing the digestibility of these nutrients to be utilized by the bird instead of the microbiota is an essential step in the prevention of necrotic enteritis. Supplementing the diet with exogenous proteases and carbohydrases can maximize the breakdown of excess proteins and non-starch polysaccharides, thereby reducing viscosity and the nutrient available to the bacteria. 

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The best-known predisposing factor for necrotic enteritis is mucosal damage caused by coccidial pathogens. Coccidiosis often precedes or occurs concurrently with field outbreaks of necrotic enteritis. Moreover, it has been shown in experimental infection studies that Clostridium perfringens and Eimeria spp. act synergistically in inducing necrotic enteritis lesions. Co-infection with Clostridium perfringens and Eimeria oocysts or an overdose of commercial coccidiosis vaccines containing attenuated Eimeria strains results in more birds with lesions or higher mortality rates than birds receiving only Eimeria or only Clostridium perfringens. Eimeria parasites colonize the small intestine and destroy epithelial cells as a consequence of the intracellular stages of their lifecycle. Plasma proteins leak into the gut lumen through the resulting gaps in the epithelial lining of the intestinal lumen, and these can be used as growth substrates by Clostridium perfringens strains. Moreover, coccidial infection induces a T-cell-mediated inflammatory response that enhances intestinal mucogenesis. This enhanced mucin production provides a growth advantage to Clostridium perfringens due to its ability to use mucus as a substrate.This leads to poor digestion and an unbalanced gut ecosystem.

Enteric pathogens & immunosuppression

Subclinical immunosuppression in chickens is an important but often underestimated factor in the subsequent development of clinical disease. Immunosuppression can be caused by pathogens such as chicken infectious anemia virus, infectious bursal disease virus, reovirus, and some retroviruses (e.g., reticuloendotheliosis virus). Mycotoxins and stress, often caused by poor management practices, can also cause immunosuppression. Mycotoxins depress the local immunity of the digestive system, which is spread through the GALT (gut-associated lymphoid tissue), Peyer's patches, mesenteric lymph nodes, and cecal tonsils. Whenever the digestive system's local immunity is compromised, opportunistic pathogens such as Clostridium perfringens are more likely to proliferate. Four types of mycotoxins impair the local immunity of the digestive system. Aflatoxins and ochratoxins decrease the production of antibodies (immunoglobulins A and M), while Fumonisins and trichothecenes reduce the production of interleukins and interferon.

Data have been published suggesting that low-level maternal immunity against Clostridium perfringens is associated with an increased risk of necrotic enteritis in broiler chickens. Birds are likely to be particularly susceptible during the time when maternal antibodies have waned, and the level of actively produced specific antibodies is still low. Published data suggest that broiler offspring from young parents, hens have lower levels of maternal antibodies against Clostridium perfringens than chicks derived from older parents.

The gastrointestinal tract (GIT) of broiler chicken is considered the most integral part of pathogen's entrance, production and disease prevention. Interaction between Clostridium perfringens and other pathogens, such as Escherichia coli and Salmonella present in the small intestine, may contribute to the development of NE in broiler chickens. The proliferation of these pathogens causes dysbacteriosis, increasing feed conversion ratio and reducing performance leading to the creation of favourable conditions for Clostridium perfringens.

It became inevitable to use an antibiotic growth promoter alternative (AGP) Since the ban of antibiotics in poultry diets and after the rise of anti-microbial resistance around the world. The evolution of using probiotics, considering the mode of action, strains and count in combination with prebiotics, represents one of the best alternatives to antibiotics. Unlike antibiotics, probiotics have no withdrawal period nor microbial resistance. The application of probiotics and prebiotics to day-old chicks provides an ideal opportunity for beneficial bacteria to colonize the digestive tract before chicks are exposed to potentially pathogenic bacteria and fungi in the broiler house, aiding the development of the digestive tract and helping to protect against enteric infections.

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Both mycotoxin contamination of feed and Clostridium perfringens-induced necrotic enteritis have an increasingly global economic impact on poultry production. Mycotoxins are the result of secondary metabolites from fungi growing on many animal feedstuffs. Contamination of broiler feed with Fusarium mycotoxins like deoxynivalenol or fumonisins or a combination of the two is a predisposing factor for necrotic enteritis in broiler chickens. Mycotoxins can directly reduce gut integrity, thus leading to decreased absorption and digestion of dietary nutrients and increased intestinal barrier permeability. Mycotoxins create ideal conditions for the proliferation of Clostridium perfringens by disrupting the intestinal barrier and damaging the epithelium. This results in a decreased absorption of dietary proteins, which leads to a higher amount of proteins in the small intestine. These proteins may serve as substrates for the pathogen.

Interaction between mycotoxin and necrotic enteritis:

  • A reduction in the small intestine's length, villi height, and crypt depth was reported following exposure to deoxynivalenol and fumonisins. By reducing the surface available to absorb nutrients, such changes promote the growth of Clostridium because non-absorbed feed proteins accumulate in the intestine lumen.
  • Alteration of epithelial barrier function by mycotoxins on tight junctions disrupts the intestinal barrier. Consequently increases epithelium permeability and plasma proteins leakage into the lumen of the intestine, promoting the growth of Clostridium.
  • Mycotoxins-contaminated feed negatively impacts the digestive microbiota. The continued ingestion of fumonisins during two weeks reduces the diversity of the ileal microbiota. In addition, exposure to fumonisins, aflatoxins and ochratoxins diminishes the count of Lactobacillus species.

In summary, whenever necrotic enteritis infection occurs or there is suspicion of subclinical infection with Clostridium perfringens, it is imperative to investigate possible mycotoxin contamination in the feed. Therefore the addition of an effective broad-spectrum mycotoxin deactivator is another essential step in the prevention of necrotic enteritis.


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