{"id":58712,"date":"2020-09-29T12:10:12","date_gmt":"2020-09-29T10:10:12","guid":{"rendered":"https:\/\/ew-nutrition.com\/necrotic-enteritis-the-complete-overview\/"},"modified":"2025-08-14T17:10:06","modified_gmt":"2025-08-14T15:10:06","slug":"necrotic-enteritis-complete-overview","status":"publish","type":"post","link":"https:\/\/ew-nutrition.com\/us\/necrotic-enteritis-complete-overview\/","title":{"rendered":"Necrotic enteritis: The complete overview"},"content":{"rendered":"

by Inge Heinzl <\/strong>and Technical Team<\/strong>, EW Nutrition<\/span><\/p>\n

Necrotic enteritis is a profit killer in poultry production<\/h2>\n

Necrotic enteritis is the cause of USD 6 billion losses every year in global poultry production, corresponding to USD 0.0625 per bird (Wade and Keyburn, 2015). This controllable disease is on the rise. One reason is the voluntary or legally required reduction of antibiotics in animal production due to the increasing occurrence of antimicrobial resistance but also consumer demand. Another reason is the administration of live Coccidiosis vaccines and partial reduction of ionophores, which also show efficacy against Gram-positive bacteria (Williams, 2005).<\/p>\n

Necrotic enteritis and coccidiosis are the most significant health problem in broilers (Hofacre et al., 2018).<\/p>\n

The disease generally occurs in broiler chickens of 2-6 weeks of age. It is caused by an overgrowth of Clostridium perfringens<\/em> type A and, to a lesser extent, type C in the small intestine. The toxins produced by C. perfringens<\/em> also damage the intestinal wall.<\/p>\n

Clinical and subclinical forms of NE \u2013 which one causes more significant losses?<\/h3>\n

The clinical form is obvious<\/h4>\n
\"\"
Intestine showing signs of NE<\/em><\/span><\/figcaption><\/figure>\n

…is characterized by acute, dark diarrhea resulting in wet litter and suddenly increasing flock mortality of up to 1% per day after the first clinical signs appear (Ducatelle and Van Immerseel, 2010), sometimes summing up to mortality rates of 50% (Van der Sluis, 2013). The birds have ruffled feathers, lethargy, and inappetence.<\/p>\n

Necropsy typically shows ballooned small intestines with a roughened appearing mucosal surface, lesions, and brownish (diphtheritic) pseudomembranes. There is a lot of watery brown, blood-tinged fluid and a foul odor during post-mortem examination. The liver is dark, swollen, and firm, and the gall bladder is distended (Hofacre et al., 2018).<\/p>\n

In the case of peracute<\/strong> Necrotic Enteritis, birds may die without showing any preliminary signs.<\/p>\n

The subclinical form often only can be noticed at the end of the cycle<\/h4>\n

When birds suffer from the subclinical form, chronic damage to the intestinal mucosa and an increased quantity of mucus in the small intestine lead to impaired digestion and absorption of nutrients resulting in poor growth performance. The deteriorated feed conversion and the resulting decreased performance become noticeable around day 35 of age. As feed contributes approximately 65-75% of the input cost to produce a broiler chicken, poor feed conversion increases production costs and significantly influences profitability. Often, due to a lack of clear symptoms, this subclinical disease remains untreated and permanently impacts the efficiency of production.<\/p>\n

\"Poultry\"<\/p>\n

The pathogen causing NE \u2013 a ubiquitous bacterium<\/h3>\n

Responsible for Necrotic Enteritis are Gram-positive, anaerobic bacteria, specific strains of Clostridium perfringens<\/em> type A and, to a lesser extent, type C (Keyburn et al., 2008).<\/strong><\/p>\n

\"Clostridium<\/p>\n

Clostridia primarily occur in the soil where organic substances are degraded, in sewage, and in the gastrointestinal tract of animals and humans. These bacteria produce spores, which are extremely resistant to environmental impact (heat, irradiation, exsiccation), some disinfectants, and can survive for several years. Under suitable conditions, C. perfringens<\/em> spores can even proliferate in feed or litter.<\/p>\n

Clostridium perfringens<\/em> is a “natural inhabitant” of the intestine of chickens. In healthy birds, it occurs in a mixture of diverse strains at 102<\/sup>-104<\/sup> CFU\/g of digesta (McDevitt et al., 2006). The disease starts when C. perfringens<\/em> proliferates in the small intestine, usually due to a combination of factors such as high amount protein, low immunity, and an imbalance in the gut flora. Then, the number rises to 107<\/sup>-109<\/sup> CFU\/g of digesta (Dahiya et al., 2005).<\/p>\n

Highly important: NetB, a pore-forming toxin is a key virulence factor for NE<\/h3>\n

To establish in the host, Clostridium<\/em> Spp. and other pathogens depend on virulence factors (see infobox). These virulence factors include for example “tools” for attachment, evasion or suppression of the host’s immune system, “tools” for getting nutrients, and “tools” for entry into intestinal cells. Over the years, the \u03b1-toxin produced by C. perfringens<\/em> was assumed to be involved in the development of the disease and a key virulence factor. In 2008, Keyburn and coworkers found another key virulence factor by using a C. perfringens<\/em> mutant unable to produce \u03b1-toxin, while still causing Necrotic Enteritis.<\/p>\n

Thus, another toxin was identified occurring only in chickens suffering from Necrotic Enteritis: C. perfringens<\/em> necrotic enteritis B-like toxin (NetB). NetB is a pore-forming toxin. Pore-forming toxins are exotoxins usually produced by pathogenic bacteria but may also be produced by other microorganisms. These toxins destroy the integrity of gut wall cell membranes. The leaking cell contents serve as nutrients for the bacteria. If immune cells are destroyed, an immune reaction might be partially imparted.<\/p>\n

Additionally, pathogenic strains of C. perfringens<\/em> produce bacteriocins \u2013 the most important is Perfrin (Timbermont et al., 2014) \u2013 to inhibit the proliferation of harmless Clostridium<\/em> Spp. strains and to replace the normal intestinal flora of chickens (Riaz et al., 2017).<\/p>\n

\n

Examples of virulence factors<\/h4>\n
    \n
  1. Adhesins<\/strong>
    \nEnable the pathogen to adhere or attach within the target host site, e.g. via fimbria. Pili enable the exchange of RNA or DNA between pathogens.<\/li>\n
  2. Invasion factors<\/strong>
    \nFacilitate the penetration and the distribution of the pathogens in the host tissue (invasion and spreading enzymes). For example: hyaluronidase attacking the hyaluronic acid of the connective tissue or flagella enabling the pathogens to actively move.<\/li>\n
  3. Toxins<\/strong>
    \nDamage the function of the host cells or destroy them (e.g. endotoxins – lipopolysaccharides, exotoxins)<\/li>\n
  4. Strategies of evasion<\/strong>
    \nEnable the pathogen to undergo the strategies of defense of the immune system (e.g. antiphagocytosis factors provide protection against an attack by phagocytes; specific antibodies are inactivated by enzymes).<\/li>\n<\/ol>\n<\/div>\n

    \"Virulence<\/p>\n

    Predisposing factors favor the development of NE<\/h2>\n

    A chicken with optimal gut health<\/strong> may be less susceptible to NE<\/strong>. Additional predisposing factors<\/strong> are necessary to allocate nutrients and make the gut environment suitable for the proliferation of these pathogens, \u00a0enabling them to cause disease (Van Immerseel et al., 2008; Williams, 2005).<\/p>\n

    1.\u00a0\u00a0 FEED: composition and particle size are critical<\/h3>\n

    Feed plays a role in the development of Necrotic Enteritis that should not be underestimated. Here, substances creating an intestinal environment favorable for C. perfringens<\/em> must be mentioned.<\/p>\n

    \"Nsp\"<\/p>\n

    \"Protein<\/p>\n

    \"Particle<\/p>\n

    <\/div>\n

    2.\u00a0\u00a0 Mycotoxins create ideal conditions for NE<\/h3>\n

    Mycotoxins harm gut integrity and create ideal conditions for the proliferation of Clostridium perfringens<\/em>:<\/p>\n

    Mycotoxins do not have a direct effect on C. perfringens<\/em> proliferation, toxin production, or NetB transcription. However, mycotoxins disrupt gut health integrity, creating a favorable environment for the pathogen. For example:<\/p>\n