Update on Necrotic Enteritis and Non-Antibiotic Solutions in Poultry
Definition of necrotic enteritis
Necrotic enteritis is an acute infection of the intestine and occasionally of the liver in chickens and turkeys caused by Clostridium perfringens. C. perfringens is a Gram-positive, rod shaped bacteria, anaerobic (although tolerating exposure to air), spore-forming pathogenic bacterium of the genus Clostridium present in the environment and inhabiting the gastrointestinal tract.
Necrotic enteritis is commonly seen in 2- to 5-week old broiler chickens raised on litter and in 7-to 12-week-old turkeys. The disease will remain in the flock for 5 to 10 days, causing 2% to 50% mortality (Merck Veterinary Manual, 1998).
Dysbiosis unleashes C. perfringens
The majority of the bacteria in the body are harmless by the protective effects of the immune system. The majority of the bacteria in the body are harmless by the protective effects of the immune system though many are beneficial, particularly in the gut microflora and so they do not cause disease.
Under normal conditions the “good bacteria” in the intestinal tract (beneficial gut microflora) keep the Clostridium perfringens popluation limited. However, several species of bacteria are pathogenic and can cause infectious diseases like necrotic enteritis, mainly in the GIT and liver (although liver lesions are rare in turkeys). When conditions change in the intestinal tract, Clostridium perfringens numbers increase, toxins are produced and the disease appears.
C. perfringens is known to be able to survive in the environment. Spores are resistant to harsh environmental conditions and persist for extended periods of time in nature, in the biofilm are resistant to disinfection and oxygen. Spore and bacteria shed in the feces of chickens have the potential to contaminate and be transmitted to subsequent flocks and might persist after disinfection.
Most times, the clinical (severe) disease symptom of necrotic enteritis is the fast and unexplained death of birds without clinical signs, eventually depressed and ruffled, progressing fast to increased mortality.
When symptoms such as severe depression, decreased appetite, dark colored diarrhea, closed eyes or ruffled feathers appear they are often short-lived because birds die rapidly. Dead birds appear dehydrated and seem to rot very quickly from the inside out.
Hepatitis and Colangiohepatitis associated with necrotic enteritis has been described (Randal et al, 1983; Hutchincon and Ridell 1990, Loveland and Kaldhusdal 1999; Sasaki et al 2000). Cholangiohepatitis induction by bile duct ligation and inoculation of C. perfringens (Onderka et al 1990, and Sasaki et al 2000 ), necrotic hepatitis due to CP in newly hatched broiler chicks (Sasaki et al 2003), cholecystitis, lesions in the bursa of fabricius, spleen and gizzard might also happen.
Classifying C. perfringens
Birds having necrotic enteritis harbor higher concentration but lower diversity C. perfringens populations than those in healthy birds, confirming previous findings. Seventeen exotoxins or enterotoxins were identified (Songer, 1996), with type A and C being the most common and type A being the most prevalent.
Toxins include Alpha toxin, Beta 2, Cpe ( enterotoxin ), net B and tce. Alpha toxin is the most virulent and net B pore-forming toxin has emerged as the most significant for broilers. Necrotic enteritis birds show prevalence for netB, although levels might vary.
When dead birds are opened, it might look like the bird has coccidiosis, but the intestines are ballooned with gas, friable and contain a foul-smelling brown fluid. Early in the disease progression, intestines may contain ulcers or light yellow spots on the surface. Later, the interior surface of intestines may contain what seems to be a tan to yellow colored membrane that is often said to resemble a “turkish towel.” Livers may show foci of necrosis.
Predisposing factors for necrotic enteritis
In general, intestinal stress leads to gastrointestinal changes that induce necrotic enteritis, including: faster passage time, lower protein absorption, lower carbohydrate absorption, changes in the protective microbiota, Increased intestinal permeability, increased Ca loss.
Here are the main predisposing factors that can lead to necrotic enteritis:
- Coccidiosis (Eimeria contamination)
Coccidiosis affects intestinal integrity and inducing inflammation, clinical or subclinical coccidiosis and noticeable for Eimeria maxima contamination. (Read How Mycotoxins Aggravate Coccidiosis in Poultry)
- Fusarium mycotoxins
Contamination of broiler feed with Fusarium mycotoxins like deoxynivalenol or fumonisins or the combination, at levels below the maximum EU level guidance (5 mg/kg feed for DON and 20 mg/kg feed for fumonisins ) is a predisposing factor for necrotic enteritis in broiler chickens.
These mycotoxins negatively influence the intestinal barrier (Fig 1). For example, duodenal villi gets shorter and enterocytes tight junctions are disrupted resulting in leakage of proteins from the plasma to the gut, less absorption of nutrient from the feed, and increasing the level of intestinal nutrients that are available for Clostridium perfringens.
Figure 1. Impacts of low level deoxynivalenol on intestinal barrier - Source: BIOMIN
- Feed composition and digestibility.
A variety of feed composition and digestibility factors can predispose birds to necrotic enteritis, including:
- Low digestibility protein
- Gut inflammation/irritation/damage
- Higher fiber diet, fast growth, high energy, high viscosity and high protein diets
- Predisposing enzymes (xylanases),
- Amino acids supplementation (low level of Arginine and glutamine)
- High level of acid lactic
Immune suppressing factors include:
- Chicken anemia virus
- Infectious bursal disease (IBD), Gumboro disease
- Marek’s disease
- Gut hemorrhagic enteritis virus
- Intestinal parasites
Round worms in particular increase the likelihood of necrotic enteritis in poultry.
- Poor water quality
The bacteria load in drinking water matters a great deal. Biofilm was found to protect C. perfringens bacterial cells from exposure to high concentrations of tested antimicrobials. Additionally, C. perfringens biofilm can protect the bacterial cells from the action of most disinfectants (University of Montreal). C. perfringens biofilm is an effective in vitro protection mechanism to antibiotics and most disinfectants commonly used on farms and in food processing.
Salmonella thyphimurium infection in young chicks is a significant predisposing factor for necrotic enteritis in broilers.
Several management variables can contribute to the occurrence of necrotic enteritis, including:
- High stocking density
- Litter quality and litter management
- Intermittent lighting versus continuous lighting
Antimicrobials and necrotic enteritis
The removal of antibiotic growth promoters (AGPs) from production systems typically leads to greater intestinal inflammation and necrotic enteritis in flocks. (Read Antibiotic Resistance Key to Understanding Efforts to Curtail Antibiotics in Poultry).
The mechanism of action with the use of AGPs was mainly anti-inflammatory through inhibition of pro-inflammatory cytokines production, shifting microbiota composition/load and altering inflammatory metabolite production by microbiome.
Long-term sub-therapeutic usage of AGPs caused an increase in antibiotic resistant C. perfringens, allowing bacteria to survive and continue to grow instead of being killed or inhibited by therapeutic doses of the drug.
Antibiotics such as bacitracin, penicillin, tylosin or lincomycin can be used to treat necrotic enteritis, however the use of antibiotics might not be so effective since the disease progresses so rapidly and the toxins involved produce irreversible intestinal damage. (Read more about the negative effects of antibiotics on poultry production).
The rise of antibiotic resistance put one of the great medical findings of all time at risk. Nowadays, innovative tools shown to be safe, effective and profitable for the industry helping reducing antibiotic usage and thus preserving the value of antibiotics for treatment.
Replacement of the entire population of C. perfringens by single, chicken virulent strains has been noted in natural outbreaks (Engstrom et al 2003) as well experimentally (Barbara et al, 2007 ). There is competition among C. perfringens in the intestinal bacteria flora.
In a previous clinical trial using a mixed C. perfringens strain inocula, only one of the strains inoculated became predominant. The dominant C. perfringens was different depending on risk factors. Bacteriocins production is not only a prerogative of pathogenic C. perfringens strains: bacteriococus other than perfrin can be produced. Bacteriocins could be used as alternatives to antibiotics.
Alternatives to antimicrobials to control necrotic enteritis
Scientific research has shown that several novel, non-antibiotic feed additives can help to reduce the incidence and severity of necrotic enteritis in flocks.
Several categories of alternative solutions are available, such as:
These supply a complex of a probiotic microbe or microbes with a prebiotic meant to be used by these organisms to replace missing function in a microbiome, establish a beneficial microflora as soon as possible, increasing bacteria colonization of gut, improve nutrient absorption, provide metabolites as essential nutrients, induce host digestive enzymes and promote host immunity. In this way, the prebiotic and probiotic combination helps ensure that less damage will be produced to the epithelial wall and less dead cell contents will be released to the lumen to feed C. perfringens.
2. Diet/nutritional therapy
Promoting beneficial microbial communities and gut function can improve both the health, digestibility and growth performance. This can be done in a number of ways. For example, feed all-vegie diets to flocks at risk or use better quality ingredients. Ingredients such as corn gluten, soy oil, high quality protein, animal by-products might increase exposure to Clostridia spores. Lower Ca will reduce predisposition. Pellet quality should make for a more consistent intake of feed which should translate into less enteritis. Higher doses of Cu or Zn+Cu seems to reduce necrotic enteritis lesions scores. Threonine is important for the feed diet for mucin production.
3. Exogenous feed enzymes
Diets that contain different anti-nutritional factors affect normal digestion and nutrient absorption. Digest different anti-nutritive factors (NSPs) impede normal digestion and nutrient absorption.
Plant-based phytogenic feed additives can promote beneficial microbial community growth and function, and enhance innate and acquired immunity. They have an antimicrobial, anti-inflammatory and antioxidant activity. Importantly, certain essential oils enhance digestibility, amino acid intake, mucin stimulation and increased adsorptive surface.
5. Organic acids
Combinations of organic acids are useful for water disinfection and sanitization, to promote feed hygiene, and to control salmonella contamination (S. hyphimurium).
Butyrate can strengthen the epithelial barrier (Tj expression, AMP expression) and anti-inflammatory effect.
Mycotoxin deactivators help to control immunosupressive effects and lesions in the gastrointestinal tract caused by Fusarium mycotoxins. Mycotoxin risk management , especially through enzymatic activity for these non-adsorbable mycotoxins, is crucial at all levels. Even low level mycotoxin contamination deserves preventive action.
Several management steps can be taken to reduce the risk of necrotic enteritis. For example:
- Reduce early fast growth
- Brood the birds warmer
- Keep the birds eating, especially during NE challenges,
- Decrease density
- Use litter acidification or build up litter
- Avoid animal by-products.
- Early exposure of chicks with C. perfringens-contaminated litter decreased the severity of the controlled NE challenge. More severe outbreaks in first flocks follow a complete cleanout and in first flocks in a new broiler house.