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Dr. Aris Malo

Control of necrotic enteritis requires attention to multiple factors that can trigger the disease, ranging from coccidiosis to the amount of protein in feed, said Dr. Aris Malo, global technical manager, Intervet/Schering-Plough Animal Health.

The leading cause of necrotic enteritis (NE) is the alpha toxin secreted by Clostridium perfringens, an opportunistic bacterium that needs the right environment to flourish and wreak havoc in the chicken’s gut, Malo said. In recent years, health surveys indicate that NE has become one of the top five concerns among poultry producers. The disease is also costing the global poultry industry millions of dollars annually.

NE may be subclinical or clinical. Economic losses from subclinical NE occur due to lost weight gain and growth as well as impaired feed conversion, while the clinical form causes increased morbidity and mortality. The disease also predisposes birds to secondary infections and increases time to market, he said.

Damage to the intestinal mucosa may be only a slight thickening, as occurs with subclinical NE, or severe necrosis, which occurs with clinical NE. In a normal gut, the villi are elongated, finger-like structures that extend out to the lumen; in a gut ravaged by NE, villi are shortened and have wide gaps between them. In some cases, the villi appear to be melted together. “You can imagine the big reduction in the absorptive surface of the intestines,” he said.

Broilers with NE also tend to have ballooning in the gut, since C. perfringens is gas forming. Another consequence is cholangiohepatitis, evidenced by an enlarged liver with a yellowish-bronze color, which results in condemnations, Malo said.

Clostridia like high pH

The veterinarian pointed out that clostridia can be found throughout the environment, including soil, dust and feed, and these bacteria are a normal part of the gut flora of all animals. Clostridia like a high pH, and, consequently, farms located in areas with high concentrations of limestone report a higher incidence of NE compared to other areas.

An important trigger for development of NE is clinical or subclinical coccidiosis. Coccidial lesions in the gut initiate increased mucus production. “It’s the gut trying to protect itself, but you could say it has the opposite effect because mucus is also food for clostridia,” he explained. “If the clostridia are the type that produces toxins, it also causes more damage to the gut and more mucus. It turns into a vicious cycle.”

It’s no coincidence that NE tends to occur during the later half of the production cycle, which is the same time that flocks on anticoccidials experience oocyst leakage if coccidial resistance has developed, he continued. Besides NE, flocks may develop other conditions associated with clostridia, such as gangrenous dermatitis.

The second half of the production cycle is the worst time for birds to develop harmful gut conditions because “that’s when they put on the meat. That’s when you’re going to have a high impact on your production performance,” Malo said.

He also cited a controlled study conducted at the University of Georgia demonstrating that NE mortality is worse if birds are challenged with coccidiosis.

Other NE triggers

Other triggers for the development of NE include reduced antibiotic sensitivity when in-feed antibiotics are used; highprotein diets, which supply clostridia with certain amino acids that the bacterium needs; and high levels of animal byproducts, particularly fish meal, which can be heavily contaminated with clostridia spores. High levels of wheat, rye and barley have been associated with the development of NE because they are coarse grains, which can irritate the gut and be difficult to digest, resulting in more nutrients for clostridia organisms and more mucus production. In addition, a change in feed can irritate the gut, making it a favorable environment for clostridia, Malo said.

When edible types of litter such as rice or oat hulls are used, they are consumed by birds, increasing ingestion of coccidia and bacteria and setting the stage for development of NE, he noted.

Measures that can reduce the incidence of NE in flocks at risk for the disease include feeding a lower protein diet, with more synthetic amino acids. Byproducts of questionable quality should be avoided, as should grains such as wheat and edible types of litter. Enzymes and microflora treatments that improve digestibility may be helpful, he advised.

Besides nutrition and management changes aimed at minimizing the risk for NE, another option is the use of a Clostridium type-A toxoid developed by Intervet/Schering-Plough Animal Health. To date, the vaccine has been used under a conditional license by producers in the US and Canada growing antibiotic-free birds and was recently approved for use in the EU. Two doses are administered to hens, which pass immunity against NE to their offspring.

The vaccine reduces mortality from NE and the incidence and severity of lesions due to C. perfringens type-A-induced NE. The vaccine has resulted in improved livability, improved weight and improved feed conversion, Malo said.

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