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Subclinical Necrotic enteritis: ‘It's a big problem’
Subclinical necrotic enteritis — the form of Clostridium perfringens infection that often goes undetected while it quietly eats away at performance — is believed to be far more common than originally thought in broiler chickens and is expected to become more prevalent as poultry operations reduce their dependence on in-feed antibiotics.
“It’s a big problem,” although no one really knows the actual incidence because it is not easily detected, says Dr. Steve Davis, president and CEO of Colorado Quality Research, Wellington. “The effect of subclinical necrotic enteritis is subtle and additive. Performance deteriorates from flock to flock, especially if you aren’t cleaning out your houses.”
Some producers miss subclinical necrotic enteritis, or NE, because they haven’t had it before, Davis continues. In other cases, there’s a gradual drop in feed efficiency and weight gain that goes unnoticed. Subclinical NE can also cause liver lesions resulting in condemnation at processing. The problems may have existed for so long that producers think they’re normal. The disease may not be identified until the health program changes and performance improves.
Dr. Charles Hofacre, a professor at the University of Georgia, Athens and a leading authority on NE, says that subclinical necrotic enteritis is estimated to cost the global poultry industry $2 billion annually — and that’s probably a conservative estimate. Put another way, NE cost producers about 5 cents per bird.
“Subclinical NE is probably more expensive to the industry than clinical NE because it often goes unnoticed, while clinical NE is obvious and gets treated,” says Hofacre.
He agrees with Davis that “You may have many flocks affected before realizing that you are losing feed efficiency and growth unless you conduct regular weekly posting sessions, which most producers do not.”
Can strike conventional flocks
While full-blown outbreaks of NE are most likely to occur in antibiotic-free birds, Davis says, subclinical NE is more likely to strike conventional flocks receiving antibiotics.
Some in-feed antibiotic growth promoters have the added benefit of controlling clostridium, these experts explain. However, fewer antibiotic growth promoters, or AGPs, are being used today to meet growing consumer demand for more birds raised without antibiotics.
Ionophores, another class of antibiotics used for coccidiosis control, also help suppress NE indirectly by controlling coccidiosis, which predisposes birds to NE infection, and by direct antimicrobial action against clostridium. However, extensive use of these additives has caused clostridial and coccidial pathogens to develop resistance to the drugs.
Hofacre and Davis both expect to see more acute and subclinical NE as the industry backs off the use of in-feed antibiotics. Hofacre cites the European experience, where the poultry industry has seen a huge surge of NE in broilers since AGPs were banned by regulators.
“In the United States, the reduction in AGPs is being driven by consumers, not by regulators as it is in Europe. I don’t know that we’ll go to zero AGPs, but I think the US poultry industry will go pretty low. Consumers don’t want AGPs used due to concerns that they may contribute to antibiotic resistance in humans,” Hofacre says.
Diagnosing NE
Diagnosing subclinical NE is challenging because there are no tests for C. perfringens. Nor is there a way to predict an increased risk for NE based on litter samples, he says.
“Culturing C. perfringens from the litter is an exercise in futility,” Hofacre says. To cause NE, a toxic strain of C. perfringens must be present, but there’s no way to tell if clostridium isolated from litter has the gene needed to produce the toxin that causes NE. In other words, “You can have clostridium in the environment, but that doesn’t prove it is causing disease,” he adds.
For now, diagnosis requires necropsy examination of intestinal mucosa. With NE, there is mucus on the small intestinal surface, which may be thick and rough. The liver may be firm and dark in color. Moderate to smaller lesions can be hard to identify, he says.
Davis says that “For diagnosis of subclinical NE, it’s very important to get anaerobic cultures of very fresh, dead birds by euthanizing if necessary.”
Adds Hofacre: The diagnosis is more of “a clinical impression” among those experienced with the disease. There’s a certain amount of enteritis, but it never gets severe enough to call it clinical NE. The term subclinical enteritis really reflects the severity of the disease.
Acute NE threatens antibiotic-free and some conventional flocks
The clinical form of necrotic enteritis (NE) results in necrosis of the intestinal lining and remains one of the most common and costly diseases of modern broiler flocks around the world.
The hallmark sign of clinical NE is a sudden, high death rate in affected flocks, which can range anywhere from 2% to 50%. In less severely affected flocks, birds may exhibit depression, poor appetite, ruffled feathers and diarrhea.
Flocks most susceptible to clinical NE are antibiotic-free birds, say experts.
According to Dr. Steve Davis, president and CEO of Colorado Quality Research, Wellington, it is a mistaken notion that coccidiosis vaccination leads to NE. Coccidiosis vaccines, like chemical anticoccidials, simply have no secondary antibacterial effect to prevent C. perfringens.
Because coccidiosis is a risk factor for the development of NE, control of coccidiosis with measures such as vaccination and management can help prevent NE, the experts say.
Other flocks that might be at risk for NE development are those receiving ionophore anticoccidials, a type of antibiotic. If coccidia and clostridium become resistant to ionophores, there’s a greater risk for development of NE, they say.
Davis has noted that among some flocks, clinical NE seems to occur earlier than before. “It used to be at 3 to 4 weeks of age and now it’s between 2 and 3 weeks of age. It may have to do with coccidiosis control; ionophore and chemical anticoccidials are allowing more infective oocysts to be excreted into the environment, known as leakage, faster than they used to.”
Poultry genetics might also play a role, he says. “We have found in our studies that acute NE is more prevalent in males, which are more likely to die from the disease than females.”
‘Once you see it, you won’t forget’
In contrast to subclinical NE, which can be subtle and difficult to diagnosis, a clinical NE outbreak is often readily apparent due to the high death rate, Hofacre says. An official diagnosis is made upon necropsy of affected birds and, “Once you see it, you won’t forget the firm liver and dark mahogany color. The surface of the small intestines is thick and rough.”
Davis cautions, however, that “I’ve seen cases so acute that the gut deteriorates rapidly and you may not see classic ‘Turkish towel’ lesions characteristic of NE.”
Conversely, a heavy growth of clostridium does not always mean NE because after a bird dies, clostridium in the gut balloons in great numbers since there are perfect anaerobic conditions with a lot of protein and mucus. Therefore, “in a full outbreak, you may need to necropsy quite a few birds before you see classic NE gut lesions,” he says.
How to control necrotic enteritis
Whether it strikes in the clinical or subclinical form, necrotic enteritis is caused by the same pathogen, Clostridium perfringens. Measures to prevent or control it are therefore similar in both situations, though specifics may vary depending on the type of broiler production system in place.
One of the first steps that can be taken to control NE, says Dr. Steve Davis, president and CEO of Colorado Quality Research, Wellington, is sound cleaning and disinfection of the environment between flocks to decrease the bacterial load, especially in facilities with a history of NE.
Litter moisture should not be too high or low. Oat or rice hull may increase the risk for NE because it is less absorptive, he says.
Attention to diet ‘crucial’
Attention to diet is crucial, Davis says. Grains high in indigestible soluble fiber, such as wheat, barley, oats and rye, have been linked to intestinal disease in poultry.
Broilers receiving a high-protein diet are easier to challenge with C. perfringens, as are broilers receiving higher density diets, possibly because nutrients remain available to the bacteria in the intestine if they are fed at higher levels than birds can utilize, he says.
“Integrators raising broilers without feed grade antibiotics may be able to decrease the incidence of NE by using lower density formulations or by concentrating on amino acid fortification and balance instead of feeding diets with higher protein levels,” Davis says. However, dramatic changes in diet are linked to development of NE and should be avoided.
Animal byproducts can be a source of C. perfringens contamination. “We have conducted research showing literally tens of thousands of clostridium spores per gram in some animal byproducts found in blends. In one study we did, fishmeal in the feed was heavily contaminated with C. perfringens. We’ve also found the pathogen in bone meal. So, in some cases, flocks are getting clostridium from their food,” Davis says.
Overeating is yet another factor linked to NE. “If you slow down feed consumption with measures such as decreased lighting, you can decrease the incidence of NE, which is the opposite of what most people think,” he says.
Cooler temperatures that chill birds and increased feed consumption should be avoided, he continues. “It appears that increasing the environmental temperature to decrease feed intake in broiler flocks breaking with NE will help curtail the severity of an outbreak.”
Davis advises producers to consider the source of their chicks. Flocks with excellent chick quality and uniformity require a greater challenge to develop disease, so continued improvements in chick quality should improve control of NE. It could be that different breeds have varying levels of maternal antibody against C. perfringens.
Last but not least, bird density is a critical factor in preventing NE, since density affects many of the other variables involved, he says.
Immunity may be key
To best control both clinical and subclinical NE in flocks — especially for producers who want to reduce the use of antibiotics — a combination approach will most likely be needed, starting with good coccidiosis control, the experts say.
“One combination might be coccidiosis vaccination, natural products such as organic acids and NE vaccination,” says Davis.
Immunity will be key to any successful combination, he says. “NE occurs early in the bird’s life, and another problem we see that’s caused by clostridium is dermatitis, which occurs late in the life of birds. I have never seen a broiler flock with NE that got dermatitis later. The reason is immunity. Birds that survive NE build immunity against clostridium.”
This observation indicates that vaccinating for NE could be helpful in flocks at risk whether they are antibiotic-free birds, birds receiving chemicals or vaccines to prevent coccidiosis or birds on a rotation program during times they transition off ionophores, he says.
Checklist for good control
- Implement a good coccidiosis control program, which may consist of a properly administered vaccine or effective in-feed products.
- Maintain good hygiene. Clean out and sanitize houses between flocks.
- Maintain appropriate flock density.
- Use absorbent litter to help maintain proper litter moisture.
- Discourage feed gorging.
- Avoid feed sources contaminated with toxic Clostridium perfringens and consider monitoring ingredients for C. perfringens spores.
- Eliminate or reduce feed ingredients associated with an increased risk for NE, such as wheat, barley, rye and other grains with a high level of indigestible soluble fiber, and animal byproducts.
- Avoid dramatic dietary changes.
- Feed a low-density, high-quality diet fortified with amino acids; avoid high-protein diets.
- Vaccinate against NE.
- Consider administration of competitive exclusion and organic acid products to promote good gut health.
- Consider bird breeding and the source of chicks, since some may be more or less prone to development of NE.
