Necrotic enteritis (NE) is the most common and financially devastating bacterial disease in modern broiler flocks. It is an infectious disease caused by Clostridium perfringens, which is a gram-positive, anaerobic bacterium that can be found in soil, litter, dust and at low levels in the intestine of healthy birds. Clostridium perfringensonly causes NE when it transforms from non-toxin producing type to toxin producing type.
There are five types of C. perfringens (A, B, C, D and E) which produce a number of toxins (alpha, beta, epsilon, iota and CPE). The α-toxin, an enzyme (phospholipase C) is believed to be a key to the occurrence of NE. However, a recent study has shown that an isolate that does not produce α-toxin can still cause disease. In addition, a new toxin called NetB has been recently identified in disease causing C. perfringens isolates. The intestine of infected birds is friable and distended with gas and gross lesions caused by toxins. In the acute form of NE, birds often die without clinical signs. However, in its subclinical form the disease is much more financially damaging for the producer. The commonly observed symptoms of the disease vary with the age of birds.
Early signs of an NE outbreak are often wet litter and diarrhoea, and an increase in mortality is not often obvious. However, the depression of growth rate and feed efficiency of birds become noticeable by day 35 because of damage to the intestine and the subsequent reduction in digestion and absorption of food. Furthermore, increased condemnations at processing due to liver lesions associated with subclinical NE can occur. It has been estimated that the average cost of NE to the poultry industry can be as high as 5 US cents per bird. The images on the right are examples of NE lesions in broiler chickens; the increasing seriousness of the lesions is scored from 1 to 4.
NE is a complex, multifactorial disease with many unknown factors influencing its occurrence and the severity of outbreaks. In particular, sporadic outbreaks of NE can occur frequently in farms where antibiotics are not used as growth promoters or coccidial infections are not controlled, the husbandry practice is not strict, and diets based on viscous grains with animal protein sources are common.
Some other dietary and husbandry factors can contribute to the outbreak of NE. For example, damage to the intestinal mucosa through coccidial infection or a change in the normal intestinal microflora as a result of a change in diet formulation, such as inclusion of a high level of viscous cereal grains and/or animal byproducts like fish meal and meat meal, can predispose birds to the rapid proliferation of C. perfringens.
The incidence of clostridial infections is high in birds fed diets based on wheat, barley, oats or rye. These grains contain a high level of indigestible soluble fibre, which increases digesta viscosity, decreases digesta passage rate and reduces nutrient digestibility. A highly viscous intestinal environment will increase the proliferation of facultative anaerobes like gram-positive cocci and enterobacteria. Furthermore, a large amount of undigested material in the small intestine together with a slow flow of digesta increases the chances of rapid bacterial colonisation of the intestine.
The use of poorly digestible protein sources alters the microflora and creates a favourable condition in the intestine for the proliferation of pathogens. Of course, the converse is also true because when a highly digestible diet is fed to animals, the chance of pathogens colonising the gut can be greatly diminished.
The use of high levels of animal protein meals such as fish meal or meat and bone meal is often associated with an increased risk of NE. In fact, the most effective model for reproduction of NE under experimental conditions uses a diet containing in excess of 25% fish meal and/or meat and bone meal prior to a challenge with Eimeria and C. perfringens.
The occurrence of NE is often associated with an outbreak of coccidial infection. Coccidial infections cause damage to the intestinal lining, making the gut susceptible to other infections including C. perfringens.
Outbreaks of NE can be effectively prevented by including antibiotics such as bacitracin and avilamycin in the feed. In addition, an effective control of coccidial infections can greatly reduce the risk of NE outbreaks. Furthermore, if antibiotics are not used in the feed, strict on-farm hygiene management practice, good climate control of the buildings and careful selection of feed ingredients for diet formulation are all important in maintaining production efficiency. In the Nordic countries, where antibiotics have been removed from the feed, ionophorous anticoccidials have been used to manage NE.
Following the ground-breaking discovery that alpha-toxin is not the main causative factor for NE, by a Monash University PhD student funded by the Poultry CRC, Anthony Keyburn, CSIRO Livestock Industries researchers have patented NetB, the toxin they believe is the culprit. The research team has identified the novel toxin and is now working on how it might be used to create the first truly effective vaccines against NE.
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