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By Maja Marien, Sharon Miller, Mark LaVorgna, Wouter Depondt and Dieter Vancraeynest, Technical Team Alpharma, EMEA and US
It is generally accepted that predisposing factors are required for Clostridium perfringens to cause Necrotic Enteritis (NE). The best known predisposing factor is mucosal damage caused by coccidiosis, in particular by Eimeria species that colonise the small intestine (E. maxima, E. mitis, E. acervulina).Coccidiosis often proceeds or occurs concurrent with field outbreaks of NE. Eimeria parasites destroy intestinal cells, causing gaps in the intestinal lining through which plasma proteins leak into the gut lumen (Figure 1). Furthermore, coccidiosis causes an impaired intestinal function resulting in poorly digested feed remaining in the intestine, as well as an inflammatory response that leads to increased mucus production. All of these - the plasma proteins, poorly digested feed and mucus - are suitable as growth-substrate for extensive proliferation of clostridial bacteria and hence support bacterial overgrowth.
Effect of the diet
The nature of the diet is an important non-bacterial factor that influences the incidence of NE. Anything that increases digesta viscosity, decreases nutrient digestibility and prolongs intestinal transit time, can be considered as a risk factor. More nutrients available in the gut can stimulate the growth of certain bacterial populations, which in its turn might change the general intestinal microbial composition. It has been shown that diets with high levels of non-starch polysaccharides (NSPs) increasing the viscosity, high dietary concentrations of animal protein (e.g. fishmeal) and/or protein-rich diets containing relatively high concentrations of poorly digestible proteins can result in heavily increased proliferation of C. perfringens resulting in clinical problems.Apart from Eimeria infections and the feed, any factor that causes stress (e.g. increased stocking density) in broilers could predispose them to NE because it could alter the intestinal environment.
Mortality rates
In the acute form of NE, the prominent feature is acute death, often without premonitory signs. Mortality rates can vary from 5-50%. Rates of about 10% are generally not unusual. Other clinical signs of NE are aspecific and include depression, dehydration, somnolence, ruffled feathers, diarrhoea, increased water, and decreased feed consumption. Wet litter can also be an early indicator of disease.
At necropsy, the small intestine is thin-walled, fragile, dilated, fibrinonecrotic and filled with gas. Confluent or focal mucosal necrosis of the small intestine covered by a yellow-brown or bilestained pseudomembrane can be found. Although NE is of importance worldwide, there are intestinal conditions that are not necessarily caused by C. perfringens, which are of even bigger concern to poultry producers. As these conditions have many resemblances with NE regarding predisposing factors, prevention and treatment, they are discussed in more detail below.
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