Dietary calcium and meat and bone meal as potential precursors for the onset of necrotic enteritis

Abstract

SUMMARY Necrotic enteritis (NE) is an enteric disease of poultry caused by Clostridium perfringens (C. perfringens). The incidence of NE has increased in several countries as a result of restrictions on the use of in-feed antibiotics. This disease may be triggered by a combination of coccidiosis and the presence of undigested nutrients in the hindgut providing nutrients and high pH that favour the proliferation of pathogens. Meat and bone meal (MBM) inclusion rates above 4% and higher dietary calcium (Ca) inclusion rates above 1.0% may potentially favour the overgrowth of enteric pathogens, including C. perfringens. High levels of elastin, collagen and keratin from MBM are refractory to gastric digestion and may act as nutrient substrates for C. perfringens. Such proteins are metabolised by C. perfringens by putrefactive fermentation, producing trimethylamine and ammonia, that affect gut health and increase the pH of digesta. Digesta pH may become elevated by feeding a diet high in Ca, as this nutrient has a high acid-binding capacity. Calcium interacts with phytic acid, forming mineral-phytate complexes that decrease the activity of exogenous dietary phytase. This reduces digestion and increases the influx of nutrients into the hindgut. Similarly, smaller particle sizes (dgw <75 μm) and high solubility of some Ca sources could increase digesta pH and chelation of Ca by phytic acid and decrease nutrient digestibility. Whether the practice of overfeeding Ca in order to ensure this nutrient is not limiting for bone development may be putting the bird at risk of a NE outbreak is not known. This review discusses the potential for dietary MBM to exacerbate NE in broiler chickens. The impact of Ca level and particle size to affect gut pH and phytase efficacy are discussed, with inferences to alter the onset of NE.