Overview
Necrotic enteritis (NE) is a significant intestinal disease in poultry, with an estimated global annual cost for the industry of $6 billion (Wade and Keyburn, 2015).
Clostridium perfringens are normal members of the gut microbiota but NetB (pore-forming toxin) producing strains cause NE (Keyburn et al., 2008). These strains colonise and proliferate when conditions in the intestine allow. Factors that contribute to the development of NE include coccidiosis, high or animal protein diets, mycotoxins, and anti-nutritional factors/nutritional imbalances that disrupt the intestinal mucosa, digestive dynamics and/or the microbiome, and thus provide nutrients for these pathogenic C. perfringens strains (Broom, 2017).
NetB creates holes in cell membranes, causing leakage of contents and cell death, most frequently in the jejunum (Smyth, 2016), and NE can present in birds as clinical (significant mortality) and sub-clinical (poor performance) forms, usually between 2 and 6 weeks of age. Definitive diagnosis of NE in live birds is not possible and can even be challenging in dead birds due to normal post-mortem changes that occur in the intestine, but characteristic, tan-coloured lesions, sloughed/thinning mucosa, foul-smelling gas and frequently dark-green (bile) discolouration of the proximal small intestine mucosa and luminal contents are strongly indicative (Smyth, 2016).
Immune responses to, and host interactions with, pathogenic C. perfringens are not well described but various cytokines and chemokines are reported to be modulated, and differential responses likely produce more or less resistant host phenotypes (Broom and Kogut, 2019), while immunosuppression can increase NE susceptibility and/or severity (Prescott et al., 2016).
Mitigation measures primarily focus on predisposing factors (e.g. coccidiosis control, appropriate diets) and feed and water additives (e.g. probiotics, prebiotics, organic acids, phytogenics, enzymes, etc.) (Broom, 2017). Attempts to develop effective vaccines continue.
References
Broom, 2017. Necrotic enteritis: current knowledge and diet-related mitigation. doi.org/10.1017/S0043933917000058
Broom and Kogut, 2019. Deciphering desirable immune responses from disease models with resistant and susceptible chickens. doi.org/10.3382/ps/pey535
Keyburn et al., 2008. NetB, a new toxin that is associated with avian necrotic enteritis caused by Clostridium perfringens. doi.org/10.1371/journal.ppat.0040026
Prescott et al., 2016. Experimental reproduction of necrotic enteritis in chickens: a review. doi.org/10.1080/03079457.2016.1141345
Smyth, 2016. Pathology and diagnosis of necrotic enteritis: is it clear-cut? doi.org/10.1080/03079457.2016.1158780
Wade and Keyburn, 2015. The true cost of necrotic enteritis. www.poultryworld.net/Meat/Articles/2015/10/The-true-cost-of-necrotic-enteritis-2699819W/
Necrotic enteritis (NE) is a significant intestinal disease in poultry, with an estimated global annual cost for the industry of $6 billion (Wade and Keyburn, 2015).
Clostridium perfringens are normal members of the gut microbiota but NetB (pore-forming toxin) producing strains cause NE (Keyburn et al., 2008). These strains colonise and proliferate when conditions in the intestine allow. Factors that contribute to the development of NE include coccidiosis, high or animal protein diets, mycotoxins, and anti-nutritional factors/nutritional imbalances that disrupt the intestinal mucosa, digestive dynamics and/or the microbiome, and thus provide nutrients for these pathogenic C. perfringens strains (Broom, 2017).
NetB creates holes in cell membranes, causing leakage of contents and cell death, most frequently in the jejunum (Smyth, 2016), and NE can present in birds as clinical (significant mortality) and sub-clinical (poor performance) forms, usually between 2 and 6 weeks of age. Definitive diagnosis of NE in live birds is not possible and can even be challenging in dead birds due to normal post-mortem changes that occur in the intestine, but characteristic, tan-coloured lesions, sloughed/thinning mucosa, foul-smelling gas and frequently dark-green (bile) discolouration of the proximal small intestine mucosa and luminal contents are strongly indicative (Smyth, 2016).
Immune responses to, and host interactions with, pathogenic C. perfringens are not well described but various cytokines and chemokines are reported to be modulated, and differential responses likely produce more or less resistant host phenotypes (Broom and Kogut, 2019), while immunosuppression can increase NE susceptibility and/or severity (Prescott et al., 2016).
Mitigation measures primarily focus on predisposing factors (e.g. coccidiosis control, appropriate diets) and feed and water additives (e.g. probiotics, prebiotics, organic acids, phytogenics, enzymes, etc.) (Broom, 2017). Attempts to develop effective vaccines continue.
References
Broom, 2017. Necrotic enteritis: current knowledge and diet-related mitigation. doi.org/10.1017/S0043933917000058
Broom and Kogut, 2019. Deciphering desirable immune responses from disease models with resistant and susceptible chickens. doi.org/10.3382/ps/pey535
Keyburn et al., 2008. NetB, a new toxin that is associated with avian necrotic enteritis caused by Clostridium perfringens. doi.org/10.1371/journal.ppat.0040026
Prescott et al., 2016. Experimental reproduction of necrotic enteritis in chickens: a review. doi.org/10.1080/03079457.2016.1141345
Smyth, 2016. Pathology and diagnosis of necrotic enteritis: is it clear-cut? doi.org/10.1080/03079457.2016.1158780
Wade and Keyburn, 2015. The true cost of necrotic enteritis. www.poultryworld.net/Meat/Articles/2015/10/The-true-cost-of-necrotic-enteritis-2699819W/