Intestinal Events and Nutritional Dynamics Predispose Clostridium Perfringens Virulence in Broilers
The changes occurring in the chicken gut that can lead to a build-up of the pathogen causing necrotic enteritis are outlined by an Auburn University professor, who adds that feed enzyme supplementation can help to create an environment in which the bacteria cannot easily proliferate.
9 December 2014
3 minute read
By: Clostridium perfringens A (CPA) entering the gastrointestinal system depends on favourable conditions to develop and subsequently extend pathogenicity, according to Dr Ed Moran of Auburn University in his latest review in Poultry Science.
Reduction in digestive dynamics progressing from the duodenum decreases lumen oxygen, leading to anaerobic conditions in the distal lumen that favor CPA, he explains. When nutritional support is concurrently provided, an expanding population threatens the mucosa.
Dietary non-starch polysaccharides that increase viscosity further impair oxygen transfer from the mucosa, improving the ability of CPA to thrive.
Incompletion of feed digestion early in the small intestine along with endogenous nitrogen provide additional support for population expansion.
Glucosidase versatility with mucin elicited by distal CPA concurrently erodes the villus unstirred water layer at the apex, providing access to underlying binding sites for colonisation.
Proteolytic destruction within the lamina propria supports colonisation to create subclinical necrotic enteritis.
Eventual vascular entry of CPA and toxins provides a portal path for instituting cholangiohepatitis. Liver condemnations from inspection detect acute flock infection compared with preceding marginal losses in nutrient absorption that decrease feed efficiency.
Enterocyte lysis by coccidia enable CPA access to binding sites, thereby extending villus necrosis and further impairing feed conversion.
Loss of bodyweight and increased mortality follow as mucosa involvement proceeds. In practice, supplemental feed hemicellulases that reduce digesta viscosity minimise a favourable environment for CPA, while superimposing a combination of amylase, phytase and protease avoids nutritional support, concludes Dr Moran.
He adds that physical dynamics of the small intestine together with characteristics of feed that modify digesta viscosity and nutritional availability are central to establishing transient CPA as a pathogen.
Reference
Moran E.T. Jr. 2014. Intestinal events and nutritional dynamics predispose Clostridium perfringens virulence in broilers. Poultry Science. 93(12): 3028-3036. doi: 10.3382/ps.2014-04313
Further Reading
You can view the full report (fee payable) by clicking here.
Find out more about necrotic enteritis by clicking here.
December 2014
