Intestinal events and nutritional dynamics predispose Clostridium perfringens virulence in broilers.

Abstract

Clostridium perfringensA (CPA) entering the gastrointestinal system depends on favorable conditions to develop and subsequently extend pathogenicity. Reduction in digestive dynamics progressing from the duodenum decreases lumen oxygen, leading to anaerobic conditions in the distal lumen that favor CPA. When nutritional support is concurrently provided, an expanding population threatens the mucosa. Dietary nonstarch 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 N 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 colonization. Proteolytic destruction within the lamina propria supports colonization 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 BW and increased mortality follow as mucosa involvement proceeds. In practice, supplemental feed hemicellulases that reduce digesta viscosity minimize a favorable environment for CPA, while superimposing a combination of amylase, phytase, and protease avoids nutritional support. 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.