A stress-induced model of acute necrotic enteritis in broiler chickens using dietary corticosterone administration

Mounting evidence indicates that stress can predispose chickens to disease. The objective of the current study was to develop a method that utilized physiological stress to predispose Ross 308 broiler chickens to acute necrotic enteritis (NE). Stress was mediated through the administration of the stress hormone, corticosterone. At 11 d posthatch (p.h.), corticosterone (20 mg kg(−1)) administration commenced. At 12 and 13 d p.h., birds were orally inoculated with a virulent strain of Clostridium perfringens, and at 14 d p.h., birds were euthanized. Birds administered corticosterone exhibited decreased weight gain, and birds co-challenged with C. perfringens and corticosterone were affected to a higher degree. Necrotic lesions were present in birds inoculated with C. perfringens (33%), but a substantially higher prevalence of birds treated with C. perfringens and corticosterone in combination exhibited lesions (100%). Clostridium perfringens densities were correlated with necrotic lesion and histopathologic scores. Both C. perfringens and corticosterone challenge altered mRNA immune responses in the small intestine. In this regard, birds infected with the pathogen showed higher relative mRNA concentrations of toll-like receptor 2A (TLR2A), transforming growth factor beta 2 (TGFβ2), and inducible nitric oxide synthase (INOS). Birds co-challenged with C. perfringens and corticosterone showed hindered TLR2A mRNA expression. A reduction in TLR2A responses mediated by corticosterone administration suggests that the glucocorticoid suppresses immune stimulation in jejunal mucosa, which may be the underlying cause for the increased prevalence and intensity of disease observed in corticosterone treated birds. Overall, the corticosterone stress model resulted in levels of NE comparable to other models of NE that currently exist without the use of a co-infection agent. This model may facilitate the exploration of mechanisms of stress-induced NE, and the development of effective alternatives to antibiotics.