Host responses to Clostridium perfringens challenge in a chicken model of chronic stress

Sarah J M Zaytsoff,G Douglas Inglis,Alexander M Garner,Richard R E Uwiera,D Wade Abbott,Wesley F Zandberg,Sarah M Lyons

doi:10.1186/s13099-020-00362-9

Abstract

BackgroundThis study utilized a chicken model of chronic physiological stress mediated by corticosterone (CORT) administration to ascertain how various host metrics are altered upon challenge with Clostridium perfringens. Necrotic enteritis (NE) is a disease of the small intestine of chickens incited by C. perfringens, which can result in elevated morbidity and mortality. The objective of the current study was to investigate how physiological stress alters host responses and predisposes birds to subclinical NE.ResultsBirds administered CORT exhibited higher densities of C. perfringens in their intestine, and this corresponded to altered production of intestinal mucus. Characterization of mucus showed that C. perfringens treatment altered the relative abundance of five glycans. Birds inoculated with C. perfringens did not exhibit evidence of acute morbidity. However, histopathologic changes were observed in the small intestine of infected birds. Birds administered CORT showed altered gene expression of tight junction proteins (i.e. CLDN3 and CLDN5) and toll-like receptors (i.e. TLR2 and TLR15) in the small intestine. Moreover, birds administered CORT exhibited increased expression of IL2 and G-CSF in the spleen, and IL1β, IL2, IL18, IFNγ, and IL6 in the thymus. Body weight gain was impaired only in birds that were administered CORT and challenged with C. perfringens.ConclusionCORT administration modulated a number of host functions, which corresponded to increased densities of C. perfringens in the small intestine and weight gain impairment in chickens. Importantly, results implicate physiological stress as an important predisposing factor to NE, which emphasizes the importance of managing stress to optimize chicken health.

Highlights

This study utilized a chicken model of chronic physiological stress mediated by corticosterone (CORT) administration to ascertain how various host metrics are altered upon challenge with Clostridium perfringens
Necrotic enteritis (NE) incited by Clostridium perfringens is an economically-important disease of the small intestine of poultry that results in high bird mortality and costs the global poultry industry US$5–6 billion per year [1]
Corticosterone treatment was associated with increased densities of C. perfringens in the small intestine Confirmation of the successful colonization of inoculated birds by CP1 C. perfringens was confirmed by conventional PCR for the NetB toxin gene, and showed that only inoculated birds (Cp+St− and Birds inoculated with C. perfringens (Cp+)St+) were positive for netB 24 h post-inoculation (Additional file 1: Fig. S1)

Summary

Introduction

This study utilized a chicken model of chronic physiological stress mediated by corticosterone (CORT) administration to ascertain how various host metrics are altered upon challenge with Clostridium perfringens. Necrotic enteritis (NE) incited by Clostridium perfringens is an economically-important disease of the small intestine of poultry that results in high bird mortality and costs the global poultry industry US$5–6 billion per year [1]. A co-infection with Eimeria spp. predisposes birds to NE by promoting epithelial damage and increasing mucus production, which provides nutrient sources that C. perfringens can competitively utilize [5, 6]. Dietary factors, such as the inclusion of fishmeal and wheat/barley in diets, may be important predisposing factors for disease [5].

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