9:00 am - 10:00 am
A graduate exam seminar is a presentation of the student’s final research project for their degree.
This is an ALES PhD Final Exam Seminar by Sarah Zaytsoff. This seminar is open to the general public to attend.
Thesis Topic: Stress predisposition to necrotic enteritis caused by Clostridium perfringens in chickens and the administration of a complex microbiota to mitigate disease
PhD with Drs. Richard Uwiera, Douglas Inglis, and Trina Uwiera.
Necrotic enteritis (NE) incited by the bacterium, Clostridium perfringens, is a disease of the small intestine of poultry that imparts a substantive economic cost and was previously controlled through the administration of in feed antibiotics. However, poultry production has entered an era of restricted antimicrobial use and this has prompted an urgent need for antimicrobial alternatives. Despite the best management practises, birds are exposed to unavoidable or unpredictable stressors that can influence various systems within the body. Limited research has examined the influence of physiological stress on the intestinal microbiota in poultry and its relationship to NE. Birds acquire many of their microbes from the environment and lack significant maternal transfer of microbes. Consequently, this results in a low diversity microbiota and renders birds susceptible to infections once exposed to pathogens on the farm. Administering a complex mixture of bacteria to birds shortly after hatch may promote colonization resistance in the intestine against incoming pathogens and expediting immune development in chicks to prevent future infections later in life. The objectives of my thesis research were: (1) elucidate the influence of stress on bird health; (2) examine the impact of stress on NE in layer chickens; (3) ascertain the impact of stress on NE in broiler chickens; and (4) determine the ability of a complex microbiota (CM) administered to day-old broiler chicks to ameliorate stress-induced NE. For all four objectives, physiological stress was incited by orally administering the glucocorticoid stress hormone, corticosterone (CORT) via water or feed. For objectives 2, 3, and 4, birds were challenged with a virulent strain of C. perfringens (CP1). For Objective 1, birds administered CORT exhibited altered lipid metabolism in the liver, and altered metabolite profiles in liver, kidney, and muscle. Moreover, stress altered the α- and β-diversity of bacterial communities within the small intestine and ceca. Notably, birds administered CORT possessed higher densities of indigenous C. perfringens. For Objective 2, layer chickens administered CORT and challenged with C. perfringens CP1 manifested subclinical NE. In this regard, body weight gain was reduced only in birds administered CORT and inoculated with C. perfringens. Moreover, small intestinal mucus glycans were altered by C. perfringens colonization. In birds administered CORT, genes encoding tight junction proteins and toll-like receptors in the intestine were altered, as were inflammatory responses in the thymus and spleen. The administration of CORT also increased densities of C. perfringens in the small intestine. For Objective 3, broiler chickens administered CORT and challenged with C. perfringens manifested clinical NE. Birds challenged with C. perfringens showed higher histopathological scores; however, only birds administered CORT and challenged with C. perfringens exhibited gross necrotic lesions in the small intestine. Clostridium perfringens densities were highest in birds administered CORT, which in conjunction with increased pathological scores, indicated that stress is a predisposing factor to NE. For Objective 4, the model of NE from Objective 3 was used to ascertain the degree to which the administration of a CM to day-old chicks influences NE. The CM was derived from cecal digesta of healthy broiler breeder adults, and was propagated in bioreactors. Birds administered the CM did not exhibit clinical signs of NE upon challenge with CORT and C. perfringens. Disease resistance was associated with an increased α-diversity and altered β-diversity of bacterial communities in the small intestine and ceca of birds administered the CM. Furthermore, birds that developed clinical NE exhibited decreased short-chain fatty acid production in the ceca, and this corresponded with a reduction in butyrate-producing bacteria in diseased birds. Evidence indicated that stress promoted disease by impairing immune and epithelial responses (e.g. TLR2A, MUC2B, CATH1) in the small intestine. Moreover, birds administered the CM counteracted responses to stress via stimulation of responses to fight infection and promote recovery (e.g. upregulation of IL2, IL22, IL17). Collectively, this thesis demonstrated physiological stress imparts alterations to bird metabolism, immune function, and the intestinal microbiota in a manner that contributed to increased susceptibility to NE. Moreover, the administration of a complex bacterial microbiota to day-old birds provided resistance to NE by increasing microbial diversity and promoting positive host responses.