Control of necrotic enteritis in poultry production with in-feed antibiotic alternative strategies

Abstract

Poultry necrotic enteritis (NE) is caused by a Gram-positive bacteria, 'Clostridium perferingens' (Cp) leading to devastating economic losses in the broiler chicken industry. The aim of this project was to develop dietary strategies to control NE in broiler chickens as an alternative to the use of in-feed antibiotics. Four experiments were conducted to investigate the roles of four test articles in controlling necrotic enteritis in broilers, following the logic flow of NE pathogenesis. Predisposing factor: The first experiment was designed to test if glycine supplementation (10 g/kg) in grower diets could replace 'Eimeria' co-infection in establishing a subclinical NE challenge model, because dietary glycine has been shown to promote the proliferation of Cp. In this experiment, a successful subclinical NE challenge was achieved, as shown by a lack of mortality but mild intestinal lesions and higher feed conversion ratio (FCR) in the Cp challenged birds. A combined challenge with Cp and 'Eimeria' presented reduced body weight gain in broilers, whereas feeding supplemental glycine resulted in increased growth performance. The highest jejunal lesion scores were found in birds with a combination of Cp challenge and supplemental glycine without 'Eimeria' among all the treatments. The first study suggested that using glycine can partially replace 'Eimeria' in a subclinical NE challenge model in promoting intestinal lesions, but not impairing chicken performance. Gut microflora management: The second experiment was designed to determine the effects of a prebiotic, yeast cell wall extract (YCW) derived from 'Saccharomyces cerevisiae' or in-feed antibiotics, Zn bacitracin and salinomycin (AB) on broiler growth, intestinal lesions, humoral immune response and gut microflora metabolites during subclinical NE challenge. The results obtained in this experiment showed that AB siginificantly alleviated the impacts of subclinical NE on performance and intestinal lesions of broiler chickens, but YCW showed limited effects. Inclusion of YCW in diets suppressed the inflammation caused by NE and promoted the production of immunoglobulins on d16, indicating its immunomodulatory effects. For short chain fatty acids (SCFA) profile in cecal contents, YCW increased formic acid concentrations during challenge and increased butyric acid concentration in unchallenged birds on d16, implying a role in altering gut microflora metabolites. This study indicates YCW may not fully replace in-feed antibiotics in controlling subclinical NE in broiler chickens however it modulates immune responses and increases short chain fatty acid production, suggesting potential benefits to bird health. Anti-inflammation: A third experiment was conducted to investigate the effects of isoquinoline alkaloids (IQA) derived from Macleaya cordata as anti-inflammatory agents on broiler performance, intestinal lesions, productive traits, gut microflora, SCFA and serum biochemical indices during NE challenge. The effects of NE on broiler performance, carcass traits and intestine lesions were significantly alleviated by including IQA in the diets. Challenge with NE altered the serum biochemical indices, whereas IQA retained triglyceride and triiodothyronine levels on d16 and increased the total cholesterol and triiodothyronine levels on d24, indicating IQA controlled the pathophysical changes of NE challenge. This was most likely related to a direct anti-inflammation effect from IQA, because no differences in gut microflora or SCFA production in chicken were detected as a result of dietary inclusion of IQA. Compensating the metabolic loss from inflammation caused by NE: A fourth experiment investigated if supplemental L-glutamine (L-Gln, 10 g/kg) could reverse the negative impacts of NE on broiler performance, intestinal morphology and lesions and serum biochemical indices. Similar to IQA, results obtained in this experiment showed L-Gln significantly increased performance and intestinal development in broiler chickens during NE challenge. However, the mode of action could be different from IQA, as L-Gln did not affect serum biochemical indices, except that it decreased uric acid levels on d24. This indicates that L-Gln could have compensated for the metabolic loss from NE challenge, provided fuel to enterocytes and increasing amino acid utilization, rather than suppressing inflammation directly. The results of these studies suggest potential dietary strategies to control NE challenge in broiler chickens. The work highlights the importance of inflammation during NE infection and indicates inflammation should be a possible target for the future development of antibiotic alternatives and nutritional strategies to enhance gut health.