Effects of Tylosin on Bacterial Mucolysis,Clostridium perfringensColonization, and Intestinal Barrier Function in a Chick Model of Necrotic Enteritis

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Abstract
Necrotic enteritis (NE) is a worldwide poultry disease caused by the alpha toxin-producing bacteriumClostridium perfringens. Disease risk factors include concurrent coccidial infection and the dietary use of cereal grains high in nonstarch polysaccharides (NSP), such as wheat, barley, rye, and oats. Outbreaks of NE can be prevented or treated by the use of in-feed antibiotics. However, the current debate regarding the prophylactic use of antibiotics in animal diets necessitates a better understanding of factors that influence intestinal colonization byC. perfringensas well as the pathophysiological consequences of its growth. We report a study with a chick model of NE, which used molecular (16S rRNA gene [16S rDNA]) and culture-based microbiological techniques to investigate the impact of the macrolide antibiotic tylosin phosphate (100 ppm) and a dietary NSP (pectin) on the community structure of the small intestinal microbiota relative to colonization byC. perfringens. The effects of tylosin and pectin on mucolytic activity of the microbiota andC. perfringenscolonization and their relationship to pathological indices of NE were of particular interest. The data demonstrate that tylosin reduced the percentage of mucolytic bacteria in general and the concentration ofC. perfringensin particular, and these responses correlated in a temporal fashion with a reduction in the occurrence of NE lesions and an improvement in barrier function. The presence of pectin did not significantly affect the variables measured. Thus, it appears that tylosin can control NE through its modulation ofC. perfringenscolonization and the mucolytic activity of the intestinal microbiota.