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Clin. Vaccine Immunol. doi:10.1128/CVI.00162-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Immunization of broiler chickens against Clostridium perfringens-induced necrotic enteritis

Department of Pathobiology, University of Guelph, Guelph, Ontario N1G 2W1, Canada

^* To whom correspondence should be addressed. Email: prescott{at}uoguelph.ca.

	Abstract

Necrotic enteritis (NE) in broiler chickens is caused by Clostridium perfringens. Currently, no vaccine against NE is available and immunity to NE is not well characterized. Our previous studies showed that immunity to NE followed oral infection by virulent rather than avirulent C. perfringens, and identified immunogenic secreted proteins apparently uniquely produced by virulent C. perfringens. These proteins were alpha-toxin, glyceraldehyde 3-phosphate dehydrogenase, pyruvate: ferredoxin oxidoreductase (PFOR), fructose 1,6-biphosphate aldolase, and a Hypothetical Protein (HP). The current study investigated the role of each of these proteins in conferring protection to broiler chickens against different severities of oral infection challenge with virulent C. perfringens. Genes encoding these proteins were cloned and purified as histidine-tagged recombinant proteins from E. coli and used to immunize broiler chickens intramuscularly. Serum and intestinal antibody responses were assessed by ELISA. All proteins significantly protected broiler chickens against a relatively mild challenge. In addition, immunization with alpha-toxin, HP and PFOR also showed significant protection against a more severe challenge. When primed with alpha-toxoid and boosted with active toxin, birds immunized with alpha-toxin showed the greatest protection against a severe challenge. The serum and intestinal washings from protected birds had high antigen-specific antibody titers. Thus, we conclude that there are certain secreted proteins, in addition to alpha-toxin, that are involved in immunity to NE in broiler chickens.

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