Clostridium perfringens epsilon toxin inhibits the gastrointestinal transit in mice

• Published in: Research in veterinary science Vol. 89; no. 3; pp. 404 - 408
• Main Authors: Losada-Eaton, D.M., Fernandez-Miyakawa, M.E.
• Format: Journal Article
• Language: English
• Published: England Elsevier India Pvt Ltd 01.12.2010; Elsevier Limited
• Subjects: Administration, Oral; Animals; Bacterial Toxins - administration & dosage; Bacterial Toxins - pharmacology; Brain; Clostridium perfringens; Clostridium perfringens - metabolism; Clostridium perfringens epsilon toxin; dietary exposure; Enterotoxemia; Enterotoxemia - metabolism; Enterotoxemia - physiopathology; enterotoxins; Epsilon toxin; Experiments; Female; Gastric Emptying - drug effects; Gastric Emptying - physiology; gastrointestinal transit; Gastrointestinal Transit - drug effects; Gastrointestinal Transit - physiology; Gram-positive bacteria; Infusions, Intravenous; Intestinal transit; intragastric administration; Male; Mice; Mice, Inbred BALB C; Motility; oral administration; Permeability; Sheep; Small intestine; Veterinary medicine; Epsilon toxin; Intestinal transit; Enterotoxemia; Clostridium perfringens
• ISSN: 0034-5288; 1532-2661
• DOI: 10.1016/j.rvsc.2010.04.006

Epsilon toxin produced by Clostridium perfringens type B and D is a potent toxin that is responsible for a highly fatal enterotoxemia in sheep and goats. In vitro, epsilon toxin produces contraction of the rat ileum as the result of an indirect action, presumably mediated through the autonomic nervous system. To examine the impact of epsilon toxin in the intestinal transit, gastric emptying (GE) and gastrointestinal transit (GIT) were evaluated after intravenous and oral administration of epsilon toxin in mice. Orally administered epsilon toxin produced a delay on the GIT. Inhibition of the small intestinal transit was observed as early as 1 h after the toxin was administered orally but the effects were not observed after 1 week. Epsilon toxin also produced an inhibition in GE and a delay on the GIT when relatively high toxin concentrations were given intravenously. These results indicate that epsilon toxin administered orally or intravenously to mice transitorily inhibits the GIT. The delay in the GIT induced by epsilon toxin could be relevant in the pathogenesis of C. perfringens type B and D enterotoxemia.