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Protection of goats against experimental enterotoxaemia by vaccination with Clostridium perfringens type D epsilon toxoid
  1. F. A. Uzal, MedVet, MSc, PhD1 and
  2. W. R. Kelly, MSc, PhD1
  1. 1 Department of Veterinary Pathology, The University of Queensland, Brisbane, Qld 4072, Australia

Abstract

Enterotoxaemia in goats is mainly characterised by enterocolitis, and it has been suggested that the poor efficacy of commercial vaccines in preventing the disease is due to the local action of Clostridium perfringens toxin/s within the intestine, where circulating antibodies might not exert their action. Five goat kids were vaccinated with an incomplete Freund's adjuvant C perfringens type D epsilon toxoid vaccine on three occasions at three-week intervals, four similar kids were vaccinated with a commercial enterotoxaemia vaccine at the same times, and five other unvaccinated kids were used as controls. All the animals were challenged intraduodenally, one week after the last vaccination, with C perfringens type D filtered culture supernatant. At the time of challenge, the level of epsilon toxin antibodies in the serum of the Freund's adjuvant- vaccinated kids ranged between 2.45 and 230 iu/ml, while the kids that received the commercial vaccine had levels between 0.22 and 1.52 iu/ml, and the unvaccinated kids had levels below 0.03 iu/ml. No clinical or postmortem changes were observed in the kids that received the Freund's adjuvant-vaccine. Three of the four kids that received the commercial vaccine developed mild, pasty diarrhoea, with a slight reddening of the colonic mucosa being observed postmortem. All the unvaccinated kids developed severe diarrhoea, respiratory distress and central nervous system signs, and were killed humanely between six and 24 hours after challenge. The postmortem changes consisted of pseudomembranous colitis, lung oedema and perivascular oedema of the brain. Moderate to high serum levels of anti-epsilon antibody appeared to protect the goats against both the systemic and the intestinal effects of C perfringens type D toxins.

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