Abstract

The ten cases observed were in calves aged 7 months to a year in four herds in central Montana between December 1978 and January 1983. The animal may at first appear normal until disturbed, when it shows muscle tremors and ataxia. In advanced stages the animal is in lateral recumbency with pronounced nervous symptoms and will usually die within 1-4 days. Gross lesions were confined to the ileum, caecum and colon in most cases with varying degrees of mucusal necrosis, haemorrhage and fibronecrotic debris. Intracellular coccidia were observed microscopically, mainly in portions of the colon. Faecal samples all contained coccidial oocysts in varying numbers. Serum magnesium values varied from normal to above normal, while calcium values were all below normal. Liver and kidney samples from several calves were negative for lead. Initial treatment consisted of 250 ml of a commercial calcium, magnesium and dextrose solution i/v and an additional 250 ml s/c. Sustained release sulfamethazine boluses were given orally. Animals in convulsions were given 7% chloral hydrate i/v or a 6% chloral hydrate/magnesium sulphate solution i/v. Supportive therapy included balanced electrolyte solutions given orally or i/v as needed. The nervous symptoms paralleled those in cows with hypomagnesaemia. A mechanism is proposed which involves stresses (including intestinal damage by coccidia) causing depletion of tissue magnesium and lowering of serum calcium. The most logical approach to the problem is the prevention of all coccidiosis through good herd management, sanitation, reduction of stress, and use of anticoccidials.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call