COBALT DELAYS THE DEVELOPMENT OF CLINICAL ANNUAL RYEGRASS TOXICITY IN SHEEP

Annual ryegrass toxicity (ARGT) is a neurological disease of livestock caused by corynetoxins found in annual ryegrass infected by Clavibacter toxicus (Riley and Ophel 1992). We have previously shown that cobalt supplements offer partial protection against apparent liver damage resulting from doses of corynetoxins sufficient to cause sub-clinical ARGT in sheep (Davies et al. 1993). The current experiment investigated the response of cobalt supplemented sheep to doses that would cause the clinical disease. Forty five Merino wethers maintained at 3.5 kg liveweight on a basal diet of oaten hay with 12% lupins were allocated to 9 treatment groups each of 5 sheep in a 3 x 3 factorial design. Toxic ryegrass seed was incorporated in the diet to provide either 0, 0.15 or 0.30 mg corynetoxins/kg liveweightday. Sheep were drenched daily with an aqueous solution of CoS03.7H,0 to provide either 0, 4 or 16 mg cobalt/day. Toxin treatment was stopped at the first appearence of clinical signs (staggering gait, convulsions). Sheep receiving cobalt supplements were able to ingest 30% more toxin before showing the clinical signs of the disease than those animals not supplemented with cobalt (P = 0.026). Increasing the level of cobalt from 4 to 16 mg/day did not confer any greater protection (P = 0.083). The cumulative dose of toxin required to induce clinical signs was slightly, but not significantly , greater for those sheep receiving toxin at the lower rate (P = 0.434).