Toxicity of bunamidine. 1. Cardiovascular effects

In New Zealand hydatid disease is of sufficient economic and medical importance to justify irksome preventive measures. A recent Committee of Inquiry (1967) concluded that the best long-term measure would be the requirement that all dog-owners feed their dogs only on specially prepared dog foods. Meanwhile, however, drugs are being used to eliminate Echinococcus granulosus and closely related cyclophyllidean tapeworms from their primary host, which is the dog. Dosing with arecoline began in 1937. When bunamidine came on the scene in 1966, it promised to be a better anthelmintic in at least some respects (Gemmell and Shearer, 1968). Bunamidine gets rid of a higher proportion of worms than does arecoline; it is easier to administer; and both laboratory and field studies carried out by the manufacturers indicated that bunamidine is less toxic than arecoline in therapeutic doses. It was therefore puzzling why in New Zealand, though not until recently elsewhere, a number of dogs died apparently as a result of having been dosed with bunamidine. Interest in the cardiovascular effects of bunamidine was stimulated by accounts of deaths which had evidently occurred with dramatic suddenness (Fastier, 1972). Some of the experiments to be described suggest a mechanism by means of which certain dogs may be killed by bunamidine given in the therapeutic dose, range. These experiments have already been briefly reported (Fastier et al 1968).