Abstract:
The specific neurotoxic principle of Tylecodon wallichii (Harv.) Toelken subsp. wallichii, the cause of
krimpsiekte in small stock, was isolated and identified as the previously described cumulative bufadienolide,
cotyledoside. Krimpsiekte was experimentally induced in two sheep by the repeated
intravenous administration of cotyledoside at the rate of 0,01-0,015 mg/kg body mass. On day 9,
both animals developed clinical signs typical of krimpsiekte, which is characterized by tremors, paresis
and recumbency. Both sheep had difficulty in controlling their hindquarters when attempting to lie
down. No significant electrocardiograph abnormalities were detected during the experiment which
confirms that cotyledoside at low doses does not overtly affect the electrical activity of the heart. No
gross lesions were observed in the sheep. The most significant microscopic lesions comprised mild
brain oedema and pronounced vacuolation of the white matter of thalamic nuclei. These lesions might
explain some of the motor function deficiencies clinically observed in this syndrome. The previously
held contention that these neurotoxic cardiac glycosides are indeed the cause of krimpsiekte is,
therefore, confirmed.
