Abstract. The ground endosperm of the seeds of Cassia occidentalis (coffee senna) administered to rabbits, orally, 0.25-3.0% body weight, produced a fatal cardiomyopathy characterized by mitochondrial degeneration, lipid accumulation, myofibrillar degeneration, myocytolysis and relatively minor reparative changes. Mitochondrial damage is probably the primary morphologic lesion and results from the specific action of the toxic principle(s) of coffee senna. The other changes reflect the disordered metabolism caused by the altered function of the damaged mitochondria. The microscopic lesions in the hearts of poisoned rabbits resembled those in cattle poisoned with coffee senna and thus the rabbit is considered a useful model for the study of the intoxication. The microscopic appearances of coffee senna poisoning in rabbits and cobalt toxicity in the rat are similar.

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A disease in Angus calves was characterised by shedding of the epidermis with ulceration and inflammation of the oral mucosa and the skin of carpus, metacarpal-phalangeal joints, phalanges, coronary border, and with partial separation of the hooves. The pathogenesis of these lesions involves a breakdown of intercellular adhesions associated with anomalous development of the desmosome-tonofilament complexes in the basal and prickle cells of the epidermis. The breeding and clinical history suggested a genetic cause. The disease was called ‘familial acantholysis of Angus calves’.