By Krook, L., Cornell Veterinarian, 1975
Description
Cestrum diurnum poisoning was described in a Florida bull. Clinical signs included chronic wasting and progressive lameness. Plasma clacium was elevated for long periods of time but decreased toward low normal values. There was pronouced C-cell hyperplasia. Osteopetrosis was very severe and reflected retarded osteocytic osteolysis and chondrolysis. Further negative effects on the osteocytes eventually lead to osteonecrosis. Soft tissue calcinosis involved tendons and ligaments, major arteries and veins but kidneys and lungs were spared. Whereas the osteopetrosis could be explained by hypercalcitoninism, the osteonecrosis was believed to result from direct action by the Cestrum diurnum factor, previously shown to have an action similar to that of 1,25-dihydroxy-cholecalciferol, which is the biologically active metabolite of vitamin D3
Cestrum diurnum poisoning was described in a Florida bull. Clinical signs included chronic wasting and progressive lameness. Plasma clacium was elevated for long periods of time but decreased toward low normal values. There was pronouced C-cell hyperplasia. Osteopetrosis was very severe and reflected retarded osteocytic osteolysis and chondrolysis. Further negative effects on the osteocytes eventually lead to osteonecrosis. Soft tissue calcinosis involved tendons and ligaments, major arteries and veins but kidneys and lungs were spared. Whereas the osteopetrosis could be explained by hypercalcitoninism, the osteonecrosis was believed to result from direct action by the Cestrum diurnum factor, previously shown to have an action similar to that of 1,25-dihydroxy-cholecalciferol, which is the biologically active metabolite of vitamin D3
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