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Neurological signs were observed in cattle consuming the roots of Marsdenia hilariana and sheep consuming leaves of Marsdenia megalantha. Similar nervous signs to those observed in spontaneous poisoning were induced experimentally by the administration of roots of M. hilariana to goats, and by the administration of leaves and roots of M. megalantha to sheep. No lesions were observed at necropsies and on histological examination of the nervous system and other tissues., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Intoxication by pods of Prosopis juliflora (mesquite beans) causes an impairment of cranial nerve function in cattle and goats. In goats, vacuolation of neurons in the trigeminal motor nuclei has been reported. To study the lesions in cattle caused by consumption of P. juliflora pods and dry ground pods, eight 6- to 12-month-old male cattle were divided into 4 groups: group 1 was fed a ration containing 50% of pods; groups 2 and 3 received a ration containing 50 and 75% of dry ground pods, respectively; group 4 was the control. After 200 days, all cattle were killed and sampled for histologic evaluation. Samples of the trigeminal motor nucleus were examined by electron microscopy. All cattle from groups 1, 2, and 3 showed clinical signs resulting from impaired function of cranial nerves V, IX, X, and XII, starting 45-75 days after consumption of the plant. The main histologic lesions were vacuolation and loss of neurons in trigeminal motor nuclei and other motor cranial nerve nuclei with Wallerian-like degeneration in the cranial nerves. Mild denervation atrophy was observed in the masseter and other masticatory muscles. On electron microscopy, neurons of the trigeminal nuclei had markedly swollen mitochondria, with the mitochondrial cristae displaced peripherally, disoriented and disintegrating. Intoxication by P. juliflora seems to have a novel pathogenesis, characterized by a selective, primary, chronic, and progressive injury to mitochondria of neurons of the trigeminal and other cranial nerve nuclei. Cranial nerve degeneration and denervation atrophy of the muscles occurs as a consequence of the neuronal lesion.

In the State of Paraiba, Northeastern Brazil, goat mortality occurred with the ingestion of Plumbago scandens. The fresh plant was then given experimentally to 4 goats at 5, 10, 17.5 or 25 g/kg bw. Depression, anorexia, salivation with foamy saliva, bellowing, bruxism, humpbacked posture, bloat, ruminal atony, continuous lateral head movements, tachycardia, dyspnea and dark brown to black urine were observed in the goats given 17.5 or 25 g/kg bw. The goats receiving 5 or 10 g/kg bw had less severe signs. The goat dosed with 25 g/kg bw died after 18-20 h. All others recovered in 3-9 d. At necropsy of the high dose goat, the main lesions were dark violet to black discoloration of the mucosa of the tongue, esophagus, reticulum and ventral sac of the rumen, and gelatinous edema in the visceral ruminal peritoneum. Histologically the reticulum and ventral rumen sac had diffuse epithelial necrosis and severe edema and neutrophilic infiltration of the submucosa. Separation of the ruminal epithelium from the submucosa was observed. Epithelial degeneration and necrosis was also seen in the omasum, esophagus and tongue. Reproduction of the disease with clinical signs similar to those observed by the farmer in the spontaneously affected goats suggests that the clinical mortality was caused by ingestion of Plumbago scandens.