This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Armién, A. G. Articles by Frese, K. Search for Related Content PubMed PubMed Citation Articles by Armién, A. G. Articles by Frese, K.

Spontaneous and Experimental Glycoprotein Storage Disease of Goats Induced by Ipomoea carnea subsp fistulosa (Convolvulaceae)

Institut für Veterinär-Pathologie, Justus-Liebig-Universität Giessen, Giessen, Germany (AGA, KF), Departamento de Nutrição Animal e Pastagem, Instituto de Zootecnia, Universidade Federal Rural do Rio de Janeiro, Brazil (CHT, PVP)

Spontaneous and experimental poisoning with the swainsonine-containing and calystegine-containing plant Ipomoea carnea subsp fistulosa is described. Three of 8 goats presenting with emaciation, weakness, symmetrical ataxia, posterior paresis, proprioceptive deficits, abnormal posture, abnormal postural reaction, and muscle hypertonia were necropsied. I fistulosa was suspected to be the cause of the neurologic disease in all cases. An experiment was conducted to confirm the diagnosis using 12 goats and diets containing 3 different concentrations of the plant. All goats fed I fistulosa developed neurological signs that were similar to those observed in the spontaneous intoxication. Muscle atrophy and pallor were the only macroscopic changes observed in spontaneous and in experimental intoxication. Histological lesions of spontaneous and experimental animals were similar. The most prominent lesion was cytoplasmic vacuolation in neurons of the central and the autonomous nervous system, pancreatic acinar cells, hepatocytes, Kupffer cells, follicular epithelial cells of the thyroid gland, and macrophages of the lymphatic tissues. Neuronal necrosis, axonal spheroids formation, and astrogliosis were additionally observed in the brain. Ultrastructurally, the cytoplasmic vacuoles consisted of distended lysosomes surrounded by a single-layered membrane. Nonreduced end-rests or sequence of -Man, -Glc, ß(1–4)-GlcNAc, and NeuNAc on lysosomal membrane were revealed by lectin histochemistry. Samples of plants used in the experimental trial contained swainsonine and calystegine and their intermediary derivate. We conclude that I fistulosa induces a glycoprotein storage disease primarily based on the inhibition of the lysosomal -mannosidase by the alkaloid swainsonine.

Key words: Ataxia; calystegine; glycoproteinosis; goat; Ipomoea carnea subsp fistulosa; lectin histochemistry; lysosomal storage disease; plant poisoning; swainsonine; ultrastructure.

Request reprints from Dr. Aníbal G. Armién, Department of Veterinary Population Medicine, College of Veterinary Medicine, University of Minnesota, 1333 Gortner Ave., St. Paul, MN 55108. E-mail: armie001{at}umn.edu

This article has been cited by other articles:

				B. L. Stegelmeier, R. J. Molyneux, N. Asano, A. A. Watson, and R. J. Nash The Comparative Pathology of the Glycosidase Inhibitors Swainsonine, Castanospermine, and Calystegines A3, B2, and C1 in Mice Toxicol Pathol, July 1, 2008; 36(5): 651 - 659. [Abstract] [Full Text] [PDF]