Experimental poisoning of goats by Ipomoea carnea subsp. fistulosa in Argentina: a clinic and pathological correlation with special consideration on the central nervous system

Abstract

Ipomoea carnea subsp. fistulosa, aguapei or mandiyura, is responsible for lysosomal storage in goats. The shrub contains several alkaloids, mainly swansonine which inhibits lysosomal α-mannosidase and Golgi mannosidase II. Poisoning occurs by inhibition of these hydrolases. There is neuronal vacuolation, endocrine dysfunction, cardiovascular and gastrointestinal injury, and immune disorders. Clinical signs and pathology of the experimental poisoning of goats by Ipomoea carnea in Argentina are here described. Five goats received fresh leaves and stems of Ipomoea. At the beginning, the goats did not consume the plant, but later, it was preferred over any other forage. High dose induced rapid intoxication, whereas with low doses, the course of the toxicosis was more protracted. The goats were euthanized when they were recumbent. Cerebrum, cerebellum, medulla oblongata, pons and colliculi, were routinely processed for histology. In nine days, the following clinical signs developed: abnormal fascies, dilated nostrils and abnormal postures of the head, cephalic tremors and nystagmus, difficulty in standing. Subsequently, the goats had a tendency to fall, always to the left, with spastic convulsions. There was lack in coordination of voluntary movements due to Purkinje and deep nuclei neurons damage. The cochlear reflex originated hyperreflexia, abnormal posture, head movements and tremors. The withdrawal reflex produced flexor muscles hypersensitivity at the four legs, later depression and stupor. Abnormal responses to sounds were related to collicular lesions. Thalamic damage altered the withdrawal reflex, showing incomplete reaction. The observed cervical hair bristling was attributed to a thalamic regulated nociceptive response. Depression may be associated with agonists of lysergic acid contained in Ipomoea. These clinical signs were correlated with lesions in different parts of the CNS.

Suspected natural lysosomal storage disease from ingestion of pink morning glory (<i>Ipomoea carnea</i>) in goats in northern Argentina

“…These are similar to those previously described in both spontaneous and experimentally induced poisoning with I. carnea [2, 10], and these aspects were reported in goats from other swainsonine-containing plants, such as locoweed, other Ipomoea sp. and Sida carpinifolia [3, 4, 7, 11].…”

“…Swainsonine-containing plants, such as Swainsona galegifolia, Oxytropis sp ., Astragalus sp ., Ipomoea sp ., Turbina cordata and Sida carpinifolia , cause a glycoprotein storage disease in livestock, which has been described in many countries, including China [4], the United States [13], Mozambique [6], Brazil [2, 3, 7, 9] and Argentina [5, 10, 11]. These poisonings were characterized by abnormal behavior of the affected animals, consisting of weakness, loss of appetite, ataxia, recumbence and death [2,3,4, 6, 7, 9].…”

“…I. carnea toxicosis was experimentally reproduced in the Corrientes province of northern Argentina [10], because it is the most prevalent toxic plant in the region. However, this is the first report of a spontaneous disease in goats by I. carnea in Argentina.…”

Haematologic alterations caused by Ipomoea carnea in experimental poisoning of guinea pig

“…It has been reported decrease of total bone marrow cellularity in adult rats intoxicated with I. carnea (Hueza and Górniak, 2011). This toxicity is characterized by lysosomal vacuolization of cells from different organs and tissues, including the lymphocytes, pancreatic acinar cells, spleen, hepatocytes, liver and macrophages of the lymphatic tissues and neurons of CNS (Armién et al, 2007;Ríos et al, 2012).…”

“…fistulosa (Convolvulaceae) has been reported in the northeastern region of Argentina (Ríos et al, 2012) and in other tropical and subtropical countries (Austin and Huaman, 1996). Different toxic alkaloids have been isolated from this plant: swainsonine (SW) and the calystegines A 3 , B 1 , B 2 , B 3 , and C 1 (de Balogh et al, 1999;Haraguchi et al, 2003;Cholich et al, 2009).…”