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The indolizidine alkaloid swainsonine, found in some Astragalus and Oxytropis (i.e., locoweed) species, is a potent cellular glycosidase inhibitor that often poisons livestock. Other toxic genera such as some Ipomoea species also contain swainsonine as well as calystegines which are similar polyhydroxy alkaloids. The toxicity of calystegines is poorly characterized; however, they are also potent glycoside inhibitors capable of intestinal and cellular glycoside dysfunction. The objective of this study was to directly compare A. lentiginosus and I. carnea poisoning in goats to better characterize the role of the calystegines. Three groups of four goats each were treated with ground alfalfa (control), I. carnea or A. lentiginosus to obtain daily doses of 0.0, 1.5, and 1.5 mg swainsonine/kg bw per day, respectively, for 45 days. Animals were observed daily and weekly body weights, serum enzyme activities, and serum swainsonine concentrations were determined. At day 45 all animals were euthanized and necropsied. Goats treated with A. lentiginosus and I. carnea developed clinical disease characterized by mild intention tremors and proprioceptive deficits. Goats treated with A. lentiginosus developed clinical disease sooner and with greater consistency. No differences in body weight, serum swainsonine concentrations and serum enzyme activity were observed between goats treated with A. lentiginosus and I. carnea. Additionally, there were no differences in the microscopic and histochemical studies of the visceral and neurologic lesions observed between goats treated with A. lentiginosus and I. carnea. These findings suggest that I. carnea-induced clinical signs and lesions are due to swainsonine and that calystegines contribute little or nothing to toxicity in goats in the presence of swainsonine., (Published by Elsevier Ltd.)

Locoweeds are perennial herbaceous plants included in Astragalus spp. and Oxytropis spp. that contain the toxic indolizidine alkaloid swainsonine. The livestock that consume locoweed feeding can suffer from a type of toxicity called "locoism." There are aliphatic nitro compounds, selenium, selenium compounds and alkaloids in locoweed. The toxic component in locoweeds has been identified as swainsonine, an indolizidine alkaloid. Swainsonine inhibits lysosomal α-mannosidase and mannosidase II, resulting in altered oligosaccharide degradation and incomplete glycoprotein processing. As a result, livestock that consume locoweeds exhibit several symptoms, including dispirited behavior, staggering gait, chromatopsia, trembling, ataxia, and cellular vacuolar degeneration of most tissues by pathological observation. Locoism results in significant annual economic losses. Recently, locoweed populations have increased domestically in China and abroad, resulting in an increase in the incidence of poisoning. Therefore, in this paper, we review the current research on locoweed, including on species variation, pathogenesis, damage and poisoning prevention measures., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Swainsonine (SW) is a toxin produced by locoweeds and harmful to the livestock industry. Degrading SW by Arthrobacter sp. HW08 was demonstrated as a promising way to deal with SW poisoning. However, it is unknown which part of the subcellular enzymes in Arthrobacter sp. HW08 is responsible for biodegrading SW and whether the metabolites are atoxic. In this study, intracellular and extracellular enzymes of Arthrobacter sp. HW08 were isolated and their enzyme activity was evaluated. The metabolites were fed to mice, and physiological and histological properties of the treated mice were investigated. The results showed that only intracellular enzyme of Arthrobacter sp. HW08 (IEHW08) could degrade SW efficiently. Compared with mice in SW treatment group, mice in SW + IEHW08 treatment group (1) increased their body weights; (2) showed higher number of platelets and lower number of white blood cells; (3) decreased the levels of creatinine, urea nitrogen, alanine transaminase and aspartate aminotransferase in serum; (4) reduced the number of vacuolated cells in cerebellum, liver and kidney. All these data demonstrate that IEHW08 was potentially safe for mice, while keeping the capacity of degrading SW. This study indicates a possible application of IEHW08 as an additive in the livestock industry to protect animals from SW poisoning.

Poisoning by Sida carpinifolia belongs to a group of plant-induced phenotype which resembles lysosomal storage diseases. Saanen goats were fed aerial parts of green S. carpinifolia for up to 3 months. Concentrates complemented the nutritional requirements. Urine and blood samples were collected for oligosaccharide study (by thin layer chromatography-TLC) and hemogram analysis, respectively. Abnormal excretion of oligosaccharides was observed from the 2nd day of S. carpinifolia ingestion until one day after withdrawal of the plant from the diet. There were no changes in hemogram. Clinical signs were typical of poisoning caused by plants of this group and were seen from the 37th day on S. carpinifolia diet until seven days after withdrawal of the plant, when signs gradually became scarce and less evident. Results presented here suggest that detection of urinary oligosaccharides by TLC may be an useful method to assess swainsonine-containing plants exposure or an early diagnostic tool for poisoning by these plants.

A disease of the central nervous system in goats was observed in the municipalities of Juazeiro, Casa Nova and Curaça, state of Bahia, and Petrolina, state of Pernambuco, Northeastern Brazil. The disease was produced experimentally in two goats by the administration of dry Turbina cordata mixed with grain. Clinical signs were observed after the ingestion of 62 and 106 g/kg body weight in 28 and 54 days, respectively. The concentration of swainsonine in the plant varied from less than 0.001% to 0.14% (dry weight). Clinical signs of natural and experimental cases included difficulties in standing, ataxia, hypermetria, wide-based stance, intention tremors, spastic paresis mainly in the hind legs, nystagmus, abnormal postural reactions, head tilting, and falling. Diffuse vacuolation of neurons, epithelial cells of pancreas, thyroids, and renal tubules were observed on the histology. From the electron microscopy of Purkinje cells the vacuoles represented dilated lysosomes. These findings demonstrated that T. cordata causes an acquired glycoprotein lysosomal storage disease. The intoxication occurs at least in an area of 27,000 km2 causing severe losses in goats, and some farmers report the disease also in cattle.

Spotted locoweed (Astragalus lentiginosus var. diphysus) is a toxic, perennial plant that may, if sufficient precipitation occurs, dominate the herbaceous vegetation of pinyon-juniper woodlands on the Colorado Plateau. Six cow/calf pairs and four horses grazed a 20-ha pasture with dense patches of locoweed in eastern Arizona during spring 1998. Locoweed density was 0.7 plants/m2 in the pasture. Locoweed averaged 30.4% NDF and 18.4% CP. Concentrations of the locoweed toxin, swainsonine, fluctuated from 1.25 to 2 mg/g in locoweed. Horses ate more (P < 0.01) bites of locoweed than did cows (15.4 and 5.1% of bites, respectively). Horses generally increased locoweed consumption over time since they ate approximately 5% of bites in the preflower stage compared with 25% of bites in the pod stage. Cattle consumed almost no locoweed (< 1% of bites) until the pod stage, when they increased consumption to 15% of bites. Horses were very avid (approximately 65 to 95% of bites) in selecting the small quantities (approximately 40 to 150 kg/ha) of available green grass, and it appeared that their propensity to eat scarce green forage influenced their locoweed consumption as well. Horses ate relatively little dry grass, even when it was abundant, whereas cattle ate large amounts of dry grass until green grasses became more abundant. Calves began eating locoweed on the same day as their dams and ate approximately 20% of their bites as locoweed. Serum concentrations of swainsonine were higher (P < 0.05) in horses than in cattle (433 vs. 170 ng/mL, respectively). Baseline swainsonine was zero in all animals, but swainsonine was rapidly increased to above 800 ng/mL in serum of horses as they ate locoweed. Horses exhibited depression after eating locoweed for about 2 wk; after 5 wk of exposure, horses became anorectic and behaviorally unstable. Although limited in scope, this study indicates that horses should not be exposed to spotted locoweed.

The effects of ionophore supplementation on selected serum constituents of sheep consuming locoweed were investigated. Sixteen sheep were allotted by weight to a 2x2 factorial arrangement of treatments: 1) no locoweed, no lasalocid, 2) no locoweed, 0.75 mg lasalocid/kg BW, 3) 0.5 mg swainsonine/kg BW, no lasalocid, 4) 0.5 mg swainsonine/kg BW, 0.75 mg lasalocid/kg BW. Swainsonine was provided by locoweed (Oxytropissericea), and sheep were fed a blue grama based diet at 2.5% BW for a 35 d treatment period. Diets were formulated to be isocaloric and isonitrogenous. Blood samples were collected on d 1, 7,14, 21, 31 and 35 to determine serum swainsonine concentration, alkaline phosphatase, total iron, aspartate aminotransferase, g-glutamyltransferase, and lactate dehydrogenase activity and total cholesterol, and triglyceride concentrations. No lasalocid by locoweed interaction (P > 0.4) was noted for any response variable measured. Average daily gains (P = 0.4) and orts (P = 0.7) were not affected by the treatments. No lasalocid treatment (P = 0.7) or day (P = 0.1) effect of serum swainsonine was observed. A locoweed by day interaction (P < 0.0001) of serum alkaline phosphatase was detected. Alkaline phosphatase levels were elevated (P < 0.01) for locoweed treated sheep at 24 h following initial exposure and remained elevated throughout the trail. Total iron was suppressed (P < 0.08) in locoweed fed sheep. A day effect (P < 0.02) was observed for serum iron. However, no linear, quadratic, or cubic effects of day were noted (P >0.2). A locoweed by day interaction (P < 0.0001) of serum aspartate aminotransferase and g-glutamyltransferase was detected. Aspartate aminotransferase levels were elevated (P < 0.0001) by d 7 for locoweed treated animals and remained elevated throughout the trial. g--Glutamyltransferase levels were suppressed (P < 0.0001) by day 7 for locoweed treated animals and remained suppressed throughout the trial. A locoweed by day interaction (P = 0.06) of serum cholesterol was detected. However, no linear, quadratic, or cubic effects of day were detected (P = 0.2). Lasalocid treatment had no effect on any serum constituent measured. Use of lasalocid in grazing animals should not increase the likelihood of locoweed intoxication.

The indolizidine alkaloid swainsonine has been identified as the toxic constituent of Sida carpinifolia, a native perennial shrub-like plant, reported to produce neurological disorders in goats and ponies in southern Brazil. Swainsonine was detected in dry ground plant material after extraction and analysis by both liquid and gas chromatography mass spectrometry. The swainsonine concentration was 0.006% on a dry weight basis. The clinical and pathological features of this lysosomal storage disease were similar to those observed in Swainsona, Oxytropis, Astragalus, and Ipomoea poisonings with multiple cytoplasm vacuoles in neurons, acinar pancreatic cells, hepatocytes, and renal tubular cells.

The Battle of Little Bighorn was fought over 100 y ago but many controversies remain. Some feel the defeat of Custer could have been avoided if Benteen and Reno had united with Custer. A slow-moving pack train may have hindered the troops of Benteen and Reno from joining up with Custer. One report indicated the horses and mules in the pack train were lame and behaved crazily. It has been previously suggested that the animals had selenium toxicosis. We propose the lameness could have been caused by selenium, but that the behavioral problems may have been caused by the ingestion of plants containing swainsonine.

Five mycotoxins found in concentrates or roughages have been shown to cause neurologic disease in livestock. Fumonisin B1 is produced by Fusarium moniliforme and causes leukoencephalomalacia in horses. Swainsonine and slaframine are produced by Rhizoctonia leguminicola and cause mannose accumulation and parasympathomimetic effects, respectively. Lolitrems from Acremonium lolii and paspalitrems from Claviceps paspali are tremorgens found in grasses.