Defensive properties of pyrrolizidine alkaloids against microorganisms

The understanding of the selection factors that drive chemical diversification of secondary metabolites of constitutive defence systems in plants, such as pyrrolizidine alkaloids (PAs), is still incomplete. Historically, plants always have been confronted with microorganisms. Long before herbivores existed on this planet, plants had to cope with microbial pathogens. Therefore, plant pathogenic microorganisms may have played an important role in the early evolution of the secondary metabolite diversity. In this review, we discuss the impact that plant-produced PAs have on plant-associated microorganisms. The objective of the review is to present the current knowledge on PAs with respect to anti-microbial activities, adaptation and detoxification by microorganisms, pathogenic fungi, root protection and PA induction. Many in vitro experiments showed effects of PAs on microorganisms. These results point to the potential of microorganisms to be important for the evolution of PAs. However, only a few in vivo studies have been published and support the results of the in vitro studies. In conclusion, the topics pointed out in this review need further exploration by carrying out ecological experiments and field studies

Poisonous Plants and Plant Toxins That Are Likely to Contaminate Hay and Other Prepared Feeds in the Western United States

Livestock poisoning by toxic plants is a relatively common problem in pastures and rangelands and it is estimated to annually cost the livestock industry more than $200 million. However, these estimates are for grazing animals and the total cost is probably much greater because many animals are poisoned by contaminated feeds. Many poisonous plants are accessible to grazing livestock, but they are generally avoided and are not eaten, or they are eaten at doses that they do not produce detectable disease. In such cases toxic plants may not be more than a problem of displacing desirable nutritious plants. However, this is not always the case, especially when toxic plants contaminate prepared feeds. Poisonous plants incorporated in preserved forages, such as hay and silage, are much more likely to be eaten. This may occur because of increased competition from herd mates or by increased feeding pressure as prepared feeds are most often used in winter when alternative food sources are exhausted. Alternatively, the plants may become more palatable as they are diluted with palatable feed or the previously distasteful plant components are altered during forage preparation or storage. In addition, normally safe forages, under certain conditions, can produce and accumulate toxins. Identifying these toxic contaminates and understanding when forages may be toxic is critical in reducing poisoning and ensuring quality animal products. Our objectives of this review are to present basic principles of identifying contaminated feeds and sampling forages, introduce several common forages that under certain conditions can be toxic, present a brief description of plants that we have found contaminating feed in the western United States, and review how to treat or avoid such poisonings. The Rangelands archives are made available by the Society for Range Management and the University of Arizona Libraries. Contact [email protected] for further information.Migrated from OJS platform March 202

The acute toxicity of the death camas (Zigadenus species) alkaloid zygacine in mice, including the effect of the methyllycaconitine coadministration on zygacine toxicity

Death camas (Zigadenus spp.) is a common poisonous plant on foothill rangelands in western North America. The steroidal alkaloid zygacine is believed to be the primary toxic component in death camas. Poisonings on rangelands generally occur in the spring when death camas is abundant, whereas other more desirable forage species are limited in availability. In most cases where livestock are poisoned by plants in a range setting, there is more than one potential poisonous plant in that area. One common poisonous plant that is often found growing simultaneously in the same area as death camas is low larkspur (Delphinium nuttallianum). Consequently, the objectives of this study were to conduct acute toxicity studies in mice and to determine if coadministration of low larkspur will exacerbate the toxicity of death camas. We first characterized the acute toxicity of zygacine in mice. The LD50 of zygacine administered intravenously (i.v.) and orally was 2.0 ± 0.2 and 132 ± 21 mg/kg, respectively. The rate of elimination of zygacine from whole blood was determined to be 0.06 ± 0.01/min, which corresponds to an elimination half-life of 13.0 ± 2.7 min. The i.v. LD50 of total alkaloid extracts from a Utah and a Nevada collection were 2.8 ± 0.8 and 2.2 ± 0.3 mg/kg, respectively. The i.v. LD50 of methyllycaconitine (MLA), a major toxic alkaloid in low larkspur, was 4.6 ± 0.5 mg/kg, whereas the i.v. LD50 of a 1:1 mixture of MLA and zygacine was 2.9 ± 0.7 mg/kg. The clinical signs in mice treated with this mixture were very similar to those of mice treated with zygacine alone, including the time of onset and death. These results suggest that there is an additive effect of coadministering these 2 alkaloids i.v. in mice. The results from this study increase knowledge and understanding regarding the acute toxicity of death camas. As combined intoxications are most likely common, this information will be useful in further developing management recommendations for ranchers and in designing additional experiments to study the toxicity of death camas to livestock

Locoweed Poisoning in Livestock

The Rangelands archives are made available by the Society for Range Management and the University of Arizona Libraries. Contact [email protected] for further information.Migrated from OJS platform March 202

Neurologic disease in range goatsassociated with Oxytropis sericea (Locoweed) poisoning and water deprivation

About 200/2500 Spanish goats foraging on mountain rangelands of western Montana developed neurologic disease with severe rear limb weakness, knuckling of the rear fetlocks, and a hopping gait. Sick goats were of all ages and in good flesh, though they often had dull, shaggy coats. Some mildly affected animals recovered after being moved to feed lots, but others progressed to recumbency, seizures and death. At necropsy both moribund and clinically affected animals had few gross lesions; 1 animal had contusions and puncture wounds on rear legs and perineum, suggestive of predator bites. Histologic lesions included mild vacuolation of neurons and visceral epithelial cells, mild diffuse cerebral edema with minimal neuronal pyknosis, and random, multifocal Wallarian degeneration of spinal cord axons. Affected animals had elevated serum sodium, potassium and chloride levels; other mineral analyses and serum biochemistries were within normal limits. Locoweed-induced depression and inhibition of neuromuscular function coupled with water deprivation due to predation pressure allowed development of neurologic disease and hypernatremia

Respiratory Elimination ofSelenium in Sheep Given the Accumulator Plant Symphyotrichum spathulatum (WesternMountain Aster)

Selenium (Se) is a necessary mineral required by mammals and poultry. If toxic amounts are ingested, expired air becomes a potentially important, but poorly investigated, route of elimination. A study was performed to evaluate respiratory toxicokinetics of Se in sheep. Sheep were gavaged with the accumulator plant Symphyotrichum spathulatum at Se equivalent doses of 0, 2, 4, 6 or 8 mg/kg BW. As positive controls an additional two sheep were gavaged with purified sodium selenite at 4 mg Se/kg BW and two sheep were gavaged with purified selenomethionine (Se-Met) at 8 mg Se/kg BW. Expired air samples were collected prior to dosing and at 1, 2, 4 and 8 hrs post dosing. Samples were collected from both sheep in the control, selenite and Se-Met groups and from 4 sheep in each of the plant-Se treatment groups. The air Se concentrations of the Se-Met group were statistically higher (P \u3c 0.05) than all other groups at each time point of collection. The selenite, 2 and 4 mg plant-Se/kg BW groups all had peak concentrations at the 2 hr collection time. The 8 mg plant-Se/kg BW group showed a linear increase in respiratory Se concentration through 8 hours. The 6 mg plant-Se/kg BW group peaked at 1 hour, then dropped and peaked again at 4 hours and finally dropped between 4 and 8 hours. At 8 hours, the 8 mg plant-Se/kg BW group was significantly higher (P \u3c 0.05) than all other groups. The elimination profile for Se-Met was dissimilar to any of the other treatments, with greater than 20 times the concentration of Se in the expired air than the high dose plant Se or the selenite treatments. The 4 mg selenite and 4 mg plant Se had similar elimination profiles, although the 4 mg plant Se had significantly greater (P \u3c 0.05) concentrations at 2, 4 and 8 hrs. The total dose of the plant Se appreciably altered the elimination profile. These findings indicate that both dose and chemical form of Se affect respiratory elimination kinetics