Solutions to Locoweed Poisoning in New Mexico and the Western United States

Graham, David L.; Creamer, Rebecca; Cook, Daniel; Stegelmeier, Bryan L.; Welch, Kevin D.; Pfister, J. A.; Panter, Kip E.; Cibils, Andrés F.; Ralphs, Michael H.; Encinias, Manny; McDaniel, Kirk C.; Thompson, David C.; Gardner, Kevin T.

doi:10.2111/1551-501x-31.6.3

Cited by 11 publications

(4 citation statements)

References 8 publications

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“…No SWA differences were detected between injured and uninjured O. sericea leaves collected from three sites in New Mexico (Parker, 2008). Although locoweed SWA can deter vertebrate herbivory, some cattle individuals are more prone to feeding on new plants; through social interactions more individuals feed on toxic locoweeds when preferred plants are unavailable (Cook et al, 2009a; Graham et al, 2009). Thus, additional studies should further explore any antiherbivory function of SWA and examine where locoweed plant–fungal endophyte symbioses fall along a mutualism–commensalism–parasitism continuum.…”

Section: Discussionmentioning

confidence: 99%

“…The primary applied ecological relevance of locoweeds is that ingestion by livestock leads to “locoism,” a disease caused by SWA that results in erratic behavior, health problems, reproductive problems, and even death (James et al, 1981; Cook et al, 2009b). Some locoweeds have widespread geographic ranges in the western United States (Fox et al, 1998) and have negatively affected ranching in several U.S. states for decades (Kingsbury, 1964; Graham et al, 2009). Thus, we need a greater understanding of genetic and environmental factors that influence SWA levels in locoweeds.…”

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confidence: 99%

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Locoweed dose responses to nitrogen: Positive for biomass and primary physiology, but inconsistent for an alkaloid

Delaney

Klypina

Maruthavanan

et al. 2011

American J of Botany

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Supplemented N led to positive dose responses for plant biomass and leaf photosynthesis and pigments, but SWA dose responses differed across locoweed taxa and time. At N levels that enhanced plant growth and reduced antioxidant protective systems, fungal endophyte alkaloid production was not strongly influenced. Production of SWA may be more strongly influenced by factors other than C:N supply (e.g., seasonality, plant age) in the locoweed-endophyte-Rhizobium complex.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Locoweed dose responses to nitrogen: Positive for biomass and primary physiology, but inconsistent for an alkaloid

Delaney

Klypina

Maruthavanan

et al. 2011

American J of Botany

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“…Also, swainsonine was present in O. sericea plants sampled from four geographic locations over a 5-month period, spanning the vegetative to the senescent stages of growth ( 53 ). In rangelands, dead locoweed stalks are toxic, demonstrating that swainsonine can persist in dead tissue and continue to be a hazard to grazing livestock ( 54 ). In M. anisopliae cultures, swainsonine was stable up to 100°C over a pH range of 2–10 ( 30 ).…”

Section: Alkaloid Production and Physiological Effectsmentioning

confidence: 99%

Blackpatch of Clover, Cause of Slobbers Syndrome: A Review of the Disease and the Pathogen, Rhizoctonia leguminicola

Kagan

2016

Front. Vet. Sci.

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Rhizoctonia leguminicola Gough and Elliott is a widely used name for the causal agent of blackpatch disease of red clover (Trifolium pratense L.). This fungal pathogen produces alkaloids (slaframine and swainsonine) that affect grazing mammals. Slaframine causes livestock to salivate profusely, and swainsonine causes neurological problems. Although the blackpatch fungus was classified as a Rhizoctonia species (phylum Basidiomycota), morphological studies have indicated that it is in the phylum Ascomycota, and sequencing data have indicated that it may be a new genus of ascomycete. The effects of the alkaloids on grazing mammals and their biosynthetic pathways have been extensively studied. In contrast, few studies have been done on management of the disease, which requires a greater understanding of the pathogen. Methods of disease management have included seed treatments and fungicides, but these have not been investigated since the 1950s. Searches for resistant cultivars have been limited. This review summarizes the biological effects and biosynthetic precursors of slaframine and swainsonine. Emphasis is placed on current knowledge about the epidemiology of blackpatch disease and the ecology and taxonomy of the pathogen. Possibilities for future research and disease management efforts are suggested.

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“…The main toxic ingredient in locoweeds is swainsonine (SW) [ 10 ], an indolizidine alkaloid whose chemical name is 1, 2, 8- trihydroxy-indolizidine alkaloid (Figure 1 ). SW was first isolated from Swainsona canescen by Colegate et al [ 11 ]; since then, large amounts of researches has focused on the bioactivity of SW, finding that the structure of SW is similar to the mannose cation formed by the hydrolysis of mannosidase.…”

Section: Introductionmentioning

confidence: 99%

The study of the Oxytropis kansuensis-induced apoptotic pathway in the cerebrum of SD rats

Zhang

Wang

et al. 2013

BMC Vet Res

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BackgroundLocoweeds cause significant livestock poisoning and economic loss all over the world. Animals can develop locoism, a chronic neurological disease, after grazing on locoweeds. Oxytropis kansuensis is a variety of locoweed that contains swainsonine as its main toxic ingredient. The purpose of this study was to investigate the apoptotic pathway induced in the cerebrum by swainsonine.ResultsTwenty-four Sprague-Dawley rats were randomly divided into four groups (experimental groups I, II, III and a control group) and 6 SD rats of each group were feed in 3 cages separately. Rats were penned as groups and fed with feeds containing 15% (SW content 0.03‰), 30% (SW content 0.06‰), or 45% (SW content 0.09‰) O. kansuensis for experimental groups I, II, and III, respectively, or complete feed in the case of the control group. One hundred and nineteen days after poisoning, and all rats showed neurological disorders at different degrees, which were considered to be successful established a chronic poisoning model of O. kansuensis. rats were sacrificed and the expression of Fas, FasL, Bcl-2, Bax as well as cleaved caspase-3, -8 and -9 proteins in brain tissues were detected by Western blot. The results showed that SW treatment up-regulated Fas and Fas ligand (FasL) (P < 0.05), and that there was an increase in Bax and a decrease in Bcl-2 protein (P < 0.01). Moreover, SW treatment significantly increases the activation of caspase-3, 8 and -9, the key effectors in apoptosis pathway (P < 0.01).ConclusionOur data suggest that SW induces apoptosis in cells of the brain through death receptor and mitochondria-mediated, caspase-dependent apoptotic pathways in the brain tissue of SD rats.

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Solutions to Locoweed Poisoning in New Mexico and the Western United States

Cited by 11 publications

References 8 publications

Locoweed dose responses to nitrogen: Positive for biomass and primary physiology, but inconsistent for an alkaloid

Locoweed dose responses to nitrogen: Positive for biomass and primary physiology, but inconsistent for an alkaloid

Blackpatch of Clover, Cause of Slobbers Syndrome: A Review of the Disease and the Pathogen, Rhizoctonia leguminicola

The study of the Oxytropis kansuensis-induced apoptotic pathway in the cerebrum of SD rats

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