1. Aconitum columbianum: Wolfbane, Monkshood
A. columbianum growing near a creek in the Pike's Peak region
General Information:
Wolfsbane is widely distributed across Colorado, putting out purple, hood-shaped flowers and preferring wet locations(1). The "petals" visible in the photo are actually the flowers sepals, which curve over to form the characteristic hood shape. If its deeply incised palmate leaf shape reminds you of the ubiquitous larkspur or perhaps your garden delphiniums, it because all three species are in the butter cup family (ranunculaceae).
Toxicity:
Monkshood is an impressively toxic plant. It was potent enough to be used by settlers in the American west to poison bait for wolf traps (hence the name Wolfbane)(2). The main toxic substance is aconitine, which has an lethal dose [LD(50)] in mice of 1.8mg/kg given orally(3). Cyanide, by comparison, kills most mammals at 1.3mg/kg(4), which means that this innocuous-looking flower by the side of the trail contains a poison almost as potent as the famous killer used in innumerable murder mysteries and intrigues.
Aconitine targets the nervous system by forcing open sodium channels on neuronal axons, disabling neurons by forcing them to fire continuously(5). Symptoms of poisoning can include nausea, vomiting, numbness and palsy of the extremities, and arrhythmia(6). The latter is what typically kills people, with ventricular fibrillation resulting in a heart attack. The numbness some people experience is due to the sodium blocking of sensory nerves, which is probably why related monkshood species have been used in Chinese medicine as analgesics(7). Not surprisingly, the use of such a potent plant in herbal medicine has also resulted in a number of accidental poisonings(7).
Finally, monkshood can have an effect on bees. I had always wondered whether plants that produce poison in all of their parts affect their pollinators, and it turns out that they do! A study(8) of bees who had been exposed to aconitine and related toxins found that while the bees did not appear to be harmed, their behaviors changed, suggesting that the toxins were making the bees a little loopy.
2. Conium maculatum, Poison Hemlock
C. maculatum stalk and flowers growing on North Table Mountain near Golden, CO
General Information
This pretty plant is dangerous not only for its poison (see below) but its sheer availability. I have encountered it in practically every place I have been in Colorado across a wide variety of environments. The common theme seems to be that it needs water, and it establishes itself in dense thickets along creeks and in ditches. It is not native to Colorado, and is considered a noxious weed(9).
Poison hemlock can be recognized by its large heads of white flowers arranged in umbels, its twice pinnately compound (bipinnate) leaves, and the red-purple dots on its stem (presumably the "macules" referenced in the scientific name, but I have not been able to find any sources to verify this).
Poison hemlock also has the misfortune to look like a number of crisp edibles such as celery and lovage, as all three plants reside in the carrot family (Apiaceae), which tends to have hollow stems, fern-like leaves, and umbel-shaped flowers. Any would-be foragers should learn to identify this plant before attempting to harvest anything in the carrot family from the wild. Unfortunately, I have not been able to locate a definitive guide to the differences between poison hemlock and its delectable look-alikes. All I can say is that the red spots are a good field mark. If you aren't 100% sure of the plant you are holding, don't put it in your mouth! I find this song to be helpful in dealing with foraging for anything in Apiaceae (replace "alive" with "unidentified").
Toxicity
Poison hemlock is not as potent as Monkshood, with the LD(50) of the active chemical, coniine, at 100mg/kg(10) in mice. This is somewhat deceptive, however, as a lethal dose can be gotten from as few as six to eight leaves (presumably leaflets, as whole leaves would constitute a colossal salad)(11). After eating said leaves, a person would initially experience abdominal pain, hypertension, and tremors, which would then be followed by hypotension, dyspnea, bradycardia, and ultimately coma and respiratory failure(12).
The symptoms of numbness and hypotension are consistent with the description of the death of C. maculatum's most famous victim, Socrates(13). Plato writes that
"the man who gave him the poison now and then looked at his feet and legs; and after a while he pressed his foot hard, and asked him if he could feel; and he said, No; and then his leg, and so upwards and upwards, and showed us that he was cold and stiff.(13)"
The treatment for coniine poisoning is supportive, involving putting the affected person on a ventilator until their symptoms resolve (14). This would have been of little help to Socrates were it developed as he was being executed anyhow, but even very vulnerable patients such as very young children have been successfully saved using a ventilator.
3. Anticlea elegans, The Elegant Death Camas
A. elegans growing at about 11,000 ft just above treeline on Pike's Peak.
General Information
The elegant death camas resides in the lily family and essentially does what it says on the tin: the slender, lily-like leaves and delicate six-petaled flowers are graceful; and the entire plant holds an incredibly potent toxin. The green dots or splotches at the base of each petal are a useful field mark, and the leaves are a more grayish or muted green(15). It favors the higher altitudes of the montane zone and above(16), and in my experience it prefers wetter areas.
It has the dubious distinction of having killed many settlers of the West who confused its bulbs for edible lily or onion(15). A very similar species, Toxicoscordion venosum, can also be found throughout the state but growing in dryer areas and lower altitudes.
Toxicity
Information on the specifics of death camas poisoning is sparse. The toxic agent, zygacine, has an LD(50) in mice of about 130mg/kg of body weight(17). It appears to cause harm by somehow affecting sodium channels(18), although the specific mechanism of this harm and its symptoms are very hard to find any information on. Some sites offer lists of symptoms, but do not seem to site any references. The little literature that is available appears to be more interested in plant's accumulation of toxins as it relates to the local environment and the likelihood that livestock will be affected by those toxins.
This is probably a good sign, since the absence of even a single case report seems to indicate that virtually nobody has been poisoned by this plant in recent memory. The plant's low profile and small size probably help to keep it out of people's mouths.
4. Astragalus and Oxytropis ssp., Locoweeds
Astragalus bisulcatus var. haydenianus growing on North Table Mountain (left) and an unidentified locoweed growing near the Devil's Backbone by Longmont (right)
General Information
The plants that are generically termed "locoweeds" actually cover two genera and a bewildering number of very similar looking species. In the Rocky Mountain Region, there are 156 species of locoweeds in the genus Astragalus alone(19), with an unknown additional number representing Oxytropis. As a rule, these members of the pea family (Fabaceae) present clusters or spikes of purple, pink, or white bilaterally symmetrical flowers, pinnate leaves, and bean-like seed pods. With a few exceptions such as A. bisulcatus above, most of these species are frustratingly similar-looking, and can often only be identified by looking at the seedpods. I do not have the patience to hash through the vagaries of locoweed seed pods, so I have satisfied myself that if I see a plant with the above field marks, I am looking at a locoweed of some sort, although I have no idea which locoweed. They are omnipresent in Colorado and I have seen some variety of these plants growing at all altitudes.
Toxicity
As locoweeds are not a single species, so they do not have just one poison. However across both genera three types of toxicity occur.
Many species produce aliphatic nitrotoxins(20), such as miserotoxin(21). I very much lack the chemistry clout to actually understand or explain what it means, but suffice to say that miserotoxin and its relatives are relatively benign (LD/50=2.5g/kg body weight) poisons which can metabolize into more dangerous substances in the gut(21). Miserotoxin hydrolizes into a substance which is at least 10 times more deadly in the gut, but its overall levels of gut hydrolization are low enough that it poses little threat except in very high doses(21). In Astragalus, concentrations of this toxin high enough to cause harm to livestock (and presumably humans) are relatively rare(22). In the event that a high enough dosage is reached to be dangerous, nitrotoxins disrupt central nervous system functioning and cause paralysis and/or death(20)
Another variety of toxicity from Astragalus and Oxitropis is via concentrating toxic levels of the element selenium(20). This causes a twofold problem from the perspective of livestock: the plants themselves have toxic levels of selenium in them, while also manufacturing that selenium into a more bio-available form which then passes into neighboring plants as successive generations of locoweeds live and die(20). Grazing may be of little concern for humans, but selenium poisoning from directly consuming locoweed may cause acute selenium poisoning. The symptoms of poisoning by selenium include diarrhea, joint pain, hair loss, nail brittleness, and nausea(23). Finding information on an LD50 in this case wasn't practical, since different selenium-based compounds have very different toxicities, and since a variety of plants may create a variety of compounds. It is, however, possible to die of selenium poisoning (24), although I cannot find any references in the literature to anyone dying of selenium poisoning from locoweed.
The final poison found in various locoweeds is also the most dangerous: a compound called swainsonine(20). Swainsonine poisoning in humans is, as far as I can find, unknown. A blog here and another one here both discuss how one of the few possible reported events of swainsonine poison likely was not. I can't vouch for these blogs or their content, but this is as close as I can find to a reference on what happens when swainsonine meets humans. In animals it causes severe neurological damage that may be irreparable(20) by damaging or destroying dopaminergic neurons(25). This means that animals who are affected tend to either die of a lack of appetite or misadventure, while humans would likely suffer permanent neurological effects along similar lines.
This concludes this post about poisonous plants in Colorado. I hope that those of you who took the time to read through it found it as interesting as I found writing it. I also want to mention that on several of my searches doing research for this post, I found questions in forums about using some of these plants for herbal or homeopathic medicine. Please, taking into account the numerous and unpleasant things that happen to people who consume these plants, only get your medicine from a licensed medical professional and don't ever eat anything you can't identify 100%! Thanks for reading!
References
- Schneider, A. (N.D.) Aconitum columbianum. Retrieved from http://www.swcoloradowildflowers.com/Blue%20Purple%20Enlarged%20Photo%20Pages/aconitum%20columbianum.htm
- Mammoser, D., & Tekiela, S. (2007). Wildflowers of Colorado. Cambridge, Minnesota: Adventure Publications, Inc.
- Fujita, Y., Terui, K., Fujita, M., Kakizaki, A., Sato, N., Oikawa, K., & ... Endo, S. (2007). Five cases of aconite poisoning: toxicokinetics of aconitines. Journal Of Analytical Toxicology, 31(3), 132-137.
- Hebert, C. D. (1993) NTP Technical Report on Toxicity Studies of Sodium Cyanide (CAS No. 143-33-9) Administered in Drinking Water to F344/N Rats and B6C3F1 Mice. Retrieved from https://ntp.niehs.nih.gov/ntp/htdocs/st_rpts/tox037.pdf
- Du, Y., Nomura, Y., Satar, G., Hu, Z., Nauen, R., He, S. Y., & ... Dong, K. (2013). Molecular evidence for dual pyrethroid-receptor sites on a mosquito sodium channel. Proceedings Of The National Academy Of Sciences Of The United States Of America,110(29), 11785-11790. doi:10.1073/pnas.1305118110
- Fujita, Y., Terui, K., Fujita, M., Kakizaki, A., Sato, N., Oikawa, K., & ... Endo, S. (2007). Five cases of aconite poisoning: toxicokinetics of aconitines. Journal Of Analytical Toxicology, 31(3), 132-137.
- Chan, T. K. (2015). Incidence and Causes of Aconitum Alkaloid Poisoning in Hong Kong from 1989 to 2010.
- Oliver, C. J., Softley, S., Williamson, S. M., Stevenson, P. C., & Wright, G. A. (2015). Pyrethroids and Nectar Toxins Have Subtle Effects on the Motor Function, Grooming and Wing Fanning Behaviour of Honeybees (Apis mellifera). Plos One, 10(8), e0133733. doi:10.1371/journal.pone.0133733
- Marx, E. (N.D.) Conium Maculatum (Poison Hemlock). Retrieved from http://www.easterncoloradowildflowers.com/Conium%20maculatum.htm
- National Institutes of Health [NIH](N.D.) Coniine. Retreived from http://hazmap.nlm.nih.gov/category-details?id=4496&table=copytblagents
- IPCS [International Programme on Chemical Safety].(N.D.) Conium Maculatum. Retrieved from http://www.inchem.org/documents/pims/plant/conium.htm#PartTitle:2. Summary
- Schep, L. J., Slaughter, R. J., & Beasley, D. G. (2009). Nicotinic plant poisoning. Clinical Toxicology (Philadelphia, Pa.), 47(8), 771-781. doi:10.1080/15563650903252186
- Plato. (trans. 1909-1914). Phaedo Benjamin Jowett (Trans). New York: P.F. Collier & Son.
- West, P. L., Horowitz, B. Z., Montanaro, M. T., & Lindsay, J. N. (2009). Poison hemlock-induced respiratory failure in a toddler.Pediatric Emergency Care, 25(11), 761-763. doi:10.1097/PEC.0b013e3181bec925
- National Park Service (N.D.) Mountain Death Camas. Retrieved from http://www.nps.gov/brca/learn/nature/mountaindeathcamas.htm
- Schneider, A. (N.D.) Anticlea elegans. Retrieved from http://www.swcoloradowildflowers.com/White%20Enlarged%20Photo%20Pages/anticlea%20and%20toxicoscordion.htm
- Welch, K. D., Panter, K. E., Gardner, D. R., Stegelmeier, B. L., Green, B. T., Pfister, J. A., & Cook, D. (2011). The acute toxicity of the death camas (Zigadenus species) alkaloid zygacine in mice, including the effect of methyllycaconitine coadministration on zygacine toxicity. Journal Of Animal Science, 89(5), 1650-1657. doi:10.2527/jas.2010-3444
- Codding, P., W. (1983). Stuctural studies of sodium channel neuro toxins 2. Crystal structure and absolute configuration of veratridine per chlorate. Journal Of The American Chemical Society, 105(10), 3172-3176.
- Cronquist, A. (1972). Intermountain Flora. New York, New York: Hafner Publishing Company
- Bioscience Dept. of University of Arizona (N.D.) Poisoning by "Locoweeds." Retreived from: http://loco.biosci.arizona.edu/astragalus/locoweedspp.html
- Majak, W., Pass, M. A., & Madryga, F. J. (1983). Toxicity of miserotoxin and its aglycone (3-nitropropanol) to rats. Toxicology Letters,19(1-2), 171-178.
- Williams, M. C., & Barneby, R.C. (1977). The occurrence of nitro-toxins in North American Astragalus (Fabaceae). Brittonia, 29, 310-326.
- MacFarquhar, J. K., Broussard, D. L., Melstrom, P., Hutchinson, R., Wolkin, A., Martin, C., & ... Jones, T. F. (2010). Acute selenium toxicity associated with a dietary supplement. Archives Of Internal Medicine, 170(3), 256-261. doi:10.1001/archinternmed.2009.495
- Nuttall, K. L. (2006). Evaluating selenium poisoning. Annals Of Clinical And Laboratory Science, 36(4), 409-420.
- Li, Q., Wang, Y., Moldzio, R., Lin, W., & Rausch, W. D. (2012). Swainsonine as a lysosomal toxin affects dopaminergic neurons.Journal Of Neural Transmission, 119(12), 1483-1490. doi:10.1007/s00702-012-0827-6
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ReplyDeleteI'm skimming through your blog. It seems that you haven't been able to continue it for quite a while. That's a shame, because you've done great work here. I've just discovered my passion for Colorado plants and you've answered so many questions and jump started my curiosity in areas I haven't considered. Thank you for your work.
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