Question:
Is Larkspur poisonous to alpacas? If so, what are the symptoms?
Thanks so much!!
Answer:
Although I do not have any information specific to toxicity in alpacas, I am forwarding a lengthy discussion of larkspur toxicity in other ruminating species. It is safe to say that Larkspur, being toxic to cattle and sheep, would also pose a risk to alpacas.
Before I wax on about Larkspur, I should share with you Dr. Anderson's simple version of his philosophy on toxic plants. "If it is ornamental it is dangerous."
The short version of the story is this... Larkspur species vary in their toxicity levels to animals. When an animal consumes a large enough quantity, that quantity depends on the species of the plant and the animal, the time of year, the climatic conditions, and the stage of growth of the plants, toxicity occurs. Generally the symptoms are severe weakness, due to the neuromuscular blocking activity of the alkaloid toxins produced by the plants. You would see your animals showing signs of weakness, like base wide stance, staggering, apparent stiffness as they try to control their muscles, then inability to rise. Other symptoms include bloat, aspiration pneumonia, and within a few hours of high doses of the toxin, sudden death. Read more about it below if you are interested.
Please see below my signature lines for more specific information regarding Larkspur toxicity. Photographs not attached.
Tracy J Miesner, DVM
ICI Associate Director
The following information is from The Guide to Plant Poisonings in Animals in
Chapter 1
Larkspur Poisoning
Larkspurs in the genus Delphinium cause more fatal poisoning of cattle in the western United States than any other native plant species.150,151 As early as 1897, livestock losses to larkspur were reported in Montana and even now larkspur poisoning remains a serious threat to cattle with access to the plants.152-154 Livestock losses to larkspur in the United States have been estimated to exceed $234 million annually, making larkspurs second only to the locoweeds in terms of economic losses to the livestock industry.155 In some areas of the intermountain states, cattle losses to larkspur poisoning average 2 to 5 percent per year and may be as high as 10 percent in some year.156,157
Larkspur, Poison Weed
Delphinium spp.
Ranunculaceae (Buttercup family)
Habitat
There are at least 60 species of larkspur found throughout
Larkspur poisoning of cattle has been attributed to relatively few species, including D. barbeyi, D. bicolor, D. geyeri, D. glaucescens, D. glaucum, D. nuttallianum, D. occidentale, D. tricorne, and D. virescens.158 It is probably wise, however, to assume that all larkspurs are potentially poisonous, including those cultivated as ornamentals. Larkspurs are often grouped for descriptive convenience into tall and low varieties according to their growth habit. Tall larkspurs (D. barbeyi and D. occidentale, D. glaucescens) grow in deep, moist, and highly organic soils at high altitudes and often reach 7 feet in height.151,159 The tall larkspurs generally grow in montane forests, especially where snow drifts occur perennially. The plants emerge as the snows recede and once established form very long-lived dense stands. Low larkspurs (D. nuttallianum, D. nelsoni, and D. virescens) grow at lower elevations in drier rangeland, seldom growing more than 2 to 3 feet (0.5 to 1 meter) tall; they die in early summer as the soil dries out. Foothills larkspur (D. geyeri) is intermediate in its growth habit, attaining a height of 3 to 4 feet (1 meter) when in flower.
Description
Larkspurs are erect herbs arising from a single or clustered, often woody root stock. Indigenous species are perennials, whereas introduced species are annuals. Leaves clustered at the base of the plant are simple, alternate, petioled, palmately lobed into three to five divisions, and in some species further deeply divided. Stems are hollow. The showy flowers, generally blue to purple in color, but ranging from white to occasionally red, are produced on terminal erect racemes. Flowers have five sepals and four petals; the upper sepal and pair of petals are elongated to form a characteristic spur that protrudes backward. Seed pods are erect, three to five-celled, splitting down the inside ridge to release numerous dark brown to black seeds.
Toxicity
Young rapidly growing larkspur plants are most toxic, with the highest concentration of alkaloids in the leaves. Cattle, however, appear to not eat tall larkspur until the plants initiate and elongate flower stalks.160,161 At this stage, the alkaloid content of the plants is generally declining, although the seed pods contain high levels of alkaloids.161,162 Tall larkspur consumption in cattle may range from virtually nothing in the preflower stage to as much as 30 percent of the animal’s diet when the plant is in the flowering stage. There is a "toxic window" of time when cattle find tall larkspur increasingly palatable, and the plants contain significant total toxic alkaloids.160,161 This window of time occurs as the tall larkspurs begin to elongate their flower stalks and until the flowers have been replaced with seed pods. Feeding studies with cattle using both fresh and dried tall larkspur showed no correlation between alkaloid concentration and palatability.160 Sheep, however, will avoid eating the plants in the preflower stage when the alkaloid content is highest, but will readily eat the flower stalks and buds as they mature. In drought years the consumption of tall larkspur by cattle almost entirely ceases, and mortality from larkspur poisoning is lowest during droughts.160,162 Another as yet unexplained phenomenon that contributes to tall larkspur poisoning is the glutinous consumption of the larkspur by cattle in a short period after a summer rain storm.163
The toxicity attributed to the tall larkspur species cannot be assumed to hold true for the low or foothills larkspur species. Unlike the tall larkspurs, the foothills larkspur (D. geyeri) is readily eaten by cattle in the early spring before it flowers, causing significant numbers of deaths in some years. By the time it flowers, the foothills larkspur is not consumed in any quantity presumably because cattle generally have plenty of other forage available by this stage.
Cattle are most susceptible to larkspur poisoning, but sheep and horses may also be poisoned if they eat sufficient quantity of the plants over a short period of time and are concurrently subjected to stress. Sheep are be able to tolerate about four times the amount of larkspur alkaloids that would be fatal to cattle.151 Establishing the toxic dose of larkspur for cattle is difficult because the toxicity varies with the species, season, stage of growth, amount ingested, and duration over which the plant is eaten.164 It has been estimated that cattle must eat 0.7 percent of their body weight of green tall larkspur in an hour to be fatally poisoned.151 If one assumes a 1200-lb cow eats about 25 lb of forage a day, it would have to eat about 6 lb of green tall larkspur containing 5 mg/g of total toxic alkaloid to be fatally poisoned. This is about 25 percent of the cow’s total daily feed intake.160 The LD50 of total toxic alkaloid for tall larkspur has been shown experimentally to be between 25 and 40 mg/kg body weight.164
Larkspurs contain many toxic and nontoxic diterpenoid alkaloids, 40 of which have been identified in the nine larkspur species most frequently associated with poisoning in cattle.158,165,166 The alkaloids may vary in quantity depending on the species and stage of growth.150,167 Even within a small area, certain stands of larkspur appear to be more toxic than others. These "hot spots" are well recognized by ranchers who frequently anticipate losses when cattle are herded in these areas. The alkaloid content of tall larkspurs also appears to be consistently higher in plants growing in full sun as opposed to those growing in the shade. Studies with D. barbeyi have shown it to be the most toxic of the larkspurs.151,159,162 As little as 17 g/kg body weight of the green plant of D. barbeyi is lethal to cattle.162,168 A rapid electrospray mass spectrometry method has been developed that may prove useful in determining the toxic alkaloid content of larkspur species at different growth stages that will facilitate the safe management of larkspur rangeland for cattle grazing.169
To date the most toxic of the alkaloids isolated from tall larkspurs are 14-deactylnudicauline and methyllycaconitine (MLA).158,170,171 Although the former alkaloid is more toxic, greater than 15 times as much MLA is produced in the plant making it the most important toxic component of the tall larkspurs.161 The foothills larkspur (D. geyeri) and the low larkspur (D. nuttallianum) contain the highly toxic alkaloid nudicauline.172 The toxicity of the different larkspur species is, however, most likely due to the combined effects of the alkaloids present in the plants.
The alkaloids act principally at the neuromuscular junction (postsynaptic nicotinic and cho-linergic receptors) causing a curare-like blockade with muscle weakness and paralysis.167,173 The alkaloids reversibly bind to and block the action of nicotinic acetylcholine receptors at the neuromuscular junction thus competing with acetylcholine for the receptors. This effect is sim-ilar to that of nicotine and the snake toxin bungertoxin.174 Bin-ding affinity of the larkspur alkaloids to the cholinergic receptors varies with the tissue and among species.175 Cholinergic receptors in cattle are possibly more susceptible to the alkaloids than are those of sheep, offering an explanation for the refractoriness of sheep to larkspur toxicity.
Clinical Signs
Sudden death in cattle is often the first indication of larkspur poisoning. Cattle frequently die within 3 to 4 hours of consuming a lethal dose of larkspur. Poisoned cattle initially show uneasiness, increased excitability, and muscle weakness that causes stiffness, staggering, and a base-wide stance.176 The front legs may be affected first causing the animal to kneel before finally becoming recumbent. Muscle weakness may cause sudden collapse especially if the animal is stressed. Frequent attempts to stand are uncoordinated and result in rapid exhaustion. Muscle twitching, abdominal pain, regurgitation, and constipation are common clinical findings. Similar signs of poisoning occur in horses, sheep, and goats that have eaten larkspur except that vomiting is uncommon and fewer deaths are likely.
Bloat is common in larkspur poisoning because of the neuromuscular blocking effect of the alkaloids impairing eructation and the fact that the green larkspur is highly fermentable by rumen microorganisms, thereby increasing the rate of gas production in the rumen. The high protein content of larkspur may also facilitate the production of a stable foam in the rumen that enhances the severity of the bloat. Inhalation of regurgitated rumen contents in the recumbent animal will lead to fatal pneumonia. Cattle appear to be able to repeatedly eat a toxic dose of larkspur without marked clinical signs of poisoning provided larkspur consumption is significantly decreased for 2 to 4 day intervals.177 This appears sufficient time for metabolism and clearance of the larkspur alkaloids to occur and reduce the cumulative effect of daily larkspur consumption.
No specific postmortem findings are seen in animals that have died of larkspur poisoning. Bloat, inhalation of rumen contents, venous congestion, and mild gastrointestinal inflammation are common secondary findings. Diagnosis of larkspur poisoning is made by searching for parts of the plants in the animal's rumen and by finding evidence of the animal having grazed larkspur. It is also possible to detect microscopically the plant cell structure of Delphinium spp. in the feces or rumen contents that will indicate the animal had consumed the plant in the recent past.178
Treatment
Ever since larkspurs were known to be poisonous to cattle, a variety of treatments have been advocated. Treatment myths abound in the early literature and have involved the use of a variety of compounds including atropine, potassium permanganate, turpentine, bacon fat, chewing tobacco, whiskey, and bleeding the animal from the tail vein.153,179 Most of these early remedies have little scientific basis and have not been proven to be effective. The use of turpentine and bacon fat given orally may have helped reduce the severity of the bloat that develops with larkspur poisoning. Apparent successes with unique remedies have not considered the variability in toxicity of the larkspurs under different growing conditions, time of year, and quantity of total toxic alkaloid consumed. If less than a lethal dose of larkspur alkaloids is consumed, an animal will likely recover despite the treatment, unless severe bloat and regurgitation of rumen contents occurs while the animal is recumbent.
Anticholinesterase drugs that allow the accumulation of acetylcholine at the neuromuscular junction by inhibiting cholinesterase are the most appropriate for the reversal of some of the effects of larkspur alkaloids. Physostigmine (0.08 mg/kg) has been effective if given intravenously to cattle about to collapse from larkspur poisoning.177 Cattle in sternal or lateral recumbency from tall larkspur poisoning recover after treatment with physostigmine (0.4-0.8 mg/kg body weight) given intravenously.180 Treatment should be repeated as needed over several hours until clinical signs have abated. Neostigmine (0.04 mg/kg) appears to be as effective in reversing some of the effects of the larkspur alkaloids but is possibly not as effective as physostigmine for treating larkspur poisoning. A formulation that has been beneficial if administered early in the course of poisoning has been the injectable mixture of physostigmine salicylate, pilocarpine hydrochloride, and strychnine sulfate.156 Some organophosphate compounds with an anticholinesterase effect may also have potential benefit in the treatment of larkspur poisoning as they will decrease the breakdown of acetylcholine.181 Because none of these drugs are approved for use in food-producing animals they must be administered under the supervision of a veterinarian in accordance with the regulations pertaining to the use of extra-label drugs.
An early diagnosis of larkspur poisoning is essential if treatment is to be successful. Stress and excitement of the affected animal should be avoided because it will exacerbate respiratory distress and hasten death. It is often better to quietly herd affected range cattle away from the area where larkspur is being grazed and not attempt to catch and restrain an animal to treat it. Affected animals should be kept sternal if they become recumbent. Bloat should be relieved by passing a stomach tube to remove excess rumen gas and reduce respiratory difficulty when possible. Trocarization of the rumen to relieve the bloat may be more effective than trying to pass a stomach tube because it is less stressful to the animal.
Acute larkspur poisoning in a range cow can resemble grass tetany (hypomagnesemia) and milk fever (hypocalcemia) especially when the affected animal is recumbent, and laboratory facilities are not readily available to differentiate these conditions. Magnesium solutions for the treatment of grass tetany are contraindicated in suspected larkspur poisoning as magnesium will exacerbate the effect of the alkaloids at the neuromuscular junction. Calcium gluconate in contrast will have a beneficial effect at the neuromuscular junction. However, calcium solutions should be administered very cautiously because of the effect of calcium on the heart.
Prevention of Larkspur Poisoning
Intuitively, cattle should be kept off of ranges containing large quantities of larkspur. However, this would eliminate vast areas of rangeland for livestock grazing, making such a management option uneconomical. By knowing the growth habits of tall larkspur, the times when it is most toxic, and when cattle like to eat the plant, it is possible to manage cattle so that they are kept away from the larkspur during a "toxic window" when chances for poisoning are highest.161 Prior to this "toxic window," cattle may be grazed on the larkspur range even though tall larkspur is most toxic at this stage, because cattle find the plant unpalatable. Similarly, after the larkspur is past flowering it is relatively less toxic and more palatable. Consequently, knowing the toxicity, palatability and growth stage of tall larkspur, it is possible to make effective use of rangeland for livestock production while minimizing the risk for tall larkspur poisoning.182 This management strategy is only valid if there is a diversity of other forages available, and the cattle are not forced into a situation where they must eat larkspur because they are without adequate food. If early season grazing of tall larkspur is used, very close attention must be paid to the eating patterns of the cattle. As soon as the tall larkspur starts to elongate its flower stalks and cattle start to eat the flower shoots, they should be moved off of the range. Early season grazing is relevant only to tall larkspur and should not be attempted with the foothills or low larkspurs that seem to be quite palatable in the early spring when they can be highly toxic.
The fact that sheep can eat larkspur without problem makes them useful biological controls for tall larkspur. Sheep if herded into larkspur stands will eat and trample the plants thereby reducing the availability of larkspur to cattle that follow the sheep.183,184 It is doubtful, however, if sheep effectively reduce the potential for larkspur poisoning in cattle unless large numbers of sheep are actively herded into areas where the plants are abundant.
Providing adequate calcium, phosphorus, and mineralized salts for cattle has been recommended as a preventive measure for larkspur poisoning. However, mineral supplementation of cattle grazing rangeland infested with tall larkspur had no effect in reducing the amount of larkspur consumed.185 A balanced mineral supplement should always be provided to cattle to prevent mineral deficiencies and should not be relied on as a preventive measure for larkspur poisoning. It has been postulated that cattle may be deficient in minerals in late winter and early spring and may crave plants like foothills larkspur that are high in calcium.
Aversion to Larkspur
Cattle unfortunately do not have a natural aversion to larkspur, but they can be trained under certain management conditions to avoid eating tall larkspur. Cattle can form a strong aversion to eating larkspur if they are given intraruminal infusions of larkspur extract with lithium chloride.186-188 Lithium is a potent irritant and emetic that induces abdominal pain that the animal associates with the last thing it was eating or was fed.
Once cattle have developed an aversion to larkspur they continue to have the aversion from year to year provided they are not exposed to cattle that are eating larkspur.187,189,191 Socializing with cattle that are not aversed to larkspur leads to the aversed animals relearning to eat larkspur.189 Training cattle to avoid eating larkspur can be accomplished by harvesting and feeding fresh larkspur to cattle. As soon as an animal has started eating the larkspur it is restrained and given lithium chloride (100 mg/kg body weight) via stomach tube. The subsequent abdominal discomfort is associated by the animal with the last thing it ate, namely the larkspur.
Induced aversion to eating larkspur has potential beneficial implications for some ranch enterprises. In closed herd situations where all cattle can be treated with lithium and not be exposed to non-averted cattle, larkspur aversion can be maintained in the entire herd for many years at minimal cost.191,192
Control of Larkspur
Although it is possible to control larkspurs with herbicides, it is economically prohibitive to do so on a wide scale.155,193-195 However, spraying of larkspur hot-spots can be effective in reducing cattle losses. The tall larkspurs can be controlled using a variety of currently available herbicides including picloram (Tordon), metsulfuron (Escort), glyphosate (Roundup).196,197 The most effective herbicide for all growth stages of larkspur is picloram. All are effective because they kill the root and not just the vegetative portion of the plant as is the case with 2,4-D.196 Surfactants enhance the efficacy of herbicides because they improve the absorption of the chemicals through the waxy surface of the leaves. The most effective time to apply herbicides is in the early vegetative or leaf stage before the flower stalks begin to form.196 A second application of the herbicide will eliminate any plants that survive the first application. Newer application methods such as vehicle mounted carpeted rollers apply the herbicides to tall larkspur without affecting lower growing useful forbs and use less chemical than conventional spraying methods. It should be noted that herbicides increase the alkaloid content of larkspur and therefore the plants should not be grazed after spraying until the plants have completely died off.196 Herbicidal control of tall larkspur has additional benefit in that significant increases in the growth of grasses for up to 5 years after spraying increases the carrying capacity of the range.197
Research is currently underway to investigate the effectiveness of insect biologic controls to control tall larkspurs. The larkspur myrid (Hopplomachus affiguratus), which sucks on the plants reducing plant vitality, has shown potential as an insect control.198 Plants infected by the myrids become stunted, fail to produce flowers and seeds, and appear to be unpalatable to cattle. The success of this insect as a biologic control will depend on whether or not it can sustain itself in large numbers once transplanted to new stands of larkspur.
References
Larkspur (Delphinium spp.)
150. Aiyar VN, Benn MH, Hanna T, et al.: The principle toxin of Delphinium brownie Rydb, and its mode of action. Experientia 1979, 35:1367–1368.
151. Cronin EH, Nielsen DB. Tall larkspur and cattle on high mountain ranges. In Effects of Poisonous Plants on Livestock. Keeler RF, Van Kampen KR, James LF, Eds.
152. Wilcox EV: Larkspur poisoning of sheep.
153. Chestnut VK, Wilcox EV: The stock-poisoning plants of
154. Glover GH: Larkspur and other poisonous plants. Agricultural Experimental Station
155. Nielsen DB, Rimbey NR, James LF: Economic considerations of poisonous plants on livestock. In The Ecology and Economic Impact of Poisonous Plants on Livestock Production. James LF, Ralphs MH, Nielsen DB, Eds. Boulder, CO: Westview Press; 1988:5–16.
156. Marsh CD,
157. Kingsbury JM: Poisonous Plants of the
158. Olsen JD, Manners GD: Toxicology of diterpenoid alkaloids in rangeland larkspur (Delphinium spp.). In Toxicants of Plant Origin. Volume 1. Alkaloids. Cheeke PR, Ed.
159. Olsen JD: Tall larkspur poisoning in cattle and sheep. J Am Vet Med Assoc 1978,173:762–765.
160. Pfister JA, Ralphs MH, Manners GD, et al.: Relationships between tall larkspur toxicity and consumption by cattle. Larkspur Symposium Proceedings.
161. Pfister JA, Manners GD, Ralphs MH, et al.: Effects of phenology, site, and rumen fill on tall larkspur consumption by cattle. J Range Manage 1988, 41:509–514.
162. Pfister JA, Manners GD, Gardner GD, Ralphs MH: Toxic alkaloid levels in tall larkspur (Delphinium barbeyi) in western
163. Ralphs MH, Jensen DT, Pfister JA, et al.: Storms influence cattle to graze larkspur: an observation. J Range Manage 1994, 47:275–278.
164. Pfister JA, Panter KE, Manners GD: Effective dose in cattle of toxic alkaloids from tall larkspur (Delphinium barbeyi). Vet Hum Toxicol 1994, 36:10–11.
165. Olsen JD, Manners GD, Pelletier SW: Poisonous properties of larkspur (Delphinium spp.) Collectanea Botanica (
166. Grina JA,
167. Pfister JA, Ralphs MA, Manners GD: Cattle grazing tall larkspur on
168. Olsen JD: Larkspur toxicosis: a review of current research. In Effects of Poisonous Plants on Livestock. Keeler RF, Van Kampen KR, James LF, Eds.
169.
170. Manners GD, Panter KE, Ralphs MH, et al.: The occurrence and toxic evaluation of norditerpenoid alkaloids in tall larkspur (Delphinium spp.) J Food Agric Chem 1993, 41:96–100.
171. Manners GD, Panter KE, Pelletier SW: Structure-activity relationships of norditerpenoid alkaloids occurring in toxic larkspur (Delphinium) species. J Nat Prod 1997, 58:863–869.
172. Manners GD, Panter KE, Ralphs MH, et al.: The toxic evaluation of norditerpenoid alkaloids in three tall larkspur (Delphinium) species. In Plant Associated Toxins: Agricultural, Phytochemical and Ecological Aspects. Colegate SM, Dorling PR, Eds. Wallingford,
173. Nation PN, Benn MH, Roth SH, Wilkens JL: Clinical signs and studies of the site of action of purified larkspur alkaloid, methyllycaconitine, administered parenterally to calves. Can Vet J 1982, 23:264–266.
174. Kukel CF, Jennings KR: Delphinium alkaloids as inhibitors of a-bungeratoxin binding to rat and insect neural membranes. Can J Physiol Pharmacol 1994, 72:104–107.
175. Ward JM, Cockcroft VB, Lunt GG, et al.: Methyllycaconitine: a selective probe for
176. neuronal a-bungeratoxin binding sites. FEBS Lett 1990, 270:45–48.
177. Olsen JD: Larkspur poisoning: as we now know it and a glance at the future. Bovine Practitioner 1994, 28:157–163.
178. Olsen JD, Sisson DV: Description of a scale for rating the clinical response of cattle poisoned by larkspur. Am J Vet Res 1991, 52:488–493.
179. Potter RL, Ueckert DN: Epidermal cellular characteristics of selected livestock-poisoning plants in
180. Knight AP, Pfister JA: Larkspur poisoning in livestock: myths and misconceptions. Rangelands 1997, 19:10–13.
181. Pfister JA, Panter KE, Manners GD, Cheney CD: Reversal of tall larkspur (Delphinium barbeyi) poisoning in cattle with physostigmine. Vet Hum Toxicol 1994, 36:511–514.
182. Stegelmeier BL, James LF, Panter KE, et al.: Mechanisms and treatment of larkspur poisoning. Larkspur Symposium Proceedings.
183. Pfister JA et al: Larkspur (Delphinium spp.) poisoning in livestock. J Natural Toxins 8:81-94, 1999.
184. Ralphs MH, Browns JE. Utilization of larkspur by sheep. J Range Manage 1991, 44:619–622.
185. Ralphs, MH, Olsen JD. Prior grazing by sheep reduces waxy larkspur consumption by cattle: an observation. J Range Manage 1992, 45:136–139.
186. Pfister JA, Manners GD: Mineral salt supplementation of cattle grazing tall larkspur infested range land during drought. J Range Manage 1991, 44:105–111.
187. Olsen JD, Ralphs MH: Feed aversion induced by intraruminal infusion of larkspur extract in cattle. Am J Vet Res 1986, 47:1829–1831.
188. Ralphs MH, Olsen JD: Comparison of larkspur alkaloid extract and lithium chloride in maintaining cattle aversion to larkspur in the field. J Anim Sci 1992, 70:1116–1120.
189. Olsen JD, Ralphs MH, Lane MA: Aversion to eating larkspur plants induced in cattle by intraruminal infusion of lithium chloride. J Animal Sci (Suppl 1) 1987, 65:218–224.
190. Lane MA, Ralphs MH, Olsen JD, Provenza FD, Pfister JA: Conditioned taste aversion: potential for reducing cattle loss to larkspur. J Range Manage 1990, 43:127–131.
191. Ralphs MH, Olsen JD: Adverse influence of social facilitation and learning context in training cattle to avoid eating larkspur. J Anim Sci 1990, 68:1944–1952.
192. Ralphs MH, Cheney CD: Influence of cattle age, lithium chloride dose level, and food type in the retention of food aversions. J Anim Sci 1993, 71:373–379.
193. Ralphs MH: Continued food aversion: training livestock to avoid eating poisonous plants. J Range Manage 1992, 45:46–51.
194. Nielsen DB, Cronin EH: Economics of tall larkspur control. J Range Manage 1997, 30:434–438.
195. Nielsen DB, Ralphs MH, Evans JO,
196. Cronin EH, Nielsen D, Madson N: Cattle losses, tall larkspur, and their control. J Range Manage 1976, 29:364–367.
197. Ralphs MH, Evans JO, Dewey SA: Timing of herbicide applications for control of larkspurs (Delphinium spp.). Weed Sci 1992, 40:264–269.
198. Ralphs MH: Long term impact of herbicides on larkspur and associated vegetation. J Range Manage 1994, 48:459–464.
199. Ralphs MH, Jones W, Mower K, Quimby C: Biological agents to control larkspur or reduce risk of poisoning. Larkspur Symposium Proceedings.
200. Stern ES: The diterpenoid alkaloids from Aconitum, Delphinium, and Garrya species. In The Alkaloids, Volume VII. Manske RHF, Ed.
201. Kingsbury JM: Poisonous Plants of the
202. Olsen JD, Manners GD, Pelletier SW: Poisonous properties of larkspur (Delphinium spp.) Collectanea Botanica (
203. Chang TY, Tomlinson B, Tse LK, Chan JC, Chan WW, Critchley JA: Aconitine poisoning due to Chinese herbal medicines: a review. Vet Hum Toxicol 1994, 36:452–455.
204. Panter KE, Keeler RF, Baker DC: Toxicoses in livestock from the hemlocks (Conium and Cicuta spp.). J Anim Sci 1988, 66:2407–2413.
205. Panter KE, Keeler RF: Piperidine alkaloids of poison hemlock (Conium maculatum). In Toxicants of Plant Origin. Volume 1. Alkaloids. Cheeke PR, Ed. CRC Press,
206. Bowman WC, Snaghvi IS: Pharmacologic actions of hemlock (Conium maculatum) alkaloids. J Pharm Pharmacol 1963, 15:1–25.
207. Lopez TA, Cid MS, Bianchini ML: Biochemistry of hemlock (Conium maculatum L) alkaloids and their acute and chronic toxicity in livestock. A review. Toxicon 1999, 37:841-865.
208. Keeler RF: Coniine, a teratogenic principle from Conium maculatum producing congenital malformations in calves. Clin Toxicol 1979, 7:195–206.
209. Keeler RF, Balls LD: Teratogenic effects in cattle of Conium maculatum and conium alkaloids and analogs. Clin Toxicol 1978, 12:49–64.
210. Panter KE, Keeler RF, Buck WB, Shupe JL: Toxicity and teratogenicity of Conium maculatum in swine. Toxicon Suppl 1983, 3:333–336.
211. Dyson DA, Wrathall AE: Congenital deformities in pigs possibly associated with exposure to hemlock (Conium maculatum). Vet Rec 1977, 100:241–243.
212. Frank AA, Reed WM: Conium maculatum (poison hemlock) toxicosis in a flock of range turkeys. Avian Dis 1987,31:386–388.
213. Jessup DA, Boermans HJ,
214. Keeler RF: Alkaloid teratogens from lupinus, conium, veratrum and related genera. In Effects of Poisonous Plants on Livestock. Keeler RF, Van Kampen KR, James LF, Eds.
215. Keeler RF, Balls LD, Shupe JL, Crowe MW: Teratogenicity and toxicity of coniine in cows, ewes and mares. Cornell Vet 1980, 70:19–26.
216. Kingsbury JM: Poisonous Plants of the
217. MacDonald H: Hemlock poisoning in horses. Vet Rec 1937, 49:1211–1212.
218. Penney RHC: Hemlock poisoning in cattle. Vet Rec 1953, 65:669.
219. Widmer WR: Poison hemlock toxicosis in swine. Vet Med 1984, 79:405–408.
220. Shupe JL, James LF: Teratogenic plants. Vet Human Toxicol 1983, 25:415–421.
221. Edmonds LD, Selby LA, Case AA: Poisoning and congenital malformations associated with consumption of poison hemlock by sows. J Am Vet Med Assoc 1972, 160:1319–1324.
222. Panter KE, Keeler RF, Buck WB: Induction of cleft palate in new born pigs by maternal ingestion of poison hemlock (Conium maculatum). Am J Vet Res 1985, 46:1368–1371.
223. Panter KE, Keeler RF, Buck WB: Congenital skeletal malformations induced by maternal ingestion of poison hemlock (Conium maculatum) in newborn pigs. Am J Vet Res 1985, 46:2064–2066.
224. Crowe MW, Swerczek TW: Congenital arthrogryposis in offspring of sows fed tobacco stalks (Nicotiana tabacum). Am J Vet Res 1974, 35:1071–1073.
225. Panter KE, Keeler RF, Bunch TD, Callan RJ: Congenital skeletal malformations and cleft palate induced in goats by ingestion of Lupinus, Conium, and Nicotiana species. Toxicon 1990, 28:1377–1385.
226. Panter KE, Keeler RF: Induction of cleft palate in goats by Nicotiana glauca during a narrow gestational period and the relation to the reduction in fetal movements. J Natural Toxins 1992, 1:25–32.
227. Panter KE, James LF, Keeler RF, Bunch TD: Radio-ultrasound observations of poisonous plant-induced fetotoxicity in livestock. In Poisonous Plants. Proceedings 3rd International Symposium. James LF, Keeler RF, Bailey EM, et al.: Eds.
228. Panter KE, Bunch TD, Keeler RF: Maternal and fetal toxicity of poison hemlock (Conium maculatum) in sheep. Am J Vet Res 1988, 49:281–283.
229. Kingsbury JM: Poisonous Plants of the
230.
231. Anet EFLJ, Lythgoe B, Silk MH, Trippett S: Oenanthotoxin and cicutoxin. Isolation and structures. J Chem Soc 1953, 66:309–322.
232. Payonk GS,
233. Panter KE, Baker DC, Kechele PO: Water hemlock (Cicuta douglasii) toxicosis in sheep: pathologic description and prevention of lesions and death. J Vet Diagn Invest 1996, 8:474–480.
234. James LF, Ralphs MH: Water hemlock.
235. Warwick BL, Runnels HA: Water hemlock poisoning of livestock.
236. Panter KE, Keeler RF, Baker DC: Toxicosis in livestock from the hemlocks (Conium and Cicuta spp.) J Anim Sci 1988, 66:2407–2413.
237. Fleming CE,
238. Smith RA, Lewis D: Cicuta toxicosis in cattle: case history and simplified analytical method. Vet Hum Toxicol 1987, 29:240–241.
Kingsbury JM. Poisonous Plants of the