Cicuta virosa L. Cowbane, Water hemlock - Manson Publishing

Cicuta virosa L. Cowbane, Water hemlock 

Cowbane is one of the most poisonous 

plants because of its poly-yne content 

and, for that reason, its extermination 

has been the subject of official 

regulations. In addition to cicutoxin and 

cicutol, which are held responsible for 

the toxic effect, other C 17 poly-ynes 

occur, amongst them falcarindiol [1] that 

occurs widely in the family. All parts of 

the plant are highly toxic when fresh, 

particularly the underground organs 

(Figure 9) whose smell is reminiscent of 

42 Apiaceae 

parsnips or celery. On drying, the polyynes 

are largely destroyed (at least in the 

outer layers of the tissue). In a case of 

suicide described by BERNDT [2], it was 

evidently chewing dried cowbane roots 

that lead to the death. Horses after being 

given 500 g of the dried herbage have 

died within 15 hours [3]. Further poisonings 

have occurred in animals: ponies 

[4], cows [5]. As the poly-yne content in 

the aerial parts of the plant is very low 

up to the summer months, these are not 

Fig. 8: Cicuta virosa – Cowbane. 

A herb, 1.0–1.5 m high, with hollow stems 

(and petioles) and tuberous, thickened, 

chambered rhizomes (see Fig. 9). 

A water or marsh plant at the edges of 

ponds or river banks, usually in shallow 

water. 

Leaves: bi- to tri-pinnatisect; lower ones 

long-petiolate, upper ones short-petiolate 

or sessile; often doubly serrate; variable, 

depending on local habitat conditions, e.g. 

apex of leaf segments linear and sparsely 

serrated. 

Flowers: staminate or androgynous, 

white, with equal petals, in stalked umbels 

with 15–25 rays bearing many-flowered 

secondary umbels; bracts (usually) 

absent; VI–VIII. 

Fruits: ovoid and mericarps (carpels) usually 

not separating from each other. 

Distribution: northern and central Europe, 

in the south rarer to absent; in North 

America many other species, including C. 

douglasii and C. maculata, are likewise 

known as poisonous plants. 

dangerous to cattle; however, when the 

cattle pull the bulbs (rhizomes) out of 

muddy ground, very serious poisoning 

can result [6]. 

While, in the older literature, many 

cases of poisoning (with a mortality rate 

of over 30%) are to be found, especially 

in children, there have been few reports 

from Europe in recent years [7, 8]; 

however, they are by no means absent. 

Poisoning in two children by eating 

‘green cabbage’, i.e. the tubers of 

cowbane, is described in detail by 

BARTEL & GERBER [9]: 

‘An 8-year-old boy who had eaten a tuber died 

from acute cardiac failure, in spite of being 

treated clinically for 12 hours. A second 

patient, a 9-year-old boy who had only bitten 

off a piece of tuber and had spat it out because 

of the unpleasant taste, was saved after six 

hours of treatment which included positivepressure 

respiration and the administration of 

muscle relaxants.’ 

More recent reports of cowbane poisoning 

have come from North America, where (in 

addition to C. virosa) other Cicuta spp., e.g. 

C. douglasii and C. maculata, occur and are 

likewise known as dangerously poisonous 

plants [10–13]. In discussing a case of poisoning 

by C. douglasii (western water hemlock), 

MUTTER [14] writes: 

‘While on a field trip with his class from school a 

13-year-old boy ate roots of the plant which 

Fig. 9: Cicuta virosa: tuberous rhizome with root scars (left); characteristic chambers and 

golden-yellow juice on the cut surface (right). 

some of the children described as “wild 

carrot”. When he arrived home about an hour 

later, he complained of abdominal pain and 

dizziness. But since he had been given garden 

chores to do his parents thought he was 

malingering and sent him out to do the work. 

About 15 minutes later his brother found him 

lying unconscious on the ground, frothing at 

the mouth, and with vomit close by. Violent 

convulsions then began and continued, along 

with vomiting, while the boy was driven to 

hospital. “It is believed that a new speed 

record for the journey (34 miles over gravel 

roads) was established.” Administration of 

oxygen and treatment with diazepam gradually 

brought the convulsions under control; 

four days later the boy was discharged, and 

six months after the incident there were no 

apparent ill-effects.’ 

Symptoms of poisoning. Even chewing 

small (thumb-size) pieces of rhizome or 

root soon leads (within 30–60 minutes) to 

burning pain in the mouth, severe and 

prolonged vomiting, and subsequent convulsions 

(see the above-mentioned case 

history). 

Treatment 

Gastric lavage with activated charcoal. 

The most important measure is 

the prevention of the convulsions; 

thiobarbiturates, e.g. thiopentone 

sodium ( Pentothal ® , Trapanal) or 

diazepam (which, according to [15], is 

supposed to be less active) have been 

indicated as antidotes. Thus, 

STARREVELD & HOPE [15] in a case of 

serious poisoning in a 54-year-old 

adult immediately after admission 

slowly injected 350 mg i.v. of a thiobarbiturate 

and followed this by 

infusing further thiobarbiturate over a 

period of eight hours (2 mg/ml in isotonic 

saline), to give a total of 2.2 g. 

In one case of severe intoxication, 

haemodialysis and haemoperfusion 

were also used successfully [8]. 

Appendix. Of the other plants which 

contain polyacetylenes, Oenanthe crocata 

(hemlock water dropwort) merits 

special attention. It occurs in southern 

Apiaceae 43

Fig. 10: Roots of Oenanthe crocata (‘Dead men’s fingers’). 

Europe, but also in western France [16] 

and in Great Britain, where it is considered 

to be one of the most dangerous poisonous 

plants [17]. O. crocata – like Cicuta virosa 

and O. aquatica (fine-leaved water 

dropwort), which is distributed in central 

Europe – has a preference for wet 

and marshy localities. Although no 

cases of poisoning due to O. aquatica 

are known (for the composition of the 

essential oil, see [17]), cases of serious 

poisonous with O. crocata have been 

described repeatedly [17–20]. Since the 

beginning of the 20th century, at least 

10 cases of fatal poisoning have been 

44 Apiaceae 

published – amongst them also some 

from more recent times: a) a vegetarian 

hippie [16], one of three young people, 

after eating a vegetarian meal [18], and 

b) a student, who had eaten the tubers 

in the hope of achieving hallucinating 

effects [18]. Of ‘two alternative young 

men’ who, whilst on a holiday in 

Portugal, had eaten an unknown quantity 

of Oenanthe crocata, one died on 

the same day as he had eaten the 

tuber [21]; the post-mortem result 

showed complete necrosis of the 

kidney parenchyma and resembled the 

observations of CARLTON [10] who, in 

connection with poisoning by cowbane, 

had noticed rhabdomyolysis and renal 

failure. 

The thickened tubers of Oenanthe 

crocata (‘dead men’s fingers’) (Figure 10) 

are attractive for eating; they taste of 

parsnips and, when cut, produce a 

golden-yellow excretion (crocata!), which 

darkens when exposed to the air; cf. illustration 

of the cut surface of the Cicuta 

rhizome! (Figure 9). 

The toxic poly-ynes in the excretion 

(oenanthotoxin etc.; for its fluorimetric 

assay, see [22]) are rapidly decomposed in 

the air, but inside the fleshy roots they 

remain stable and hence active for longer. 

The highest poly-yne content is in the 

roots in winter and in the early part of 

spring. In the case described by MITCHELL 

& ROUTLEDGE [17], an ecology student 

had been working on a farm during his 

holidays and had prepared a salad from 

the roots of some nearby plants, since a 

little piece of the root had a ‘pleasant 

taste’. The serious poisoning that resulted 

was caused by the root of Oenanthe crocata, 

but fortunately was not fatal. 

However, the case illustrates the point 

that without adequate knowledge the 

present-day endeavour to find an ‘alternative’ 

diet can have quite dangerous 

consequences. 

Toxic concentrations of poly-ynes 

also occur in Aethusa cynapium (fool’s 

parsley) (Figure 11) and in Chaerophyllum 

temulum (rough chervil) (Figure 

12); both plants are also said to contain 

‘coniine-like volatile alkaloids’. While 

there are no recent reports of poisoning 

by C. temulum, in 1975 SWART [23] 

reported poisoning of goats by Aethusa 

cynapium. Cases of human poisoning 

with fool’s parsley are known only from 

older literature, in which its confusion 

with real parsley was pointed out. As 

fool’s parsley does not produce crispate 

leaves, Petroselinum crispum (parsley), 

which does have crispate leaves, is preferred 

for cultivation. Microscopically, 

fool’s parsley and parsley can be distinguished 

by the number of stomata on the 

undersurface of their leaves (Figure 13), 

the former having about twice as many as 

the latter. According to investigations by 

TEUSCHER [24], the poisonousness of 

fool’s parsley is questionable, as the isolated 

C 13 poly-ynes (aethusin and aethusanol 

A) showed only slight toxicity in 

animal experiments. Even eating larger 

amounts of this plant did not produce 

poisoning symptoms in mice and guinea 

pigs. The authors presumed that the older 

reports possibly referred to Conium poisoning 

or that only plants infected with 

the rust fungus Puccinia aethusae produce 

larger amounts of the poison. 

Symptoms of poisoning and 

treatment: See Cicuta virosa. 

In a serious case of poisoning, owing 

to insufficient breathing, artificial respiration 

had to be given; also, metabolic 

acidosis, signs of rhabdomyolysis and 

renal failure had to be corrected 

therapeutically [22]. 

Fig. 11: Aethusa cynapium L. – Fool’s 

parsley. 

Fig. 12: Chaerophyllum temulum L. – 

Rough chervil. 

Apiaceae 45

Fig. 13: Lower epidermis of the leaves of: Aethusa cynapium (left) and Petroselinum 

crispum (right); gelatin impression. The scale line corresponds to 50 µm. 

References 

[1] Wittstock, U., F. Hadacek, G. Wurz, E. 

Teuscher and H. Greger: Polyacetylenes from 

Water Hemlock, Cicuta virosa. Planta Med. 

61, 439–445 (1995). 

[2] Berndt, H.: Vergiftungen durch Cicuta virosa 

L., Wasserschierling. Pharmazie 2(11), 

521–523 (1947). 

[3] Bentz, H.: Nutztiervergiftungen, Erkennung 

und Verhütung. Gustav Fischer Verlag, Jena 

1969. 

[4] Dijkstra, R.G. and R. Falkena: Een geval 

van cicutoxine-intoxicatie bij ponys. 

Tijdschr. Diergeneesk. 106(20), 1037–1039 

(1981). 

[5] Van Inzen, C. and S.D. Gunn: Poisoned 

cows. Vet. Rec. 125(8), 212 (1989). 

[6] Smith, R.A. and D. Lewis: Cicuta toxicosis in 

cattle: Case history and simplified analytical 

method. Vet. Hum. Toxicol. 29(3), 

240–241 (1987). 

46 Apiaceae 

[7] Van Heijst, A.N.P., S.A. Pikaar, R.G. van 

Kesteren en J.M.C. Douze: Een vergiftiging 

door de waterscheerling (Cicuta virosa). 

Ned. Tijdschr. Geneeskd. 127, 2411–2413 

(1983). 

[8] Knutzen, O.H. and P. Paszkowski: New 

aspects in the treatment of water hemlockpoisoning. 

Clin. Toxicol. 22(2), 157–166 

(1984). 

[9] Bartel, J. and H.U. Gerber: Ein Beitrag zur 

Vergiftung mit Wasserschierling (Cicuta 

virosa) bei Kindern. Kinderärztl. Praxis 

30(12), 543–547 (1962). 

[10] Carlton, B.E., E. Tufts and D.E. Girard: 

Water hemlock poisoning complicated by 

rhabdomyolysis and renal failure. Clin. 

Toxicol. 14(1), 87–92 (1979). 

[11] Landers, D., K. Seppi and W. Blauer: 

Seizures and death on a white river float 

trip. West. J. Med. 142(5), 637–640 (1985). 

[12] Sweeney, K., K.F. Gensheimer, 

J. Knowlton-Field and R.A. Smith: Water 

hemlock poisoning – Maine, 1992. J. Am. 

Med. Assoc. 271(19), 1475–1577 (1994). 

[13] Heath, K.B.: A fatal case of apparent water 

hemlock poisoning. Vet. Hum. Toxicol. 

43(1), 35–36 (2001). 

[14] Mutter, L.: Poisoning by western water 

hemlock. Can. J. Public. Health 67, 386 

(1976). 

[15] Starreveld, E. and C.E. Hope: Cicutoxin 

poisoning (water hemlock). Neurology 25, 

730–734 (1975). 

[16] Anger, J.-P., F. Anger, Y. Chauvel, 

R.L. Girre, N. Curtes et J.-P. Curtes: 

Intoxication mortelle par Oenanthe safranee 

(Oenanthe crocata). Europ. J. Toxicol. 

9(2), 119–125 (1976). 

[17] Mitchell, M.I. and P.A. Routledge: 

Hemlock water dropwort poisoning – a 

review. Clin. Toxicol. 12(4), 417–426 

(1978). 

[18] King, L.A., M.J. Lewis, D. Parry, P.A. 

Twitchett and E.A. Killner: Identification of 

oenanthotoxin and related compounds in 

hemlock water dropwort poisoning. Hum. 

Toxicol. 4, 355–364 (1985). 

[19] Ball, M.J., M.L. Flather and J.C. Forfar: 

Hemlock water dropwort poisoning. 

Postgrad. Med. J. 63, 363–365 (1987). 

[20] O’Mahonney, S., P. Fitzgerald and M.J. 

Welton: Poisoning by hemlock water dropwort. 

Irish. J. Med. Sci. 156(8), 241 (1987). 

[21] Theus, L.: Schwere und tödliche 

Pflanzenvergiftungen der Schweiz. Bevölkerung 

von 1966–1992. Dissertation, Basel 

1994. 

[22] Del Castillo, B., A.G. De Marina and M.P. 

Martinez-Honduvilla: Fluorometric determination 

of oenanthotoxin. Ital. J. 

Biochem. 29(4), 233–237 (1980). 

[23] Swart, F.W.J.: Vergifting van geiten door 

Hondspetersilie. Tijdschr. Diergeneesk. 

100(18), 989–990 (1975). 

[24] Teuscher, E., H. Greger and V. Adrian: 

Untersuchungen zur Toxizität von Aethusa 

cynapium L., der Hundspetersilie. Pharmazie 

45(7), 537–538 (1990). 

Conium maculatum L. Hemlock 

Although hemlock is one of the most 

widely known poisonous plants, it plays 

only a minor role in the advice given by 

the Central European Toxicological 

Information Centres. Thus, for instance, 

the Centre in Berlin registered only 37 

cases in 24 years. Children who had eaten 

the fruits, flowers, stalks or leafy parts 

experienced gastrointestinal pains in 16% 

of the cases [1]. The unpleasant odour of 

the plant – it smells of mouse urine – is 

due to the free base coniine, and it 

becomes stronger after crushing the plant 

material and on making it alkaline. It 

effectively deters consumption of the 

plant. Also, the addition of hemlock fruits 

to aniseed rarely occurs nowadays. 

Figure 15 shows some umbelliferous 

fruits, including the very similar-looking 

ones of hemlock and Pimpinella anisum 

(aniseed). A more recent report of three 

deaths in Australia [2] shows, however, 

Fig. 14: Conium maculatum – Hemlock, 

Poison-hemlock. 

An annual or biannual plant (1.0–2.5 m in 

height) with finely grooved, round and at 

ground level and, higher up, spotted 

stems; distinctly smaller and with similarly 

spotted but dirty-reddish stem: 

Chaerophyllum temulentum (see Fig. 12). 

Grows along hedges, fences, roadsides 

and on waste ground. 

Leaves: intense green, 2–4-pinnate, 

glabrous. 

Flowers: whitish, umbels with bracts. 

Fruits: ovoid with wavy ridges, glabrous 

(unlike aniseed). 

Distribution: throughout Europe, rarer in 

the north. 

that this plant can be the cause of serious 

poisoning at any time. Two young men 

were found dead on New Year’s Day 

1993: 

‘Both had consumed large amounts of alcohol 

the previous night. They were observed going 

out after midnight and returning an hour later 

carrying a quantity of green vegetable matter. 

They were seen boiling this leaf matter in a pot 

full of water, and then were not seen from 2.30 

a.m. until their discovery at 10.00 a.m.’ 

Apiaceae 47

Fig. 15: Examples of Apiaceaen fruits: left to right – Cicuta virosa, Aethusa cynapium, 

Conium maculatum, Pimpinella anisum, Heracleum sphondylium (with the vittae 

visible). 

The stomach content of one, as well 

as the blood and urine of the other, was 

shown, by means of GC-NMR spectroscopy, 

(in addition to alcohol and 

THC) to contain -conicein and the plant 

material was identified as C. maculatum. 

The third fatal case refers to a 3-yearold 

child who, together with other children, 

had eaten from a plant known as 

‘carrot weed’. Whereas the other children 

spat the leaves out again, the stomach 

content of the dead child contained 142 g 

of leaf material belonging to C. maculatum. 

The stomach contents, as well as the 

blood, were shown to contain -conicein. 

After eating the leaves the child sat in its 

pram and was observed to be sleeping as 

if narcotized. Death occurred 2 hours 

after ingestion. 

Less serious was a case of Conium 

poisoning in a 4-year-old. After he had 

eaten leaves of the ‘wild carrot’, he 

luckily had to vomit, before falling into a 

narcotic-like sleep. After gastric lavage 

with activated charcoal, it took 90 minutes 

before he responded to questioning 

and recovered without further damage. 

The fresh leaves of the ‘wild carrot’ were 

shown to contain 850 g -conicein/g [3]. 

In Turkey, a woman had to receive 

artificial respiration for over 16 hours 

and, thus, survived a serious case of 

Conium poisoning. Apparently, she had 

confused hemlock with Chaerophyllum 

macropodum, a plant which, in Turkey, is 

used for the production of a certain type 

of cheese [4]. 

Toxic constituents. The piperidine alkaloids, 

such as coniine and -conicein, are 

the main alkaloids [5]. They are present 

in all parts of the plant and accumulate in 

particularly high concentrations (up to 

3.5%) in the not quite ripe fruits, where 

they are localized in the inner wall (endocarp 

and adjoining mesocarp), the 

so-called coniine layer. In dried plant 

material, i.e. in hay, the alkaloid content 

is smaller, owing to the volatility of the 

free bases. 

Toxic effects. Coniine and -conicein 

have acute toxic and in animals teratogenic 

effects. The alkaloids in hemlock, of 

which the minor ones have not been individually 

investigated, act on the central 

and peripheral nervous system. They have 

a nicotin-like effect on the autonomic 

ganglia and sensitive nerve endings, but 

N 

H 

N 

Coniine 

-Coniceine 

also exhibit curare-like effects, in which 

with higher doses the striated musculature 

is paralysed. As the alkaloids are readily 

absorbed by the skin and the mucous 

layer of the gastrointestinal tract, symptoms 

of poisoning become apparent 

within 1–2 hours after ingestion: at first 

burning in the mouth, nausea, vomiting 

and salivating, stomach pains and diarrhoea 

as well as muscle tremor and convulsions. 

In severe cases of poisoning, 

paralysis of the striated musculature sets 

in, starting at the extremities, until death 

takes place as a result of respiratory 

paralysis. Plato’s classical description of 

the death of Socrates gives rise to speculation 

even today [6]. A more recent toxicological 

valuation of coniine is given by 

SEEGER [7]. 

Several publications by a group of 

Italian doctors [8, 9] describe, apart from 

the symptoms of neuro-toxic poisoning, the 

occurrence of rhabdomyolysis (destruction 

of the striated muscle fibres) and myoglobinuria 

combined with acute renal failure. 

According to the authors, all cases (including 

three fatal ones owing to renal failure) 

were caused by indirect coniine poisoning: 

all patients had eaten song-birds, which 

themselves had eaten buds (and also possibly 

the ‘seeds’) of Conium maculatum in 

the spring. Coniine was found to be present 

in the urine of the patients and partly also 

in the serum (shown by means of thinlayer 

chromatography). There are no 

quantitative data on the concentration of 

the coniine (or of the coniine content in the 

corresponding animals); it is difficult, therefore, 

to determine whether, in fact, it was 

coniine poisoning [10]. The liver, kidneys 

and pancreas of a 14-year-old girl, who had 

died as a result of Conium poisoning, could 

be used for transplantation without 

problems [10]. 

48 Apiaceae Apiaceae 49 

Treatment 

Primary removal of poison; immediate 

activated charcoal; also, suspected 

cases to be admitted to hospital. 

Prompt endotracheal intubation and 

artificial respiration, as long as respiratory 

arrest persists. 

Animal poisonings. Poisoning in animals 

is not rare and occurs mainly in the 

spring, when no other forage is available 

in sufficient quantities for grazing animals. 

The affected animals salivate, 

excrete a lot of faeces and urine; in serious 

cases, muscle tremor and muscle 

paralysis is followed by death as a result 

of respiratory failure. According to [11], 

pigs are less sensitive than sheep and 

goats, whereas Conium is very poisonous 

to cattle. This information from PANTER 

et al., who probably have the most experience, 

do not coincide with other reports, 

according to which pigs, in particular, are 

supposed to be very sensitive [7, 12]. Pigs 

and piglets [13, 14], dairy cattle [15], elks 

[16], turkeys [17], sheep [18] and rabbits 

[19] are affected by the poisoning, 

whereas song-birds (according to observations 

in Italy) (see above) are less sensitive. 

A review of accidental poisoning and 

experimental work on ‘hemlocks’ (i.e. 

Conium and Cicuta) is given by PANTER 

et al. [11]. 

Apart from the acute toxicity, teratogenic 

effects have also been attributed to 

Conium alkaloids and have been verified 

in feeding experiments [20–22]. Doses 

that are toxic to the pregnant mother 

animal, cause skeletal malformations 

(congenital arthrogryposis, scoliosis, cleft 

palate), as are already known from 

poisoning by Lupinus and Nicotinia alkaloids 

[23]. Coniines used in experiments 

on laboratory animals gave no reaction 

with rats and have only weak teratogenic 

effects with rabbits [24]. 

References 

[1] Ritter, S.: Vergiftungsunfälle mit Pflanzen, 

in: Vergiftungen im Kindesalter, K.E. von 

Mühlendahl, U. Oberdisse, R. Bunjes und S. 

Ritter (Hrsg.), Ferdinand Enke Verlag, 

Stuttgart 1995. 

[2] Drummer, O.H., A.N. Roberts, P.J. 

Bedford, K.L. Crump and M.H. Phelan: 

Three deaths from hemlock poisoning. 

Med. J. Aust. 162(11), 592–593 (1995). 

[3] Frank, B.S., W.B. Michelson, K.E. Panter 

and D.R. Gardner: Ingestion of poison 

hemlock (Conium maculatum). Western J. 

Med. 163(6), 573–574 (1995). 

[4] Biberci, E., Y. Altuntas, A. Cobanoglu and 

A. Alipinar: Acute respiratory arrest following 

hemlock (Conium maculatum) intoxication. 

Clin. Toxicology 40(4), 517–518 

(2002). 

[5] Lopez, T.A., M.S. Cid and M.L. Bianchini: 

Biochemistry of hemlock (Conium maculatum 

L.) alkaloids and their acute and 

chronic toxicity in livestock. A review. 

Toxicon 37, 841–865 (1999). 

[6] Ober, W.B.: Did Socrates die of hemlock 

poisoning? N. Y. State J. Med. 77(2), 

254–258 (1977). 

[7] Seeger, R.: DAZ-Giftlexikon: Coniin. 

Dtsch. Apoth. Ztg. 131(15), 720–723 

(1991). 

[8] Rizzi, D., C. Basile, A. Di Maggio, A. 

Sebastio, F. Introna, R. Rizzi, S. De Marco 

and J.E. Smialek: Clinical spectrum of accidental 

hemlock poisoning: Neurotoxic 

manifestations, rhabdomyolysis a. acute 

tubular necrosis. Nephrol. Dial. Transplant. 

6, 939–943 (1991). 

[9] Scatizzi, A., A. Di Maggio, D. Rizzi, A.M. 

Sebastio and C. Basile: Acute renal failure 

due to tubular necrosis caused by wildfowlmediated 

hemlock poisoning. Renal Failure 

15(1), 93–96 (1993). 

[10] Foster, P.F., R. McFadden, R. Trevino et al.: 

Succesful transplantation of donor organs 

from a hemlock poisoning victim. Transplantation 

76(5), 874–876 (2003). 

[11] Panter, K.E., R.F. Keeler and D.C. Baker: 

Toxicoses in livestock from the hemlocks 

(Conium and Cicuta ssp.). J. Anim. Sci. 

66(9) 2407–2413 (1988). 

[12] Liebenow, H. and K. Liebenow: 

Giftpflanzen. Gustav Fischer Verlag Jena, 

Stuttgart 1993. 

[13] Hannam, D.A.R.: Hemlock (Conium maculatum) 

poisoning in the pig. Vet. Rec. 

116(12), 322 (1985). 

[14] Markham, K.: Hemlock poisoning in 

piglets. Vet. Rec. 116(1), 27 (1985). 

[15] Galey, F.D., D.M. Holstege and E.G. Fisher: 

Toxicosis in dairy cattle exposed to poison 

hemlock (Conium maculatum) in hay: isolation 

of Conium alkaloids in plants, hay 

and urine. J. Vet. Diagn. Invest. 4(1), 60–64 

(1992). 

[16] Jessup, D.A., H.J. Boermans and N.D. 

Kock: Toxicosis in tule elk caused by ingestion 

of poison hemlock. J. Am. Vet. Med. 

Assoc. 189(9), 1173–1175 (1986). 

[17] Frank, A.A. and W.M. Reed: Conium maculatum 

(poison hemlock) toxicosis in a 

flock of range turkeys. Avian diseases 31(2), 

386–388 (1987). 

[18] Panter, K.E., T.D. Bunch and R.F. Keeler: 

Maternal and fetal toxicity of poison 

hemlock (Conium maculatum) in sheep. 

Am. J. Vet. Res. 49(2), 281–283 (1988). 

[19] Short, S.B. and W.C. Edwards: Accidental 

Conium maculata poisoning in the 

rabbit. Vet. Hum. Toxicol. 31(1), 54–57 

(1989). 

[20] Keeler, R.F. and L.D. Balls: Teratogenic 

effects in cattle of Conium maculatum and 

Conium alkaloids and analogs. Clin. 

Toxicol. 12(1), 49–64 (1978). 

[21] Panter, K.E., R.F. Keeler, W.B. Buck and J.L. 

Shupe: Toxicity and teratogenicity of 

Conium maculatum in swine. Toxicon 

Suppl. 3, 333–336 (1983). 

[22] Panter, K.E., R.F. Keeler and W.B. Buck: 

Induction of cleft palate in newborn pigs by 

maternal ingestion of poison hemlock 

(Conium maculatum). Am. J. Vet. Res. 

46(6), 1368–1371 (1985). 

[23] Panter, K.E., L.F. James and D.R. Gardner: 

Lupines, poison-hemlock and Nicotiana 

ssp.: Toxicity and teratogenicity in livestock. 

J. Nat. Toxins 8(1), 117–134 (1999). 

[24] Forsyth, C. and A.A. Frank: Evaluation of 

developmental toxicity of coniine to rats 

and rabbits. Teratology 48(1), 59–64 

(1993).

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