Conium maculatum

Conium maculatum (hemlock or poison hemlock) is a highly poisonous biennial plant herbaceous flowering plant in the carrot family Apiaceae, native to Europe and North Africa.

It is a herbaceous biennial plant that grows to 1.5–2.5 m (5–8 ft) tall, with a smooth, green, hollow stem, usually spotted or streaked with red or purple on the lower half of the stem. All parts of the plant are hairless (glabrous). The leaves are two- to four-pinnate, finely divided and lacy, overall triangular in shape, up to 50 cm (20 in) long and 40 cm (16 in) broad. The flowers are small, white, clustered in umbels up to 10–15 cm (4–6 in) across. When crushed, the leaves and root emit a rank, unpleasant odor often compared to that of parsnips. It produces a large number of seeds that allow the plant to form thick stands in modified soils.

Conium maculatum is native in temperate regions of Europe, West Asia, and North Africa. It has been introduced and naturalised in many other areas, including Asia, North America, Australia, and New Zealand. It is often found on poorly drained soils, particularly near streams, ditches, and other surface water. It also appears on roadsides, edges of cultivated fields, and waste areas. It is considered an invasive species in 12 U.S. states.

Poison
Hemlock seed heads in late summer
Conium contains the piperidine alkaloids coniine, N-methylconiine, conhydrine, pseudoconhydrine, and gamma-coniceine (or g-coniceïne), which is the precursor of the other hemlock alkaloids.


Coniine has a chemical structure and pharmacological properties similar to nicotine, and disrupts the workings of the central nervous system through action on nicotinic acetylcholine receptors. In high enough concentrations, coniine can be dangerous to humans and livestock. Due to high potency, the ingestion of seemingly small doses can easily result in respiratory collapse and death. 

Coniine causes death by blocking the neuromuscular junction in a manner similar to curare; this results in an ascending muscular paralysis with eventual paralysis of the respiratory muscles which results in death due to lack of oxygen to the heart and brain. Death can be prevented by artificial ventilation until the effects have worn off 48–72 hours later.
For an adult, the ingestion of more than 100 mg (0.1 gram) of coniine (about six to eight fresh leaves, or a smaller dose of the seeds or root) may be fatal.

Effects on animals
Conium maculatum is poisonous to animals. In a short time, the alkaloids produce a potentially fatal neuromuscular blockage when the respiratory muscles are affected. Acute toxicity, if not lethal, may resolve in the spontaneous recovery of the affected animals provided further exposure is avoided.

It has been observed that poisoned animals tend to return to feed on this plant. Chronic toxicity affects only pregnant animals. When they are poisoned by C. maculatum during the fetus' organ formation period, the offspring is born with malformations, mainly palatoschisis and multiple congenital contractures (MCC; frequently described as arthrogryposis). Chronic toxicity is irreversible and although MCC can be surgically corrected in some cases, most of the malformed animals are lost. Such losses may be underestimated, at least in some regions, because of the difficulty in associating malformations with the much earlier maternal poisoning.


Since no specific antidote is available, prevention is the only way to deal with the production losses caused by the plant. Control with herbicides and grazing with less susceptible animals (such as sheep) have been suggested. C. maculatum alkaloids can enter the human food chain via milk and fowl.