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POISON HEMLOCK - Conium maculatum

POISON HEMLOCK PLANT
POISON HEMLOCK PLANT
POISON HEMLOCK PLANT
POISONOUS HEMLOCK PLANT
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POISON HEMLOCK PLANT

POISON HEMLOCK PLANT

POISON HEMLOCK PLANT

POISON HEMLOCK PLANT

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Distinguishing features

Poison hemlock is a coarse biennial herb 3-6 feet tall: the stem is smooth, purple-spotted, and hollow; the leaves are alternate, with bases sheathing the stems, appearing much like parsley; the flowers are in compound umbels, small and white. The leaves smell like parsnips when bruised and are extremely nauseating when tasted. 

DescriptionPoison hemlock is a perennial member of the Umbelliferae (parsley) family.  The plants are up to 6 feet tall with smooth, hollow stems covered with purple spots.  Leaves are finely divided, resembling those of parsley or carrots.  Crushed leaves have a mouse-like odor.  The plant is sometimes confused with wild carrot (Daucus carota, Queen Anne's lace).  There is a large white to pale yellow taproot.
Geographic rangePoison hemlock grows on fertile, moist soils across the United States in locations such as woodlots, fencerows and waste areas.
Toxic principle.  Coniine and related pyridine-type alkaloids are present in the root, young plants and seeds.  As plants mature, the foliage loses alkaloid content, but the seeds accumulate the alkaloid.  Hay can retain toxicity.
Toxicity.  The whole green plant is toxic at dosages of approximately 1% of body weight.
Diagnosis

Poison hemlock can also cause birth defects in ruminants and swine, with cattle and swine more susceptible than sheep and goats.  The most often reported birth defects are cleft palate and spinal abnormalities.  The gestational ages that have been associated with birth defects are: for goats, days 30 through 60; for cattle, days 40 through 70; for pigs, days 30 through 60.  The birth defects resemble those seen with lupine, with lupine being the more dangerous plant.

Clinical signsThe clinical course is rapid, and animals may be found dead or die within a few hours.  Initial consumption may cause a burning sensation in the mouth, salivation, emesis and diarrhea.  Rapidly developing neurologic signs include muscle tremors, muscular weakness, dim vision, convulsions and coma.  Death results from respiratory failure.  Frequent urination and defecation may also occur.

 Laboratory diagnosisThe alkaloid may be detected in the stomach contents and urine.

 Lesions are not present in poisoned animals.

Treatment.  The stomach should be evacuated, and activated charcoal administered.  Respiratory support by mechanical ventilation may be lifesaving in small animals.


 


Copyright 2002

University of Pennsylvania
Created by:    Alexander Chan (2003), Daphne Downs (2002), Chris Tsai (2001), Brett Begley (2000), Janet Triplett (1997)
Faculty Advisor:  Dr. Robert Poppenga