Etiology

• Cattle will eat water hemlock readily, particularly new growth although this may be tolerated due to low concentrations of toxins.
• The concentration of cicutoxin varies throughout the year. It is present in greatest concentration between autumn and early winter, and is found mainly in the yellow oily juice of the roots.
• In spring the concentration in leaves and stems increases to concentrations sufficiently high to prove fatal, if ingested in sufficient quantity.
• Most cases of poisoning occur in the early spring, when other plants may be unavailable or less attractive. The tuber is palatable and also most toxic in early spring.
• As the plant grows toxicity decreases until the flowers and seeds develop; deaths have been reported from ingestion of mature umbrels and fruits. Mature leaves in late spring and summer are less hazardous and poisoning generally only occurs in these seasons if the tubers are consumed.
• Wet weather may make water hemlock roots more accessible to animals, leading to episodes of poisoning. In early spring the roots may be partially above ground due to winter frost and ice and may be available when other plants have little material available for forage.

Predisposing factors

General

• Roots may be exposed following wet weather.
• Grazing along water courses.
• Lack of availability of other vegetation.

Pathophysiology

• All Cicuta species appear to be similar in toxicity.
• All parts of the plant are toxic, particularly the root.
• The main toxin is cicutoxin, a polyacetylene alcohol. Another compound, cicutol, an alcohol, is relatively non-toxic as demonstrated in a mouse bioassay.  There may also be other substances present in the plant that are equally or more toxic that cicutoxin.
• The concentrations of cicutoxin and other components vary with geographical location and season.
• The exact mechanism of poisoning is unknown.
• Cicutoxin affects Na+ and K+ channels and delays repolarisation. Prolongation of the action potential at excitatory synapses could promote excitatory activity.
• Cicutoxin is a powerful CNS stimulant (having similar actions to strychnine) that blocks gamma-amino butyric acid A (GABAA) receptors causing neuronal depolarisation resulting in grand mal convulsions and death.
• Cicutoxin may also have cardiopulmonary effects.

Timecourse

• Signs may occur suddenly, usually within 15-60 minutes, death can occur quickly (within 15 minutes) or up to 8 hours after ingestion.
• Animals may be found dead with evidence of a violent terminal struggle.
• Recovery may take 4-5 days.

Epidemiology

• Cicuta poisoning in cattle occurs mainly in North America and Europe.