Poisoning occurs as horses eat small seedlings when other forage is unavailable. Poison hemlock is toxic when included in
fresh forages or hay, but the toxin degrades with time under most storage conditions.
The toxins have been identified as piperidine alkaloids, gamma conicine, conine and n-methyl conine. Horses can be poisoned
by eating as little as 0.25 percent of their body weight.
Signs are those of CNS stimulation, followed by depression. They include muscle tremors, ataxia, excessive salivation, frequent
defecation, excessive urination, abdominal pain, increased respiratory rates, weakness leading to muscular paralysis, recumbence
and death. Most horses that survive a couple hours post ingestion will recover. As some piperidine alkaloids are teratogenic,
there is a potential for birth defects when pregnant mares eat poison hemlock.
No antidotes are known. However, most animals become ill before they ingest a fatal dose. Consequently, most recover if they
are allowed to clear the toxin; all signs of poisoning will resolve in one to two days.
5 Datura spp. (Jimsonweed, Photo 4).
Jimsonweed is an invasive weed containing the toxic tropane alkaloids atropine and scopolamine. The highest toxin concentrations
are found in the seeds that often contaminate prepared feeds and grains. As little as 0.5 percent contamination in hay can
be lethal and even lower contamination of grain has been linked to equine colic.
Photo 4: Datura spp. (Jimsonweed) is an erect, branching annual that is 1 m to 2 m tall. The large leaves are simple, alternate
with large-toothed margins. The flowers are large, white and funnel-shaped (6 cm to10 cm). The spine covered seed capsule
easily splits, releasing small brownish-black, kidney-shaped seeds that often contaminate harvested grains. Jimsonweed is
found in disturbed areas, such as corrals, roadsides and field edges.
Jimsonweed exposure also is problematic for the racing industry, as these toxins are easily detected by the routine racetrack
Clinical signs include anorexia, weight loss, rapid heart and respiratory rates, dilation of pupils, excessive thirst and
urination, sweating, severe gastrointestinal atony and abdominal pain.
Lesions are variable and mostly related to the cause of colic (obstructive, entrapment or some volvulus resulting in vascular
compromise). Most diagnoses are made by identifying the alkaloids in serum or ingesta, or finding the seeds or plant in the
6. Pteridium aquilinum (brakenfern, Photo 5).
Brakenfern usually is not eaten by horses, but they will eat it when they have inadequate forage or when it is included in
Photo 5: Pteridium aquilinum (brakenfern) is found throughout the world in moist, open woodlands. It expands with fire and
disturbances. It is a perennial fern and its branching root system can extend for several meters to dominate areas with dense
monocultures. The leaves arise from the rhizome up to 2 m high, forming large, triangular, bipinnately compound fronds. The
underside of the leaf is haired with prominent brown spores around the leaf edges in late summer.
Brakenfern contains several toxins, including a carcinogen, but in horses the primary toxin is a thiaminase. This enzyme breaks
down thiamine, vitamin B1, causing neurologic disease.
Another toxic plant (Equisetum spp or horsetail) contains similar thiaminases and produces similar disease.
Clinical signs require one to two months of exposure to develop and, once initiated, they become markedly worse over two to
three days. Changes include weight loss, incoordination, excessive staggers, wide base stance with arched back, muscle tremors,
recumbency, inability to rise and other injuries related to struggling.
Some horses may live for up to 10 days without treatment, but treatment is essential if the disease is going to be reversed.
Sometimes the clinical signs and subsequent disease develop after the horse is removed from the brakenfern source.