Treatment includes the use of activated charcoal and cathartics to prevent absorption and reduce exposure. As myocardial lesions
are likely to cause permanent damage, preventing exposure is essential.
Photo 2a: Nerium oleander (oleander) is one of the many toxic plants that contains cardioglycosides. It is a Mediterranean
plant that has become naturalized in many warmer climates. It is most often used as a drought-tolerant ornamental hedge along
roads and gardens. It is an evergreen perennial that grows 2 to 6 m. The leaves are simple oblong to lanceolate, with prominent
midrib and secondary veins. Most oleander poisonings occur when clippings are discarded into paddocks. Photo 2b: Adonis aestavalis
(pheasant's eye) also contains cardioglycosides. It was introduced from Eurasia and has escaped cultivation in many parts
of North America. It is glabrous, 10 to 20 cm tall, with simple or branched stems. The leaves are 2 to 6 cm long with narrow
segments and the flowers are reddish-orange. As an invading weed, it grows in disturbed sites in pastures and fields. When
harvested with forage, it contaminates prepared feeds.
Cardiac glycoside-containing plants
Nerium oleander (oleander — Photo 2a)
Digitalis spp. (foxglove)
Apocynum spp. (dogbane)
spp. (Western azalea, white laurel, California rose bay, rose bay, great laurel azalea, smooth azalea, purple azalea, flame-colored
azalea, rhodora, Lapland rose bay — 250 species are toxic, many are U.S. natives.)
Kalmia angustifolia, K. latifolia, K. polifolia (Lambkill, sheepkill, calfkill, dwarf laurel, wicky, mountain laurel, calico bush, ivy bush, pale laurel, bog laurel)
Asclepias spp. (milkweeds)
Adonis aestavalis (pheasant's eye — Photo 2b)
- Others (Pieris spp. — andromeda and pieris, Ledum spp. — wild rosemary)
As cardiac glycoside-containing plants are relatively common, this list is incomplete. The preceding are examples of those
likely to poison horses in North America. Most are ornamentals that are used in residential landscaping and as hedges. They
rarely are eaten fresh; however, livestock, including horses, generally will eat the clippings or prunings. Others can escape
cultivation and may invade fields and pastures. They remain toxic when they are included in hay and prepared feeds.
Most contain mixtures of toxins, including cardiac glycosides that are similar to digoxin. Toxicity varies according to the
glycoside, with highly toxic oleandrin, andromedotoxin or grayanotoxin causing poisoning at doses as low as 0.2 percent of
body weight. All these glycosides alter membrane sodium/potassium channels and calcium homeostasis, with toxicity generally
resulting in A-V block and ventricular fibrillation.
Initial signs of poisoning that occur hours after ingestion include GI upset, salivation, anorexia, frequent defecation, diarrhea,
colic, depression, weakness, incoordination, stupor, leg paralysis, weak heart rate, recumbence, coma and death.
With high doses, animals may quickly die without developing the classic microscopic lesions. Lower doses, when the initial
myocardial necrosis is non-fatal, nearly always produce microscopic heart lesions (myocardial necrosis, fibrosis and regeneration).
Heart damage may lead to congestive heart failure (stocking up, ventral edema, jugular pulse, etc.). Little is known of possible
sequelae of poisoning but sub-lethally poisoned animals are likely to have impaired endurance and performance.
Treatment is limited and generally related to minimizing absorption or enhancing transient through the gastrointestinal tract
(activated charcoal and cathartics). Immunologic antidotes used in small animals are very expensive and have not been recommended
for use in horses. Care should be taken to avoid exposing horses to these plants and their clippings.