Kalmia poliifolia
Ericaceae
Bog Laurel; Pale Laurel; Bog Kalmia; Swamp Laurel; Pale Kalmia; Kalmia; Kalmia poliifolia
Grayanotoxins, also known as andromedotoxin, acetylandromedol, rhodotoxin, and asebotoxin; arbutin glucoside and related Ericaceae glycosides. All parts of the plant should be treated as potentially poisonous, especially the foliage, flowers, nectar, and young growth.
Dose-dependent signs may include burning or irritation of the mouth, excessive salivation, drooling, perspiration of the nose or foot pads, vomiting, diarrhea, dizziness, weakness, twitching, impaired vision, depression, dyspnea, prostration, low blood pressure, sinus bradycardia, and paresthesia or a tickling, tingling, burning, pricking, or numb sensation around the mouth or extremities. If large amounts are consumed, signs may include total loss of coordination, severe and progressive muscular weakness, severe bradycardia, paradoxical ventricular tachycardia, nodal rhythm, atrioventricular block, Wolff-Parkinson-White-type rhythm disturbance, coma, cardiovascular collapse, and possibly death.
The primary toxic principle in Bog Laurel, Kalmia poliifolia, is grayanotoxin, also known as andromedotoxin, acetylandromedol, rhodotoxin, and asebotoxin. Grayanotoxins are neurotoxic diterpenoid compounds found in a variety of plants in the family Ericaceae, including Rhododendron species such as rhododendrons and azaleas, Kalmia angustifolia, or Sheep Laurel, Kalmia latifolia, or Mountain Laurel, Kalmia poliifolia, or Bog Laurel, and Pieris species, commonly known as Andromeda.
Bog Laurel, also known as Pale Laurel or Bog Kalmia, is associated with wet, acidic, boggy, or peaty environments where it may grow among other Ericaceae shrubs. This makes it a greater concern for grazing animals, browsing animals, and pets that have access to wetland edges, bog margins, damp woodland openings, acidic shrublands, or ornamental plantings that include laurel-type species. As with other grayanotoxin-containing plants, the foliage and flowers are of particular concern, but all parts of the plant should be treated as potentially poisonous.
Grayanotoxin may also be found in honey made from the nectar of these plants. This is the source of the historically famous “mad honey” poisonings, in which honey produced from grayanotoxin-containing nectar caused intoxication in humans and animals. The first recorded poisoning involving grayanotoxin comes from the Greek professional soldier and writer Xenophon. In his most famous work, Anabasis, he describes the effects of tainted honey on the army of Cyrus the Younger during the unsuccessful attempt to overthrow Artaxerxes II in 401 to 400 B.C.:
“The number of bee hives was extraordinary, and all of the soldiers that ate of the honey combs lost their senses, vomited and were affected with purging, and none of them was able to stand upright; such as had eaten only a little were like men greatly intoxicated, and such as had eaten much were like mad men and some like persons at the point of death. They lay upon the ground, in consequence, in great numbers, as if there had been a defeat; and there was general dejection. The next day, no one of them was found dead; and they recovered their senses about the same hour they had lost them on the preceding day.”
The mechanism of grayanotoxin poisoning is well described in toxicologic literature. Grayanotoxins work by binding to sodium channels in cell membranes, particularly at a receptor site associated with voltage-dependent activation and inactivation. By preventing inactivation of these channels, grayanotoxins keep excitable cells, including nerve and muscle cells, in a state of depolarization. In practical terms, this means that the normal electrical reset function of the cell is disrupted, leaving affected nerves and muscles abnormally excited.
The U.S. Food and Drug Administration Center for Food Safety and Applied Nutrition described the mechanism as follows in Foodborne Pathogenic Microorganisms and Natural Toxins:
“Grayanotoxins work by binding to sodium channels in cell membranes. The binding unit is the group II receptor site, localized on a region of the sodium channel that is involved in the voltage-dependent activation and inactivation. These compounds prevent inactivation; thus, excitable cells (nerve and muscle) are maintained in a state of depolarization, during which entry of calcium into the cells may be facilitated. This action is similar to that exerted by the alkaloids of veratrum and aconite. All of the observed responses of skeletal and heart muscles, nerves, and the central nervous system are related to the membrane effects.”
In layman’s terms, grayanotoxins disrupt the natural electrical current present in cells, preventing those cells from returning to normal after firing. The result is a toxic effect on nerves, skeletal muscle, heart muscle, and the central nervous system. This explains why grayanotoxin poisoning can produce both gastrointestinal signs, such as vomiting and diarrhea, and more dangerous cardiovascular signs, such as low blood pressure, slow heart rate, heart block, rhythm disturbance, collapse, coma, and death.
Symptoms of poisoning occur after a dose-dependent latent period that may range from a few minutes to two or more hours. When plants containing grayanotoxins are ingested, blood pressure may begin to drop, which can lead to dizziness, weakness, vomiting, diarrhea, tremors, heart disturbances, and breathing problems. If a large amount of the plant is consumed, such as may occur when cattle, horses, goats, or sheep are allowed to graze in areas containing plants known to contain grayanotoxins, convulsions, coma, and death may result.
All parts of the plant are poisonous, especially the foliage, and contain glycosides including andromedotoxin. Andromedotoxin can burn or irritate the mouth, which tends to discourage many animals from consuming dangerous quantities. As a result, plants containing andromedotoxins are often not highly palatable to horses unless they are hungry or the plant is the only available food source. Cattle, goats, and sheep tend to be more at risk because they are less selective about what they ingest and may readily eat the leaves or flowers of laurel-type Ericaceae plants when accessible.
In order for serious clinical signs to develop, an animal may generally need to ingest a meaningful quantity of green leaves, flowers, or stems containing grayanotoxins, although the amount required can vary substantially depending on plant species, toxin concentration, growing conditions, animal species, body size, and health of the animal. Toxic-dose estimates reported for grayanotoxin-containing plants vary, with Rhododendron and Kalmia not necessarily sharing the same threshold. For that reason, any numerical estimate should be treated only as a rough toxicologic reference point, not as a safety line. Any amount could pose a potentially serious problem in a small, sensitive, medically fragile, or heavily exposed animal.
Exercise common sense and keep hungry livestock away from areas where these plants are known to grow. If a pet is prone to chewing plants, browsing shrubs, or grazing the backyard for roughage, prevent access to Bog Laurel, Mountain Laurel, Sheep Laurel, rhododendron, azalea, Andromeda, and other related grayanotoxin-containing plants.
Immediate Response to Bog Laurel Ingestion
- Remove the Source: Prevent further ingestion by removing the animal from the plant, pasture, bog margin, shrub, clippings, leaves, flowers, nectar source, honey source, or any area containing Bog Laurel or related grayanotoxin-containing plants.
- Remove Plant Material from the Mouth: If the animal is witnessed eating the plant, or if identifiable plant matter is found in the mouth, remove visible plant material and flush the mouth thoroughly with water.
- Identify the Exposure: Determine whether the animal ate leaves, flowers, stems, nectar, honey, clippings, or unknown plant material. Foliage and flowers are especially important exposure sources, and any suspected ingestion should be treated seriously.
- Watch for Early Signs: Burning or irritation of the mouth, excessive salivation, drooling, vomiting, diarrhea, dizziness, weakness, twitching, perspiration of the nose or foot pads, and impaired vision may appear within minutes to a few hours.
- Watch for Cardiac or Severe Signs: Low blood pressure, slow heart rate, irregular rhythm, severe weakness, loss of coordination, collapse, dyspnea, coma, or cardiovascular collapse should be treated as emergency signs.
- Contact Veterinary Help Immediately: Consult a veterinarian, emergency veterinary clinic, ASPCA Animal Poison Control, or Pet Poison Helpline promptly if ingestion is suspected, if any symptoms are present, if the amount is unknown, or if the exposed animal is a cat, dog, horse, goat, sheep, cow, small animal, young animal, elderly animal, pregnant animal, or medically fragile animal.
Inducing Vomiting and Decontamination
- Getting Plant Material Out Matters: If a dog has recently swallowed Bog Laurel, removing remaining plant material from the stomach may reduce continued exposure to grayanotoxins. In appropriate dog exposures, vomiting may be one of the least disruptive ways to remove recently ingested leaves or flowers before additional toxin is absorbed.
- Inducing Vomiting in Dogs Only: If ingestion was very recent and the dog is alert, breathing normally, able to swallow, and not showing weakness, collapse, slow heart rate, abnormal rhythm, severe depression, tremors, repeated vomiting, breathing difficulty, or neurologic signs, a veterinarian or animal poison-control professional may recommend inducing vomiting with fresh 3% hydrogen peroxide.
- Cat Warning: Hydrogen peroxide should not be used to induce vomiting in cats unless a veterinarian specifically directs it. Cats are more prone to irritation and complications from hydrogen peroxide, and home vomiting attempts may create more risk than benefit.
- Do Not Induce Vomiting in an Unstable Animal: Vomiting should not be attempted in any animal that is weak, collapsed, sedated, having trouble breathing, unable to swallow normally, already vomiting repeatedly, showing neurologic signs, or showing cardiac signs such as slow heart rate or abnormal rhythm.
- Veterinary Decontamination: When a large amount has been ingested, gastric lavage and activated charcoal may be considered by a veterinarian depending on the timing, amount, species, and clinical signs.
- Repeated Activated Charcoal: In cases involving large ingestions, activated charcoal may be administered repeatedly during the first day under veterinary direction to reduce ongoing absorption or reabsorption of toxin.
Cardiac, Respiratory, and Supportive Treatment
- Supportive Care: Symptomatic and supportive therapy is the primary treatment because there is no simple household antidote for grayanotoxin poisoning.
- Fluid Replacement: Fluid replacement therapy may be necessary to support blood pressure, correct dehydration, and assist recovery from vomiting, diarrhea, or hypotension.
- Respiratory Support: Animals with dyspnea, air hunger, rapid shallow breathing, aspiration risk, severe weakness, or prostration may require respiratory support and close monitoring.
- Bradycardia Treatment: For severe bradycardia, atropine is commonly recommended under veterinary supervision.
- Heart Block and Rhythm Support: Sodium channel blockers, such as quinidine, or isoproterenol may be used by a veterinarian to treat heart block or significant rhythm disturbances when clinically appropriate.
- Aspiration Pneumonia: Aspiration pneumonia can develop secondary to vomiting if food, liquids, vomit, or fluids from the mouth are inhaled into the lungs or airways. Animals with coughing, labored breathing, fever, or worsening respiratory signs after vomiting should be evaluated by a veterinarian.
Livestock and Grazing Animal Management
- Remove from Pasture: Grazing animals should be removed from areas containing Bog Laurel, Mountain Laurel, Sheep Laurel, rhododendron, azalea, Andromeda, or related Ericaceae plants.
- Prevent Hungry Grazing: Hungry livestock are more likely to consume unpalatable toxic plants when desirable forage is unavailable, sparse, or inaccessible.
- Monitor for Bloat: Ruminant animals may bloat after significant ingestion and should be monitored closely for abdominal distension, discomfort, prostration, or worsening systemic signs.
- Inspect Clippings and Brush: Do not throw ornamental shrub clippings into livestock areas, and remove pruned Ericaceae material from areas accessible to animals.
Prognosis and Recovery
- Small Ingestions: Grayanotoxins are metabolized and excreted relatively rapidly, so animals that consume only a small amount may begin to improve within hours. Heart rate and blood pressure may return to normal within 2 to 9 hours, and full recovery may occur within 24 hours in mild cases.
- Large Ingestions: If larger amounts are ingested, dyspnea, depression, prostration, severe weakness, cardiac disturbance, coma, or death may occur within 1 to 2 days.
- Guarded Severe Cases: In severe cases, prognosis is guarded because the animal may improve with treatment or may become comatose and die despite supportive care.
- Primary Dangers: Bradycardia, hypotension caused by vasodilation, atrioventricular block, aspiration pneumonia, respiratory compromise, and cardiovascular collapse are among the most serious complications.
- Prevention: Prevent further ingestion of the plant and keep pets and livestock away from Bog Laurel and related grayanotoxin-containing plants. Consult a veterinarian promptly whenever exposure is suspected.