Laburnum (Laburnum Anagyroides, Laburnum X Watereri)
Laburnum (Laburnum anagyroides, Laburnum x watereri) is one of the most highly toxic ornamental plants in our gardens. This popular plant with its characteristic yellow flower clusters poses a significant danger to pets. All parts of the plant are toxic, with the seeds having the highest toxin content. The main active ingredient is the alkaloid cytisine, which is chemically similar to nicotine and acts on similar receptors in the body.
The toxicity of laburnum is classified as very high (+++). Even chewing a single branch or ingesting just three seeds can be life-threatening for a dog or cat. The LD50 (Lethal Dose 50) for subcutaneous injection is 3 mg/kg body weight for cats and 4 mg/kg body weight for dogs. These values highlight the extreme toxicity of this plant for our pets.
Laburnum is found as an ornamental shrub in many gardens and public areas. The plant blooms in spring with striking yellow flower clusters, which later mature into bean-like pods containing the poisonous seeds. There is an increased risk of poisoning for pets, especially during the flowering and seeding period (May to September).
The most important facts at a glance
Laburnum poisoning is a serious and potentially life-threatening condition for dogs and cats. All parts of the Laburnum plant contain the highly toxic alkaloid cytisine, with the seeds having the highest concentration. Even small amounts can cause severe poisoning symptoms.
Symptoms develop rapidly after ingestion and initially include gastrointestinal complaints such as vomiting and salivation, followed by neurological symptoms such as agitation, seizures, and, in severe cases, respiratory paralysis. The diagnosis is primarily based on the patient’s history and clinical presentation, supported by laboratory tests.
Therapy aims at removing the toxin through decontamination, stabilizing vital functions, and symptomatic treatment. No specific antidote exists. With early and adequate treatment, the prognosis is favorable, with the first 24–48 hours being crucial for the outcome.
Preventive measures such as removing Laburnum from gardens with pets or securely fencing off the plants are important to prevent poisoning cases. Pet owners should be informed about the dangers of Laburnum and seek immediate veterinary help if poisoning is suspected.
Causes, development and progression
Laburnum poisoning typically occurs through oral ingestion of plant parts. Dogs and cats may ingest parts of the laburnum for various reasons:
Cytisine acts on the central nervous system (CNS), particularly in the vomiting, vasomotor, and respiratory centers. It binds to nicotinic acetylcholine receptors, initially causing excitation and later paralysis of these systems. The mechanism of action explains the characteristic symptoms: initially, there is stimulation of the nervous system with states of excitement, followed by paralysis up to respiratory arrest.
The toxin is rapidly absorbed after oral ingestion, so the first signs of poisoning can appear as early as 15 minutes after ingestion. In the body, cytisine affects blood pressure, which increases due to both central stimulation of the vasomotor center and peripheral vasoconstrictive effects, along with the emptying of blood stores (spleen). Simultaneously, heart rate increases.
Young, curious animals are particularly at risk, as are dogs that generally tend to chew on plants. The risk of poisoning exists year-round, but is especially high during flowering and seed ripening.
Mechanism of action
Cytisine acts on the CNS, particularly in the vomiting, vasomotor (regulation of blood vessel diameter), and respiratory centers. It has an effect similar to nicotine, as it targets the same receptors. Initially, an excitatory effect dominates, followed by a paralyzing one.
Blood pressure is increased centrally via stimulation of the vasomotor center and peripherally via a vasoconstrictive effect with simultaneous emptying of blood stores (spleen). Heart rate also increases. The LD50, i.e., the dose that leads to death in 50% of cases, is 3 mg/kg body weight for cats and 4 mg/kg body weight for dogs when the toxin is injected subcutaneously.
Milk from grazing animals can also be toxic.
Supplements
1. Main Toxic Substances in Laburnum (Laburnum Spp.)
The toxicity of laburnum is due to the alkaloid cytisine, a highly potent neurotoxic quinolizidine alkaloid. Cytisine is chemically related to nicotine and primarily affects the central and peripheral nervous systems.
Particularly toxic are:
- Seeds (especially toxic!)
- Pods
- Flowers
- Leaves in lower concentration
2. Mechanism of Action of Cytisine
Cytisine acts as an agonist at nicotinic acetylcholine receptors (nAChRs) – both in the central nervous system and in the peripheral, especially at the neuromuscular junction.
A) Phase 1 – Stimulation (Nicotine-Like Effect)
- Cytisine mimics acetylcholine and binds to nicotinic receptors.
- This initially leads to overstimulation of ganglia and muscle fibers:
- Salivation, excitement, tremors
- Nausea, vomiting
- Muscle cramps, tachycardia
B) Phase 2 – Blockade Due to Continuous Stimulation
- Continuous stimulation leads to receptor desensitization → functional collapse.
- This causes a neuromuscular blockade:
- Muscle relaxation, movement disorders
- Bradycardia
- Respiratory paralysis
C) Central Effect
- In the brain, cytisine also acts via nicotinic receptors and can lead to restlessness, coordination disorders, seizures, or unconsciousness.
3. Clinical Manifestation in Dogs and Cats
Symptoms usually appear 1–3 hours after ingestion and can escalate rapidly depending on the amount.
Early Symptoms (Stimulating Phase):
- Salivation, vomiting, abdominal pain
- Restlessness, excitement
- Muscle tremors, tachycardia
Late Symptoms (Inhibitory Phase):
- Apathy, paralysis, ataxia
- Dyspnea up to respiratory paralysis
- Bradycardia, circulatory weakness
- Seizures, coma
In severe cases, death occurs due to respiratory arrest or cardiovascular failure.
4. Species-Specific Characteristics
- Dogs: Particularly at risk from eating fallen seeds or pods. Young dogs and puppies often show severe CNS and respiratory symptoms, as they are more sensitive to nicotine-like substances.
- Cats: Less frequently affected, as they are pickier eaters. Nevertheless, even a small amount of seeds is enough to trigger central nervous disorders, salivation, weakness, and respiratory depression. Cats often react very sensitively to neuromuscular blockade.
5. Summary of the Toxic Mechanism of Action
| Level of Action | Mechanism | Consequences |
| Nicotinic acetylcholine receptors | Agonistic continuous stimulation → desensitization | First excitation, then blockade of nerve signals |
| CNS | Effect via nicotinic receptors in the brain | Restlessness, seizures, central respiratory depression |
| Neuromuscular junction | Impaired signal transmission → paralysis | Weakness, ataxia, respiratory arrest |
| Autonomic nervous system | Ganglion stimulation, then blockade | Salivation, pupil dilation, circulatory problems |
Conclusion
Poisoning with common laburnum (Laburnum spp.) is potentially life-threatening in dogs and cats. The alkaloid cytisine it contains acts on nicotinic receptors, initially stimulating and then paralyzing – with dramatic consequences for the nervous, respiratory, and cardiovascular systems. Ingestion of seeds or pods is particularly dangerous, as even small amounts can be fatal. Immediate veterinary care is essential if poisoning is suspected.
Symptoms of intoxication
The toxin is rapidly absorbed, so toxic symptoms can appear as early as 15 minutes after ingestion.
It is also stated that this is possible after ingesting as few as three seeds.
The first symptoms are:
- Drooling
- Vomiting, prolonged, sometimes bloody
- Increased heart rate
- Dilated pupils
- States of excitation
With higher toxin levels in the blood, additional symptoms include:
- Anxiety
- Disorientation
- Shivering
- Ataxia
- Seizures
- Coma
- Shock (circulatory failure)
- Respiratory paralysis
The symptoms of laburnum poisoning develop rapidly after the plant is ingested. The first signs can appear as early as 15 minutes after ingestion. The course can be divided into early and advanced symptoms:
Early symptoms:
- Increased salivation (hypersalivation)
- Persistent, sometimes bloody vomiting
- Increased heart rate (tachycardia)
- Dilated pupils (mydriasis)
- States of excitement and restlessness
With higher toxin levels in the blood or progressive poisoning:
- Pronounced anxiety
- Disorientation and behavioral changes
- Muscle tremors and muscle stiffness
- Coordination disorders (ataxia)
- Seizures up to status epilepticus
- Impaired consciousness up to coma
- Circulatory collapse (shock)
- Respiratory paralysis with cyanosis (bluish discoloration of mucous membranes)
Supplements
The intensity of symptoms can vary depending on the amount ingested, the animal’s size, and its health status. Neurological symptoms and respiratory problems are particularly concerning, as they indicate severe poisoning and can be life-threatening.
In cats, symptoms may begin more subtly but often progress more rapidly to severe neurological disorders than in dogs. This is due to differences in toxin metabolism between species.
Diagnosis
The diagnosis of Laburnum poisoning is primarily based on the patient’s history and clinical presentation. Crucial is the evidence or reasonable suspicion that the animal had access to Laburnum and may have ingested plant parts.
The diagnostic process includes:
A thorough history taking with targeted questions about access to Laburnum or other poisonous plants is essential. Pet owners should be asked if they observed their animal chewing on the plant or if plant parts were visible in the vomit. The chronological sequence of symptoms also provides important diagnostic clues.
Clinical examination often reveals tachycardia, hypersalivation, mydriasis, and neurological abnormalities. The combination of gastrointestinal and neurological symptoms is characteristic of Laburnum poisoning.
Laboratory tests can be used supportively. A complete blood count with differential, electrolytes, kidney and liver values, and blood gas analysis help assess the severity of the poisoning and any potential organ damage. Direct detection of cytisine in blood or urine is rarely available in practice but can be performed in specialized laboratories.
The differential diagnosis includes other poisonings with similar symptom profiles (e.g., nicotine, strychnine, organophosphates), neurological diseases, and metabolic disorders. These must be ruled out, especially if no clear exposure to Laburnum can be proven.
In unclear cases, the identification of plant residues in vomit or stomach contents by a botanist or toxicological analysis of stomach contents can be helpful.
Therapeutic principles
There is no antidote.
The measures to be taken depend on the patient’s condition.
In life-threatening situations, securing vital functions such as respiration and circulation is paramount. Artificial ventilation may be necessary in some cases.
Decontamination of fur and skin is indicated if seed pods or other plant parts are still present in the fur.
The stomach and intestines should be emptied, and activated charcoal should then be administered.
The safest method of decontamination is gastric lavage, which, however, should only be performed under the necessary safety measures such as intubation.
Gastric lavage is also useful after previous vomiting and without a time limit.
Further symptomatic therapy consists of substitutions in water, electrolyte, and acid-base balance, depending on current laboratory findings. Antispasmodic medications are sometimes necessary.
Kidney function should be stimulated.
Supplements
The treatment of laburnum poisoning requires rapid action and primarily aims at toxin removal, vital function support, and symptomatic therapy. No specific antidote exists.
Therapeutic measures include:
- Stabilization of vital functions: In life-threatening situations, securing respiration and circulation is paramount. Artificial ventilation may be necessary in cases of respiratory paralysis. Intravenous fluid therapy supports circulation and promotes toxin excretion.
- Decontamination: If plant parts adhere to the fur, they should be carefully removed. If ingestion occurred recently (within 1–2 hours) and the patient is stable without neurological symptoms, vomiting can be induced. However, this should only be done by a veterinarian, as there is a risk of aspiration if consciousness is already impaired.
- Gastric lavage: The safest method of decontamination is gastric lavage under intubation protection. This is also useful after previous vomiting and without a strict time limit, as plant parts can remain in the stomach for longer.
- Adsorbents: After gastric emptying, activated charcoal (1–4 g/kg body weight) is administered to bind unabsorbed toxin. Administration can be repeated every 4–6 hours.
- Symptomatic therapy:
- Anticonvulsants for seizures (e.g., diazepam, phenobarbital)
- Thermoregulation for hyper- or hypothermia
- Oxygen administration for respiratory distress
- Heart rate and blood pressure management as needed
- Correction of electrolyte and acid-base balance
- Intensive care monitoring: Continuous monitoring of heart rate, respiratory rate, blood pressure, body temperature, and neurological status is essential. Regular laboratory checks help assess treatment success and detect complications early.
- Fluid therapy: Intravenous fluid administration supports kidney function and promotes toxin excretion. Electrolytes and buffers are supplemented as needed based on laboratory findings.
Therapy must be individually adapted to the patient’s condition and often requires hospitalization with intensive care for 24–48 hours.
Prognosis & follow-up care
Laburnum intoxications can be potentially fatal.
Since one of the main effects of laburnum toxin is centrally induced vomiting, any remaining plant parts may be expelled even before therapeutic measures are initiated.
The prognosis is good.
The prognosis of laburnum poisoning largely depends on the amount of toxin ingested, the time until treatment begins, and the animal’s individual health status.
With early and adequate treatment, the prognosis is generally favorable. A positive factor is that the toxin cytisine causes centrally induced vomiting, which means that plant parts may be expelled even before therapeutic measures begin.
Animals that survive the acute phase of poisoning (24–48 hours) have a good chance of full recovery without long-term consequences. However, in severe poisonings with prolonged seizures or prolonged hypoxia, neurological sequelae may remain.
Aftercare includes:
- Regular monitoring of organ functions (especially liver and kidneys) through laboratory tests
- Dietary adjustments for persistent gastrointestinal symptoms
- Neurological follow-up examinations for patients with central nervous symptoms
- Monitoring of heart function using ECG in patients with cardiovascular complications
For pet owners, comprehensive education on preventive measures is helpful. This includes, in particular, the recommendation to remove laburnum from gardens with pets or to safely prevent pets’ access to these plants.
For animals that have survived severe poisoning, a rehabilitation phase with adapted exercise and, if necessary, physiotherapeutic support may be necessary to promote full recovery.
Research outlook
Research into plant poisonings in small animals has gained increasing importance in recent years. In the field of Laburnum poisoning, current studies focus on several aspects:
New insights into the toxicokinetics of cytisine enable a better understanding of the toxin’s absorption, distribution, and excretion in the animal body. Current research investigates species-specific differences in metabolism that could explain why cats react more sensitively to cytisine than dogs. These findings could lead to more targeted therapeutic approaches.
In the field of diagnostics, more sensitive and faster detection methods for cytisine are being developed. Point-of-care tests could enable rapid confirmation of poisoning directly in veterinary practice in the future, thus accelerating diagnosis.
Therapeutically, work is being done on improved treatment protocols. Studies on the optimal dosage and duration of activated charcoal application, as well as the efficacy of newer adsorbents, are currently underway. The development of specific antagonists for nicotinic acetylcholine receptors could also enable more targeted therapy in the future.
The epidemiology of plant poisonings is being increasingly systematically recorded. International animal poison control centers collect data on the frequency, seasonal fluctuations, and regional differences in Laburnum poisonings. This data helps identify risk groups and implement preventive measures more effectively.
Another research focus is on the development of biomarkers that enable early detection of organ damage and can thus contribute to prognostic assessment. Specific markers are being evaluated, particularly for kidney and liver damage.
Interdisciplinary collaboration between veterinarians, toxicologists, and botanists is intensifying to expand knowledge about plant poisonings and integrate it into clinical practice.
Frequently asked questions (FAQs)
Literature
- Bäumer, W. (2008). Intoxications by ornamental plants in dogs and cats. Leipziger Blaue Hefte, 202.
- http://www.toxcenter.org/stoff-infos/c/cytisin.pdf
- GWALTNEY-BRANT, S.M. Plants. In: PETERSON, M.E., TALCOTT, P.A. Small Animal Toxicology. 3rd ed. St. Louis: Elsevier, 2013, p. 499-548. ISBN 978-1-4557-0717-1.
- KOVALKOVIČOVÁ, N., ŠUTIAKOVÁ, I., PISTL, J., ŠUTIAK, V. Some food toxic for pets. Interdisciplinary Toxicology, 2019, 12(3): 93-99. DOI: 10.2478/intox-2019-0012.
- MEROLA, V., DUNAYER, E. The 10 most common toxicoses in cats. Veterinary Medicine, 2018, 113(8): 34-43.
- Löwe G, Löwe O. Poisoning in Dogs and Cats – A Veterinary Guide. 2nd edition. Kreuztal: Kynos-Verlag. 2021; 208 p.