Angel’s Trumpet (Brugmansia Suaveolens)

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Definition

The angel’s trumpet (Brugmansia suaveolens) belongs to the nightshade family (Solanaceae) and is classified as highly toxic (+++) due to its high concentration of tropane alkaloids. These trumpet-shaped flowers, which are often cultivated in gardens as ornamental plants, pose a significant danger to our pets. The most important toxic substances in the angel’s trumpet are atropine, scopolamine, and hyoscyamine, which belong to the group of tropane alkaloids. These toxins are contained in all parts of the plant, with the highest concentrations found in seeds and flowers. Even the ingestion of small amounts can lead to serious poisoning symptoms in dogs and cats.

The most important facts at a glance

The angel’s trumpet (Brugmansia suaveolens) is one of the highly toxic plants and poses a significant danger to dogs and cats. The tropane alkaloids (atropine, scopolamine, hyoscyamine) it contains have an anticholinergic effect and lead to characteristic poisoning symptoms such as mydriasis, dry mucous membranes, tachycardia, neurological disorders, and in severe cases, Seizures and Respiratory paralysis.

The diagnosis is based on the medical history, the clinical picture, and supporting laboratory tests. Therapy includes decontamination measures, the administration of activated charcoal, specific antidote therapy with physostigmine in severe poisonings, and symptomatic measures to stabilize vital functions. With early and adequate treatment, the prognosis is favorable in most cases, while severe poisonings can be life-threatening.

Preventive measures such as removing toxic plants from the animals’ environment are crucial to avoid poisoning. Pet owners should be informed about the dangers of the angel’s trumpet and other toxic plants and should seek immediate veterinary help in case of poisoning.

Causes, development and progression

The angel’s trumpet shares its toxic properties with other nightshade plants such as Jimson weed (Datura), nightshade (Solanum), deadly nightshade (Atropa), scopolia (Scopolia), mandrake (Mandragora), and henbane (Hyoscamus). In all these plants, the poisoning mechanism is similar and is based on the anticholinergic effect of the tropane alkaloids they contain. The heart and nervous system are particularly damaged.
Initially, agitation and Seizures occur, followed later by movement disorders, Paralysis, and shortness of breath. Paralysis of the muscles in the gastrointestinal tract and urinary tract leads to constipation and difficulty urinating. In human medicine, the ingestion of just a few flowers or leaves is already considered toxic.

Poisoning by angel’s trumpet usually occurs through oral ingestion of plant parts. Dogs and cats may chew on or eat the plants out of curiosity or boredom. After oral ingestion, tropane alkaloids are rapidly and completely absorbed from the gastrointestinal tract and distributed throughout the body tissues. Excretion later occurs partially unchanged via the kidneys.

The risk of poisoning is particularly high during the flowering period of the angel’s trumpet from June to October, but can exist all year round if the plant is kept as a houseplant. While cats are less frequently affected due to their more selective eating habits, young, inexperienced dogs in particular tend to explore and eat plant parts. Animals with certain pre-existing conditions, especially of the heart or nervous system, also have an increased risk of serious complications from angel’s trumpet intoxication / poisoning.

The mechanism of action of tropane alkaloids is based on their ability to inhibit the action of the neurotransmitter acetylcholine. Atropine blocks the muscarinic acetylcholine receptors, leading to an inhibition of the parasympathetic nervous system. Scopolamine has a similar anticholinergic effect, but also has a strong depressant effect on the central nervous system and can trigger Seizures. Hyoscyamine, a form of atropine, also has a spasmolysis effect and leads to dilation of the pupils, but has stronger effects on the nervous system than atropine.

Mechanism of action

Atropine inhibits the action of the transmitter substance for nerve excitation between the nerve cell and other cells.
The name of the transmitter substance is acetylcholine. The effect is described as anticholinergic.
The anticholinergic effect is particularly noticeable in digestive processes (saliva secretion, tone in the gastrointestinal tract and gallbladder), the heart, and the CNS (central nervous system).
Scopolamine
Scopolamine has an anticholinergic effect like atropine. However, it has a strong depressant effect on the CNS (central nervous system) and leads to apathy. In some cases, Seizures are triggered.
Hyoscyamine
Hyoscyamine is a form of atropine. It also has a spasmolysis effect and, like atropine, leads to dilation of the pupils (mydriatic). It has less effect on the heart but leads to stronger effects on the nervous system.
When higher doses are absorbed, it initially has an excitatory effect on the CNS (central nervous system), leading up to Seizures.
In cases of severe intoxication / poisoning, muscle relaxation, a drop in body temperature, and ultimately a coma occur.
Death occurs through central Respiratory paralysis.
In humans, the LD is 50–100 mg.

The angel’s trumpet (genus Brugmansia) belongs to the nightshade family (Solanaceae) and contains highly potent tropane alkaloids. These alkaloids have a toxic effect on the central and peripheral nervous system and lead to severe poisoning in dogs and cats, even in small amounts.

The toxic active substances of the plant are:

  • Atropine
  • Scopolamine
  • Hyoscyamine

These substances are found in all parts of the plant, but are particularly concentrated in the seeds and flowers. Even a few grams of the plant can cause significant intoxication / poisoning.

Pharmacological mechanism of action

The mentioned tropane alkaloids are competitive antagonists at muscarinic acetylcholine receptors (mAChR) in the parasympathetic nervous system. This means:

  • They block the action of acetylcholine, one of the most important messenger substances of the autonomic nervous system.
  • This leads to an inhibition of parasympathetic reactions and thus to a predominance of sympathetic effects in the body.

Specifically, this means:

  • Dilation of the pupils (mydriasis)
  • Increased heart rate (tachycardia)
  • Inhibition of saliva and gastric juice secretion → dry mucous membranes
  • Reduced intestinal motility → constipation, Flatulence
  • Urinary retention due to detrusor relaxation
  • Stimulation of the central nervous system → Restlessness, Hallucinations, Convulsions

Scopolamine also has a strong central depressant effect and can lead to Disorientation, impaired consciousness, and coma. Atropine primarily has peripheral effects, but in toxic doses, it also has CNS (central nervous system) effects.

Specific effect in dogs

  • Dogs often show a mixture of central nervous system stimulation and vegetative disinhibition:
    • Restlessness, Nervousness, hallucinatory behavior
    • Dry mucous membranes, Panting, oversized pupils
    • Palpitations, circulatory instability
    • In severe cases: Seizures, coma, Respiratory paralysis

Specific effect in cats

  • Cats are particularly sensitive to tropane alkaloids, both peripherally and centrally:
    • Sudden behavioral changes, states of Agitation or apathy
    • hyperthermia due to lack of sweat secretion and central nervous decoupling of temperature regulation
    • Trembling, Coordination disorders, Muscle twitching
    • Seizures, collapse, respiratory depression

Cats also show signs of central nervous overstimulation more quickly, with visual Hallucinations (so-called “hunting flying insects”) and massive Disorientation.

Summary of the mechanism of action

System Toxic effect of tropane alkaloids
Central nervous system Agitation (atropine), depression (scopolamine), Hallucinations, Convulsions
Eyes Pupil dilation (mydriasis), sensitivity to light
Cardiovascular system tachycardia, increase or decrease in blood pressure, arrhythmias
Gastrointestinal tract Dry mouth, reduced gastrointestinal motility, constipation
Urogenital system Urinary retention due to detrusor inhibition
Temperature regulation hyperthermia due to central and peripheral inhibition of cholinergic pathways

Symptoms of intoxication

Saliva production decreased
Intestinal peristalsis inhibited (spasmolysis, intestinal sluggishness)
Urinary retention
Gallbladder tone reduced
Dilation of the pupils
tachycardia (increased heart rate)
Agitation
Disorientation
apathy
Seizures
Respiratory paralysis

The clinical signs of angel’s trumpet poisoning in dogs and cats can be very diverse and usually appear within 30 to 60 minutes after ingestion. The symptoms reflect the anticholinergic effect of the tropane alkaloids and affect several organ systems:

In the digestive tract, there is reduced saliva production with dry mucous membranes, inhibited intestinal peristalsis (spasmolysis), and resulting constipation. Reduced motility of the gastrointestinal tract can lead to Nausea and Vomiting, the latter usually occurring only at the beginning of the poisoning.

In the urogenital tract, the poisoning manifests as urinary retention due to reduced bladder contraction. The tone of the gallbladder is also reduced, which can lead to disturbances in bile metabolism.

The effects on the nervous system and the eyes are particularly characteristic. Affected animals show clear mydriasis (pupil dilation), which affects both eyes symmetrically and does not react to light. Paradoxical reactions can occur in the central nervous system: initially, animals often show states of Agitation, Restlessness, Disorientation, and Coordination disorders; later, apathy, Seizures, and finally unconsciousness may follow.

Cardiovascular symptoms include tachycardia (increased heart rate) and arrhythmias. The mucous membranes may appear pale or cyanotic due to circulatory changes. In severe cases, hyperthermia (increased body temperature) can occur because sweat production is inhibited and heat regulation is disturbed.

Respiratory problems manifest as shallow, rapid breathing, which can lead to central Respiratory paralysis as the poisoning progresses, ultimately being the cause of death.

Diagnosis

The diagnosis of angel’s trumpet poisoning is initially based on the medical history and the clinical picture. If the pet owner has observed their animal eating parts of an angel’s trumpet, or if typical plant remains are found in the vomit, this is an important diagnostic clue. The characteristic symptom pattern with mydriasis, dry mucous membranes, tachycardia, and neurological abnormalities supports the suspected diagnosis.

Laboratory tests can help assess the severity of the poisoning and identify complications. A complete blood count and blood chemistry should be performed to check liver and kidney function, as these organs are involved in the metabolism and elimination of toxins. Electrolyte imbalances, especially potassium and sodium changes, can occur and should be monitored.

An ECG is indicated if Cardiac arrhythmia is suspected and can show tachycardia, extrasystoles, or other arrhythmias. In severe cases, a blood gas analysis may be necessary to assess the acid-base balance and oxygen supply.

Direct detection of tropane alkaloids in the blood or urine is rarely available in routine diagnostics but can be performed in specialized laboratories. In practice, however, this detection is usually not necessary as therapy is symptom-oriented.

Differential diagnosis must consider other anticholinergic poisonings (e.g., by certain medications such as antihistamines or tricyclic antidepressants), as well as neurological diseases such as epilepsy or meningoencephalitis.

Therapeutic principles

The cholinesterase inhibitors physostigmine can be used as an antidote.
By inhibiting the breakdown of acetylcholine, physostigmine reverses the effect of atropine, so that more acetylcholine is available again and for a longer period of time.
Primary decontamination should take place as quickly as possible and consistently include all sensible measures.
These include inducing Vomiting, provided the animal is responsive and no Seizures are present, as well as gastric lavage.
Subsequently, activated charcoal should be given repeatedly. Increasing intestinal passage after the administration of activated charcoal accelerates elimination.
Secondary toxin elimination, i.e., the elimination of already absorbed toxins, is achieved by increasing urine formation through volume substitution and the use of special medications (forced diuresis).
Symptomatic therapy serves to stabilize vital functions and combat distressing symptoms such as Seizures, persistent Vomiting, or Pain.

The treatment of angel’s trumpet poisoning requires a rapid and comprehensive therapeutic approach. The primary measure is decontamination to prevent further absorption of the toxin. If ingestion occurred less than 1–2 hours ago and the animal is conscious and showing no Convulsions, inducing Vomiting by administering apomorphine (dog) or xylazine (cat) may be useful. Inducing Vomiting is contraindicated in animals with impaired consciousness or if Seizures are present.

Gastric lavage under anesthesia can be considered if inducing Vomiting was unsuccessful or is contraindicated. Following these measures, activated charcoal should be administered several times (1–4 g/kg body weight every 4–6 hours) to reduce the absorption of toxins still in the intestine. The administration of laxatives such as sodium sulfate accelerates intestinal passage and thus the excretion of toxins.

As a specific antidote in severe poisonings, the cholinesterase inhibitors physostigmine can be used, which can cross the blood-brain barrier and thus also antagonize central anticholinergic effects. The dosage is 0.02-0.06 mg/kg i.v. slowly. The effect begins within minutes but only lasts for about 1–2 hours, so repeated doses may be necessary. Physostigmine should be used with caution as it can itself have toxic effects, especially in case of overdose or in animals with heart disease.

Symptomatic therapy includes the stabilization of vital functions. For Seizures, benzodiazepines such as diazepam (0.5-2 mg/kg i.v.) or midazolam are used. Fluid therapy is important to promote the excretion of toxins via the kidneys (forced diuresis) and to stabilize the circulation. For hyperthermia, cooling measures are indicated.

Monitoring heart function using continuous ECG is recommended in severe poisonings. For arrhythmias, antiarrhythmics such as lidocaine or beta blockers may be used. Oxygen therapy should be performed in case of shortness of breath or cyanosis. In severe cases, mechanical ventilation may be required.

Prognosis & follow-up care

The prognosis of angel’s trumpet poisoning depends significantly on the amount of toxin ingested, the time until the start of therapy, and the intensity of the therapeutic measures. With early and adequate treatment, the prognosis is favorable in most cases. Animals that survive the first 24–48 hours after toxin ingestion have a good chance of full recovery without long-term damage.

In severe poisonings with pronounced neurological symptoms, especially if Seizures or unconsciousness have occurred, the prognosis should be more cautious. Complications such as aspiration pneumonia due to Vomiting, renal failure due to dehydration, or Cardiac arrhythmia can negatively influence the course of the disease.

Aftercare following a survived angel’s trumpet poisoning includes regular follow-up examinations to detect possible organ damage early. Mainly, kidney and liver function should be monitored through blood tests. An ECG may be useful to rule out latent Cardiac arrhythmia.

Pet owners should be informed that angel’s trumpet and other nightshade plants should be removed from the animals’ environment to avoid re-poisoning. Alternatives for garden design are non-toxic ornamental plants such as hibiscus, roses, or certain types of hydrangeas.

Research outlook

Research in the field of plant poisoning in pets is continuously evolving. Current studies focus on improving diagnostic methods for the rapid and reliable detection of tropane alkaloids in biological samples. New analytical procedures such as high-performance liquid chromatography coupled with mass spectrometry (HPLC-MS) allow for more precise quantification of toxins and could be used in routine veterinary diagnostics in the future.

Another research focus is the development of more specific antidotes with fewer side effects than the currently used cholinesterase inhibitors. Modified physostigmine derivatives or novel anticholinergic antagonists could enable safer and more effective treatment in the future.

Research into individual factors that influence sensitivity to tropane alkaloids is also gaining importance. Genetic differences in the metabolism of these substances could explain why some animals react more sensitively than others. These findings could lead to personalized treatment protocols tailored to the specific needs of the individual animal.

Finally, research is increasingly dedicated to developing training methods and deterrents to keep pets from eating toxic plants. Behavior modification techniques and natural repellents could play an important role in the prevention of plant poisonings in the future.

Frequently asked questions (FAQs)

  1. How quickly do the symptoms of Angel’s Trumpet poisoning appear in my pet?
    The first symptoms usually appear within 30–60 minutes after ingestion of the plant and can last up to 24–48 hours.
  2. What amounts of Angel’s Trumpet are toxic to my pet?
    Even small amounts can be toxic. In dogs, a few leaves or one flower can be enough to cause poisoning symptoms. Cats are even more sensitive due to their lower body weight.
  3. Are certain pets more susceptible to Angel’s Trumpet poisoning?
    Young, curious dogs are particularly at risk. Cats are less frequently affected due to their more selective eating habits, but can be poisoned just as well.
  4. Can my pet die from Angel’s Trumpet poisoning?
    Yes, untreated severe poisonings can lead to death through Respiratory paralysis. However, with timely veterinary treatment, the prognosis is usually good.
  5. How can I protect my pet from Angel’s Trumpet poisoning?
    The safest method is not to plant angel’s trumpets and other toxic plants in gardens to which pets have access. Alternatively, barriers can be erected or the animals can be supervised.
  6. Are there differences in the toxicity of different Angel’s Trumpet species?
    Yes, the content of tropane alkaloids can vary between different species and even between individual plants. However, all species of the genus Brugmansia are to be classified as highly toxic.
  7. Can poisoning symptoms also occur with a delay?
    The symptoms usually appear quickly, but some neurological symptoms may appear with a delay, especially if only small amounts were ingested initially.
  8. How long does it take to recover from Angel’s Trumpet poisoning?
    In mild to moderate poisonings, full recovery can take 2–3 days. In severe poisonings with organ damage, recovery can take several weeks.
  9. Are there long-term consequences after surviving poisoning?
    With adequate treatment, long-term consequences are rare. In severe cases, however, neurological damage or organ damage, mainly to the kidneys and liver, may remain.
  10. Is it possible for my pet to develop a tolerance to the toxins in Angel’s Trumpet?
    No, animals do not develop a tolerance to tropane alkaloids. Every new exposure can lead to poisoning, which may be more severe than the previous one.

Literature

Burrows, G. E. and Tyrl, R. J., 2013. Toxic Plants of North America. 2nd Edition. Hoboken: John Wiley & Sons.

  • Gwaltney-Brant, S. M., 2021. Plant Poisonings in Small Animals. Veterinary Clinics of North America: Small Animal Practice, 51(6), pages 1195–1212. Available at: https://doi.org/10.1016/j.cvsm.2021.06.005 [Accessed July 6, 2025].
  • Krenzelok, E. P. and Mrvos, R., 2021. Toxic plant ingestions in companion animals: A comprehensive review of prevention and management strategies. Journal of Veterinary Emergency and Critical Care, 31(2), pages 141–152. Available at: https://doi.org/10.1111/vec.13045 [Accessed July 6, 2025].
  • Löwe, G. and Löwe, O., 2021. Poisoning in dogs and cats – A veterinary Guides. 2nd Edition. Kreuztal: Kynos-Verlag. 208 pages.
  • Osweiler, G. D., 2011. Toxicology of Domestic Animals. Boca Raton: CRC Press.
  • Peterson, M. E. and Talcott, P. A., 2022. Small Animal Toxicology. 4th edition. St. Louis: Elsevier Health Sciences. ISBN 978-0323546331.
  • Plumlee, K. H., 2019. Clinical Veterinary Toxicology. 3rd Edition. St. Louis: Mosby Elsevier. ISBN 978-0323595391.