Toxicology Brief: Brunfelsia species: Beautiful but deadly - Veterinary Medicine
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Toxicology Brief: Brunfelsia species: Beautiful but deadly



Several biologically active compounds have been isolated from Brunfelsia species, although the exact toxins responsible for neurotoxicosis are unknown. The compound responsible for causing the clinical signs of toxicosis appears to be similar to a compound that interferes with neurotransmission such as that seen with strychnine toxicosis.

Two compounds that cause neurotoxicosis in mice or rats are hopeanine and brunfelsamidine.1 Hopeanine causes decreased activity, paralysis, seizures, and hypersensitivity, whereas brunfelsamidine produces excitement, tonic-clonic seizures, and death. It appears that brunfelsamidine may be the toxin responsible for neurotoxicosis in animals because of its ability to cause excitement and tonic-clonic seizures.1 According to one report, the unknown toxins isolated from B. calycina var. floribunda are water-soluble and highly stable, maintaining lethality for four months.2


A diagnosis of Brunfelsia species toxicosis in dogs is based on a history or evidence of exposure to the plant (flowers, leaves, berries, or seeds present in the vomitus or stool), an onset of clinical signs within hours after exposure, and the characteristic CNS signs (muscular rigidity, paddling, tonic-clonic seizures) and vomiting or diarrhea. The differential diagnoses should include toxicoses with strychnine, metaldehyde, methylxanthine, organochlorine pesticides, lead, or illicit drugs (e.g. amphetamines, cocaine) and infectious diseases such as canine distemper.


The main treatment objectives are decontamination, seizure control, and supportive care. If the animal has CNS signs, stabilize it (control seizures as described below) before starting decontamination or supportive care. In the case of a recent exposure (within two hours of ingestion) when no clinical signs are present, induce emesis with 3% hydrogen peroxide (1.5 ml/kg orally; repeat in 10 minutes if emesis does not occur after first dosing) or apomorphine (0.02 to 0.04 mg/kg intramuscularly or intravenously).

After emesis, administer activated charcoal (1 to 2 g/kg orally) mixed with a cathartic such as 70% sorbitol (1 to 2 ml/kg) or magnesium sulfate or sodium sulfate (250 mg/kg). Do not give a cathartic if the animal already has diarrhea. Repeated doses of charcoal (six to eight hours apart) can be useful if seeds or fruit have been ingested. If large amounts of seeds or berries have been consumed, consider gastric or enterogastric lavage followed by charcoal administration.

Control seizures with intravenous pentobarbital sodium (given to effect and repeated as needed) or with methocarbamol (100 to 200 mg/kg intravenously; maximum dose of 330 mg/kg/day). Intravenous propofol (4 to 6 mg/kg) or diazepam (1 to 2 mg/kg) may also be useful, although success varies with diazepam. If seizures are not controlled with the preceding treatment, administer isoflurane gas anesthesia. Severely affected animals may require intubation and artificial respiration.

Animals should be kept in a dark, quiet place. Monitor for hyperthermia or hypothermia, and treat as needed with cooling baths, fans, or heating pads. Monitor complete blood counts and serum chemistry profiles as needed. Intravenous fluid diuresis may be required for one or two days or longer. Complete recovery may take several days or weeks.


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