Veterinary Medicine - March 2008 - (Page 143)

Toxicology Brief PEER-REVIEWED hours to several days with or without treatment. Brunfelsia species poisoning does not seem to cause marked hematologic, serum chemistry, or pathologic changes in animals. TREATMENT 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) MECHANISM OF ACTION 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 tonicclonic 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 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. CONCLUSION Although there are only a few published reports of Brunfelsia species toxicosis in dogs, the information collected by the Do not give a cathartic if the animal already has diarrhea. 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 ASPCA APCC from 2001 to 2006 indicates that the number of cases is on the rise, probably because of the increased popularity and availability of Brunfelsia species in the United States. Clinical signs of Brunfelsia species toxicosis are usually observed within the ﬁrst few hours after exposure and mainly consist of CNS and gastrointestinal effects. Some CNS signs may be similar to those caused by strychnine. Treatment is aimed at decontamination, seizure control, and supportive care. Since Brunfelsia species toxicosis can cause potentially life-threatening effects, all exposures should be taken seriously and treated aggressively. REFERENCES 1. Burrows GE, Tyrl RJ. Brunfelsia L. In: Toxic plants of North America. Ames: Iowa State University Press, 2001;1107-1108. 2. Spainhour CB Jr, Fiske RA, Flory W, et al. A toxicological investigation of the garden shrub Brunfelsia calcyina var. oribunda (yesterdaytoday-and-tomorrow) in three species. J Vet Diagn Investi 1990;2(1):3-8. 3. Mason J, Khan SA, Gwaltney-Brant S. Toxicant exposures in small animals: recently recognized animal toxicants. In: Kirk RW, Bonagura JD, eds. Current veterinary therapy small animal practice (in press). 4. AnTox Database. Urbana, Ill: ASPCA Animal Poison Control Center, 2001-2006. 5. McBarron EJ, de Sarem W. Letter: Poisoning of dogs by the fruits of the garden shrub Brunfelsia bonodora. Aust Vet J 1975;51(5):280. 6. Neilson J, Burren V. Intoxication of two dogs by fruit of Brunfelsia australis. Aust Vet J 1983;60(12):378-380. 7. Banton MI, Jowett PL, Renegar KR, et al. Brunfelsia pauci ora (“yesterday, to-day and tomorrow”) poisoning in a dog. Vet Hum Toxicol 1989;31(5):496-497. DIAGNOSIS 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. VETERINARY MEDICINE March 2008 143

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Veterinary Medicine - March 2008

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