Kiss-me-quick

Brunfelsia is a genus of about 50 species of plant to include Yesterday, Today, Tomorrow; Kiss-Me-Quick; Lady-of-the-Night; Fransiscan Rain Tree and Morning-Noon-and-Night. This genus falls into the family Solanaceae whose more toxic members include Deadly Nightshade, Mandrake, and Jimson’s weed; as well as some better known less toxic and non toxic members like potato, tomato, and eggplant. Brunfelsia can typically be found in lightly wooded areas, thickets and as an ornamental shrub around the home. The leaves are simple and alternate, with shapes generally elliptic to ovate. The flowers are large and tubular, with five broad petals.

Toxicologic studies performed with members of this genus have demonstrated that all parts of the plant are toxic, but unequally so. The leaves, flowers and stems appear to be the least toxic, whereas the berries are the most. Poisonings related to Brunfelsia are extremely rare and very few could be found in the literature. The best documentation regarding Brunfelsia related intoxication comes from A toxicological investigation of the garden shrub Brunfelsia calcyina var. floribunda (yesterday-today-and-tomorrow) in three species, by Charles B. Spainhour, Jr., Robert A. Fiske, Wayne Flory, and John C. Reagor:

“In January 1989, a case of acute death of an 11-wk-old intact female Schipperkee was submitted to the Texas Veterinary Medical Diagnostic Laboratory. The local veterinarian reported that the client presented the dog to him with a complaint of an acute onset of anxiety, persistent sneezing, vomiting, moderate to severe whole body muscle tremors, and pyrexia (40.7 C). The physical status of the animal progressively worsened over a 2-hr period, culminating in a state of severe disorientation, staggering, ataxia, proprioceptive deficits, an inability to right itself, and seizures. The vomitus and loose stool contained numerous small dark brown seeds and intact medium green spherical, firm seed pods. The vaccination history was current and there was known, suspected, or possible exposure to any heavy metal, insecticide, pesticide, herbicide, or methylxanthine. The remarked that the puppy was seen eating mulch around bushesin the owner’s back yard approximately 2 hr prior to the first noted presentation of clinical signs. Treatment by the local veterinarian included Valium, prednisolone, and activated charcoal. hematoxylin and eosin (HE) by standard methods.

“There are only 2 reports in the literature of the intoxication of a canine by Brunfelsia spp. All of these reports originate from Australia and involve Brunfelsia australis (formerly known as Brunfelsia bonodora). Although Brunfelsia calcyina is known to grow in New South Wales, it does not set fruit in that climate, and its toxicity has not been definitively established. This paper reports the first intoxication of a canine with Brunfelsia calcyina and is the first documented intoxication of Brunfelsia spp. in the Western Hemisphere. In the Australian reports, 1 dog showed clinical signs of gastric and buccal irritation, nystagmus, salivation, vomition, nervous irritation, extensor rigidity, and opisthotonous, but recovered with treatment in 2 days. Another dog died within 10 hours after ingestion of berries after exhibiting vomition, dementia, and severe hematuria. An experimental dog fed 5.4 g/kg of body weight of minced Brunfelsia showed depression, antisocial behavior, vomition, diarrhea, reluctance to stand, decreased motor activity, generalized fine muscle tremors, polyuria, involuntary rhythmic limb extension, convulsions, and opisthotonous. The animal was euthanized at 40 hours post dosing. Gross necropsy revealed only edema and hyperemia of the terminal ileum. Histopathologic findings were not specific.”

Another documented U.S. case, involved a 6-year-old female Siberian husky that was presented to her local veterinarian for evaluation with the clinical signs of salivation, coughing, gagging, dilated pupils, muscular contractions, horizontal involuntary eye movement, and clonic-tonic convulsions (formerly known as grand mal seizures) after eating Yesterday-today-and-tomorrow (B. pauciflora) seeds. The dog was provided symptomatic and supportive care that included activated charcoal, intravenous fluids, anticonvulsants (pentobarbital or primidone), corticosteroids, and a topical ophthalmic ointment. On the fifth day the convulsions stopped, and by the three week mark the dog had completely recovered.

The toxins in Brunfelsia spp. preparations have not been completely characterized. However, the biodynamic compounds of Brunfelsia spp. could very well be tropane alkaloids, as these are common to plants in the Solanaceae family. Laboratory tests on Brunfelsia spp. have identified the following chemicals in varying concentrations throughout the plant: aesculetin, alpha-ionone, alpha-terpineol, benzylbenzoate, benzylsalicylate, beta-bisabolene, beta-cyclocitralbrunfelsene, beta-damascenone, beta-eudesmol, beta-safranal, brunfelsene, brunfelsamidine, elemol, 2-ethylfuran, farnesol, farnesyl, geraniol, geranyl hopeanine, ionones, isobutylsalicylate, lavandulal, limonene, linalool, linoleic acid, linolenic acid, manaceine, manacine, mandragorine, methylfurans, methylanisoles, myrcene, myristic acid, n-decane, n-heneicosane, n-heptadecane, n-heptane, n-hexadecane, nerolidol, n-nonadecane, nonanes, n-octane, n-pentacosane, n-pentadecane, neophytadiene, n-tricosane, ocimene, pentadecanoic acid, palmitic acid, pinoresinols, salicylic acid esters, scopoletin, scopolin, and terpinolene.

Of these the exact toxic principle of Brunfelsia that causes severe and potentially fatal toxicosis is not known, only that it affects the body by interfering with neurotransmission in a way that is similar to strychnine toxicosis. In studies involving rats and mice both hopeanine and brunfelsamidine were shown to cause neurotoxicosis similar to that found in pets presenting after having ingested Brunfelsia. In the study Hopeanine effected the test subjects by causing decreased activity, paralysis, seizures, and hypersensitivity, whereas brunfelsamidine produced excitement, tonic-clonic seizures (grand mal seizures), and death. Based on this study it is likely that brunfelsamidine may be the toxin responsible for the neurotoxicosis in animals due to its ability to cause excitement, seizures and death.