CASE REPORTS

Brunfelsia australis (Yesterday, Today, and

Tomorrow Tree) and Solanum Poisoning
in a Dog
Robert Clipsham, PhD, DVM

ABSTRACT
A 2.5 yr old female beagle presented for acute abdominal pain and vomiting after consuming limited offerings of green potato
skins. Progressive complications associated with suspected ingestion of a higher potency toxin followed within 5 hr. Subse-
quent investigations revealed a signicant ingestion of an Australian shrub commonly called a Yesterday, Today, and
Tomorrow tree (Brunfelsia australis). The toxic principle for this emerging toxicity is referred to as strychnine-like and is
potentially lethal with gastrointestinal, central nervous system, and cardiac pathology. This plant is currently being aggres-
sively promoted by United States nurserymen for its dramatic tri-colored blooms and drought resistance. (J Am Anim Hosp
Assoc 2012; 48:139144. DOI 10.5326/JAAHA-MS-5725)

Introduction Belladonna, Jimson weed, Mandrake, etc.), which function as

The Solanaceae family consists of between 1,500 and 2,000 species,
including the more familiar members, such as Deadly Nightshade
(Atropa belladonna), tobacco (Nicotiana spp.), Jimsonweed (Datura
stramonium), and Mandrake (Mandragora ofcinarum). The nal
determination of familial assignment is in ux as cladistic investi-
gation using DNA analysis is currently rening family designation.
Not all species are determined to be toxic, and although toxin
distribution can be extensive (with especially high concentrations in
berries and/or seeds), not all toxic plant components are dangerous.
Several important cultivars are included in this family, such as the
commercial potato (Solanum tuberosum), eggplant (S. melongena),
domestic tomato (S. lycopersicum), and paprika peppers (Capsicum
spp.), the latter of which includes the familiar bell pepper. All cul-
tivars have worldwide consumption. In a minority of societies,
Solanum spp. are used for their psychoactive substances, such as
some indigenous peoples of South America who include native
1
Brunfelsia spp. in infusion brews for their scopoletin content.
Collectively, species within the Solanaceae family generally
contain an amalgamation of toxic alkaloids that are often in concert
with various other toxic principles. These include tropanes (in
anticholinergics and block acetylcholine in neurotransmission.2,3
Nicotine (in Nicotiana, Horsetail, Nightshades, Jimson weed,
potato, etc.) is also widely distributed among the family and is
a cholinergic agonist that activates nicotinic acetylcholine recep-
tors.3,4 Diverse glycoalkaloids (sugar-decorated alkaloids) can also
be present (in Black Nightshade, Bittersweet, wild and domestic
potatoes, etc.) and have manifold mechanisms.2,47 Solanine has
also been shown to be an active toxin (neurotoxin) and experi-
mentally has been shown to reduce mitochondrial membrane
potential by opening potassium channels and simultaneously re-
leasing excessive Ca to the cytosol.8,9 Due to a variable composi-
tion, concentration, and distribution within plant parts of these
toxic organic compounds, it is problematic to describe the effects
of Solanaceae ingestion as a sole clinical portrait. The purpose of
this report is to provide an information update for an emerging
toxin source not readily accessible in the literature or data bases.
Case Report
A 2.5 yr old spayed female beagle weighing 9.5 kg presented to the
local emergency facility after several hours of vomiting following

From the Sherman Oaks Veterinary Group, Sherman Oaks, CA. ASPCA American Society for Prevention of Cruelty to Animals; BP systolic
blood pressure; PO per os
Correspondence: clipsham@ucla.edu

2012 by American Animal Hospital Association JAAHA.ORG 139

the ingestion of small fragments of potato skins during an evening
meal preparation. The owner stated that the few pieces with green
skin fell where the dog was allowed to ingest them. The dog had no
signicant pre-existing medical history, but had a history of a few
limited episodes of gastroenteric upset and one incident of insect
hypersensitivity. The dog recovered without complication from all
previous episodes. She was not on any medications, was in good
body condition, and all vaccinations were current. The patient
resided in the house and a fenced backyard. No additional envi-
ronmental, pharmaceutical, or topical toxin exposure source could
be identied by the owners.
Physical examination revealed the patient to be alert, restless,
6% dehydrated (determined by skin turgor), had moderate pty-
alism, injected mucous membranes with normal capillary rell
time, signicant mydriasis, substantial abdominal pain on pal-
pation, and a signicant bradycardia (heart rate was 55 beats/min).
Systolic blood pressure (BP) was mildly elevated at 178 mm Hg
(reference range, 125155 mm Hg). Body temperature (38.58 C),
respiratory rate (36 breaths/min), and blood glucose concentra-
tion (111 mg/dL) were all normal. The dog was neurologically
normal for motor function, pain, and conscious proprioception
on initial presentation. On-site blood analysis revealed a mild
elevation in g-glutamyltransferase (21 U/L; reference range, 014
U/L), mild hyperproteinemia (8.0 mg/dL; reference range, 5.17.8
mg/dL), a slight hemoconcentration (packed cell volume was 56%;
reference range, 3755%), mild lactate elevation (2.7 mmol/L;
reference range, 0.52.0 mmol/L), mild hyponatremia (143
mmol/L; reference range, 146156 mmol/L), moderate hypoka-
lemia (2.98 mmol/L; reference range, 3.85.10 mmol/L), and
hypocalcemia (0.79 mmol/L; reference range, 1.121.40 mmol/L).
All other electrolyte levels (including chloride), hematologic, and
serum enzymes were normal. Pancreatic lipase testing determined
by Spec cPLIa was negative. Abdominal radiographs taken 4 hr
postpresentation revealed a signicant amount of diffuse material
along the rugal folds of the gastric fundus, pylorus, and colon.
Following consultation with the American Society for Pre-
b
vention of Cruelty to Animals (ASPCA) Poison Control Center ,
a putative diagnosis of potato (S. tuberosum) toxicity was con-
curred and appropriate treatment was initiated. Differential di-
agnoses included marijuana intoxication, oleander exposure, and
other nonspecic gastroenteric irritant etiologies.
Initial therapy included a 200 mL IV bolus balanced elec-
trolyte uids followed by 45 mL/hr of the same uid to correct
c
secondary dehydration. For potassium replacement, 40 mEq/L of
potassium chloride was added. IV ondansetrond (1 mg or 0.1 mg/kg
q 12 hr) was initiated for emesis. Atropine sulfatee was injected
as an IV bolus in response to the bradycardia. The heart rate
140 JAAHA | 48:2 Mar/Apr 2012
increased from 55 beats/min to 100 beats/min. Subcutaneous
famatidinef (5 mg q 12 hr) to reduce gastritis and ameliorate
vomiting was also administered. The patient was hospitalized for
care overnight until she could be transferred to the dogs primary
veterinarian.
During the night, vomiting persisted despite the antiemetic,
and tiny fragmented pieces of green potato skins were noted. Due
to the severity of signs, the owner speculated that the dog may have
ingested more potato fragments than suspected, and the owner
postulated the dog had consumed additional pieces from the
kitchen garbage. Over the following 4 hr the dog became in-
creasingly vocally distressed and painful on abdominal palpation.
Abdominal radiographs were taken, indicating that a larger volume
of materials and/or potatoes than previous postulated by the
owners estimation and may have been contributing to the patients
signs. Approximately 5 hr after presentation, the dog exhibited
manic-type behavior (with intense and persistent muzzle rubbing
of her bedding) followed by ataxia. The dog then rapidly devel-
oped numerous neurologic decits, including muscular weakness
and muscular fasciculation, and rapidly became obtunded. The
dog was offered activated charcoal in food, but either refused or
was incapable of deglutition due to neuromuscular weakness.
Force feeding the activated charcoal slurry was not performed due
to the risk of inhalation pneumonia. Alternatively, a warm water
enema was administered to induce vomiting. A signicant
amount of material consistent with plant root ingestion was
voided. Vomiting continued intermittently throughout the re-
mainder of the dogs overnight hospitalization. BP remained
slightly elevated and the heart rate ranged from 60 beats/min to
120 beats/min.
The beagle was transferred to the primary veterinarian in the
morning for continued care. The dog presented to the primary
veterinarian in lateral recumbency with marked lethargy, a poor
response to tactile stimulation, a body temperature of 37.68 C,
moderate abdominal distension with extreme pain on palpation,
and frank blood on rectal palpation. Auscultation revealed
a normal heart rate (90 beats/min) but with an arrhythmia.
An electrocardiogram displayed at T waves and frequent
premature ventricular contractions (Figure 1). BP was normal
at 141 mm Hg.
The therapeutic plan was continued from the previous night
with subcutaneous maropitantg (1.0 mg/kg) replacing the previ-
ous ondansetron for additional emetic control. Buprenorphineh
(0.012 mg/kg IV q 8 hr) was added to control visceral pain. Addi-
tionally, ampicillini was instituted at 250 mg (25 mg/kg) IV q 8 hr
and 250 mg of a sucralfatej suspension was administered orally
q 8 hr as a gastrointestinal protectant. An external air-blown

FIGURE 1 Electrocardiogram of an affected patient showing
abnormal activity, including premature ventricular contractions.
blanketk was also applied, and a 2% lidocaine solutionl (60 mg/kg/min)
was administered to desensitize the myocardium. Subsequent elec-
trocardiograms over the next 11 hr showed discontinuation of any
previous arrhythmias.
Subsequent discussion with the owners revealed that the root
substances produced via the enema had prompted further in-
vestigation of their yard to dene alternate toxins beyond the
suspect potato skins. Holes dug by the dog were found to contain
chewed roots matching the size and character of those collected
following the enema. The holes were located at the base of
a Yesterday, Today, and Tomorrow tree (Brunfelsia australis). The
ingestion was estimated to be very recent due to daily inspection
of the yard during oversight of family children.
Symptomatic treatment of Solanum spp. toxicity was con-
tinued, but as the nature and intensity progressed, the etiologic
diagnosis was quantitatively shifted from the potato ingestion to
the newly discovered B. australis source. Because of the overlap in
toxic principles, this case was therefore considered a compound
Solanum spp. toxicity. Brunfelsia spp. are members of the Sol-
anaceae family and produce related glycoalkaloids in their owers,
roots, seeds, bark, leaves, and roots. The signs of toxicity mirror
those of the classic Solanaceae family, which includes potatoes.
The dog continued to recover in strength, coordination, and
mental capability over the following 24 hr, accompanied by an
increase in appetite and resolution of the diarrhea and associated
hematochezia. The dog was discharged approximately 48 hr after
j Diarrhea6blood
the onset of the episode. A bland diet and sucralfate (0.5 gm PO q
8 hr 3 days) were prescribed for 48 hr to assist in gastrointestinal
regeneration. The dog continued to improve the following day
and appeared in good condition on the scheduled follow-up ex-
amination 2 wk after discharge.
Discussion
Patients affected by Solanum spp. poisoning generally exhibit early
systemic signs and clinically progress from gastrointestinal to
B. australis and Solanum Poisoning in a Dog
cardiovascular to neuromuscular to neurologic disease in their
pathophysiology. These signs are consistent between three dogs
intentionally fed Brunfelsia berries and two previous accidental
case reports.1013 Solanine and chaconine, another frequent toxic
component, both possess tissue distribution and bioelimination
that parallel each other.14,15 A general list of signs noted in Sola-
num and Brunfelsia clinical poisonings are noted and are generally
considered to occur secondary to the anticholinergic neuro- and
cardiovascular toxic effects (Table 1). For purposes of this specic
case presentation, further discussion of Solanum-origin toxicity is
restricted to Brunfelsia and potato species.
Yesterday, Today, and Tomorrow Tree Poisoning
The genus Brunfelsia includes around 40 neotropical (New World
south of the Tropic of Cancer) species, including shrubs, vines,
and small trees originating from South and Central America,
Australia, Caribbean Islands, and southern Florida.1618 The
common name is derived from the large, brightly star-shaped,
colored owers with ve petals that change from deep blue to
lavender to white over time, giving the impression that three
sets of blossoms are produced independently (Figure 2). Other
common names include: Morning, Noon, and Night Tree; Lady-
of-the-Night; Paraguay Jasmine; Kiss-me-Quick; Cuban Raintree;
and Franciscan Raintree. The United States Department of Agri-
culture lists nine separate American species, apart from those
cultivated south of the United States and/or in Africa and Aus-
tralia.18 Indigenous nomenclature used by nurserymen further
complicate accurate case etiology assignment and include:
Manac, Manacn, Chiric Sanango, Chuchuwasha, Manaka,
Vegetable Mercury, Manag Caa, Gamb, Jeratacaca, Bloom
Of The Lent, Camgaba, Christmas Bloom, Chuchuwasha,
Gerataca, Geratacaca, Good Night, Jerataca, Moka Pari, Santa
TABLE 1
Clinical Signs of Solanum/Brunfelsia Toxicity: General
Temporal Progression
Nausea
CNS depression/ headache
Vomiting
Abdominal pain
Cardiac arrhythmias
Mydriasis6hypothermia
Disorientation
Ataxia
Muscle tremors
Muscular paralysis6fever
JAAHA.ORG 141

FIGURE 2 Photo of Brunfelsia australis in full bloom showing
the ower color progression from blue to lavender to white.
Maria, Umburapuama, and White Tree.17 Alternative names used
for Brunfelsia spp. are widely diverse, frequently restricted by
specic locales, and often incorrectly referenced as Brunsfelsia
spp., which severely convolutes case management during data
searches. Case in point, B. australis was previously designated B.
bonadora, B. francissia, and B. latifolia, and these prior names
10
persist in the very limited literature.
The primary alkaloids responsible are largely unreported or
under-reported in the literature as to their full actions. However,
two substances are described: brunsfelsamidine, which produces
central nervous system depressant actions, and scopoletin, which is
a psychoactive substance and a derivative of coumarin.2,5,1922
Hopeanine has also been isolated, and along with brunfelsamidine,
has been reported to cause neuropathology when adminis-
tered to rodent test subjects. 16,19,20
The primary mechanisms
involved in scopoletin toxicity in animal models include negative
chronotropic and inotropic responses, plus inhibition of
acetylcholine-mediated skeletal muscle contractions. 23
Clinical signs reported for veterinary patients include pain,
vomiting, diarrhea, salivation, lethargy, ataxia, cough, muscular
tremors progressing to rigidity (sawhorse stance), and seizures.1013,19
Nystagmus has also been reported.19 Accidental poisoning cases by
ingestion parallel those of dogs intentionally fed berries or super-
natants of berry mash by researchers.1013,19 Signs generally last 4872
hr and either terminate in recovery with no lingering effects or
progress to fatality, probably in a dose-dependent manner. Symp-
tomatic therapies are indicated, including emetics, cathartics, acti-
vated charcoal, atropine, muscle relaxants, antiarrhythmics, and
anticonvulsants (diazepam or phenobarbital), which have been
used successfully for both canine patients and rodent test subjects.
Denitive toxin analysis is not yet possible as it is not offered by
either academic or commercial labs (oral communication with
Safdar A. Khan at the ASPCA poisoning center [October 2010] and
Robert H. Poppenga and Birgit Puschner at the California Animal
Health & Food Safety Laboratory at UC Davis School of Veterinary
142 JAAHA | 48:2 Mar/Apr 2012
Medicine [October 2010]). The toxic principle is still referred to as
being strychnine-like. The litany and progression of clinical signs
are most likely due to the mlange of various suspect and known
toxic components, as seen in this case.
Potato (Solanum) Poisoning
All potato species are derived from a wild Peruvian ancestral tuber,
but 99% of all recognized modern potato species, including the
commercial potato, S. tuberosum, are descended from a Chilean
subspecies of S. tuberosum tuberosum, resulting from early selec-
tion and domestication. Currently, potatoes are the worlds fourth
largest staple crop with only a very few cultivars dominating
global markets. The primary glycoalkaloids toxins are solanine
and chaconine, which are largely found in the leaves, stems, and
tubers.2,5,6,22 The highest concentrations are just under the skin
and account for up to 80% of the total solanine plant load. Wild
varieties generally have higher glycoalkaloid content due to se-
lective crop selection and manipulation for safe human con-
sumption. Both toxins act as natural botanical pesticides and
fungicides for plant host defensive purposes. Light exposure,
temperature, age, and physical trauma act to elevate glycoalkaloid
content dramatically over a 24 hr period.23 Light exposure also
results in chlorophyll synthesis and subsequent greening of the
skin, but does not directly correlate with increased toxin levels, as
these are independent biologic events. However, light exposure
can accelerate solanine production at ve times faster than po-
tatoes in dark storage.23
Solanine content of commercial potatoes is generally ,0.2
mg/gm (200 ppm) due to primary plant breeder screening, but
can approach 1 mg/gm (1,000 ppm) when green.2,5 Human
studies show 25 mg/kg of ingestion is toxic, while 36 mg/kg can
be fatal.23 Toxic signs are initially noted above 25 mg total intake,
with life-threatening consequences at 400 mg intake for an adult
human. Commercial potato varieties range from 180 g to 560 g in
total uncooked weight. Therefore, ingesting a large, green raw
Idaho potato or even a smaller red or gold raw potato following
bruising can easily result in severe poisoning of a 20 kg (44 lb)
dog, with the potential existing for subsequent lethality, especially
if untreated.
Fortunately, solanines are poorly absorbed from the intestinal
tract, have rapid excretion via the feces and biliary tract, and are
rapidly hydrolyzed to nontoxic substrates in the stomach and
intestines.15 Rodent models show retention in the liver, gut epi-
thelium, and urinary bladder during the initial 24 hr after expo-
sure.2426 Furthermore, cooking partially denatures and/or degrades
the cyclic structure, especially when deep fried (1708 C).23 Micro-
waving at lower temperatures has signicantly less destructive effect

on these glycoalkaloids, but often renders toxin levels to a non-
clinical level. Freeze drying and dehydration have no affect in re-
ducing active toxin levels. Alternative sources of Solanum toxicity
include drinking potato leaf tea, and potentially, the practice of
using the boiled leaf and stem solution for pesticide spraying of
organic garden produce. However, potato leave tops are consumed
as a vegetable source in Bangladeshi diets with no apparent dele-
terious affects. Chaconines are thought to be synergistic with so-
lanine, but have been shown to possess a lower LD50 in mice when
administered separately.27
Clinically, potato poisoning cases have been treated symp-
tomatically similarly to Brunfelsia cases for their assumed com-
mon glycoalkaloid principles. Gross pathologic ndings are
limited to gastrointestinal edema and hemorrhage without obvi-
24
ous neuropathology. Severe and nonresponsive cases in human
patients have been successfully treated with physostigmine or
7
pilocarpine. To date, no absolute subcellular, molecular mecha-
nisms have been assigned to either solanines or chaconines to
account for their full range of clinical pathophysiologic actions
in vivo.
Conclusion and Clinical Relevance
This case report is offered as an update to intoxication via ingestion
of B. australis (Yesterday, Today, and Tomorrow) and is one of
several very limited reports available through the National Insti-
tute of Health Pubmed database. The others reported as separate,
12,19
but related, species listed as B. pauciora and B. calcyina. The
patients signs and clinical progression were identical to those
reported in the small number of other dogs with exposure to
unidentied species, and one report in 1983 for B. australis.11 One
brief letter of a toxicity study referencing B. bonodora (in Australia
in 1975) is also noted.10 Readily available information and ther-
apeutic guidelines for practitioners for this toxicity were found to
be scarce despite text reviews and numerous consultations with
toxicologists and veterinary specialists. Case in point is a fairly
informative review available through the ASPCA poison control
website, but was located only by using the search term for the
toxin brunfelsamide. This restricted identication terminology
and alternative name variations used for this group of Brunfelsia
spp. (over 25), often incorrectly referenced as Brunsfelsia, can
result in case mismanagement.
This landscape tree, along with other Solanaceae family
members, are becoming more widespread in their distribution in
the United States in the warmer climes due to inherent drought
resistance, as well as its appeal as an indoor potted plant. Un-
doubtedly this case presentation will confront practitioners with
increasing frequency. Case in point, the authors clinic was
B. australis and Solanum Poisoning in a Dog
presented with yet another Brunfelsia poisoning within 2 wk
subsequent to the dismissal of this specic case. Additionally, the
author was informed by his wife during manuscript development
that both a Yesterday, Today and Tomorrow tree and a related
Solanaceae family member, S. macranthum (Potato tree), had been
purchased and were now residing in their back yard based on
recommendations for hardiness.
Furthermore, this case is somewhat unique in that it is
a combined Solanum poisoning, but with the majority of the toxic
principle contributed by the Morning, Noon and Night Tree.
While the treatment here was relatively straightforward, rational,
and successful, the potential for a complex case of toxicity always
exists. A traditional poisonous substance was intensely com-
pounded by an emerging source of a related toxin, resulting in
a life-threatening toxicosis. When patients inappropriately ingest
one aberrant item, the probability of consuming a second toxic
item is inherently statistically elevated and compels consideration.
This case is presented for practitioners to provide enhanced
information and therapeutic support due to limited data for which
summaries or details are largely inaccessible by name and/or
completely unrecognized in many online databases and current
textbooks.
The author wishes to acknowledge the clinical contributions of Dr.
Amanda Payne at the Animal Emergency Center, Studio City, CA,
in regard to this case presentation.
FOOTNOTES
a
Idexx Labs, Westbrook, ME
b
American Society for Prevention of Cruelty to Animals (ASPCA)
Poison Control Center; College of Veterinary Medicine, University
of Illinois, Urbana, IL
c
Normasol; Hospira, Inc., Saint-Laurent, Qubec, Canada
d
Zofran; GlaxoSmithKline, Research Triangle Park, NC
e
Atropine sulfate; Butler Schein Animal Health, Dublin, OH
f
Pepcid; Merck, Whitehouse Station, NJ
g
Cerenia; Phizer, New York, NY
h
Buprenex; Reckitt Benckiser Group, plc, Slough, Berkshire, England
i
Ampicillin; Sandoz Inc., Broomeld, CO
j
Carafate suspension; Axcan Scandipharm Inc., Birmingham, AL
k
Bair Hugger; Airzant, Inc., Eden Prairie, MN
l
2% lidocaine; Sparhawk Laboratories, Inc., Lenexa, KS
REFERENCES
1. Plowman T. Brunfelsia in ethnomedicine. In Botanical Museum
Leaets Harvard University. 1977;25:289320.
2. Friedman M. Analysis of biologically active compounds in potatoes
(Solanum tuberosum), tomatoes (Lycopersicon esculentum), and
jimson weed (Datura stramonium) seeds. J Chromatogr A 2004;1054
(1-2):14355.
JAAHA.ORG 143
 3. Vanderhoff BT, Mosser KH. Jimson weed toxicity: management
of anticholinergic plant ingestion. Am Fam Physician 1992;46(2):
52630.
4. Schep LJ, Slaughter RJ, Beasley DM. Nicotinic plant poisoning. Clin
Toxicol [Phila] 2009;47(8):77181.
5. Slanina P. Solanine (glycoalkaloids) in potatoes: toxicological eval-
uation. Food Chem Toxicol 1990;28(11):75961.
6. Barceloux DG. Potatoes, tomatoes, and solanine toxicity (Solanum
tuberosum L., Solanum lycopersicum L.). Dis Mon 2009;55(6):391
402.
7. Ceha LJ, Presperin C, Young E, et al. Anticholinergic toxicity from
nightshade berry poisoning responsive to physostigmine. J Emerg
Med 1997;15(1):659.
8. Gao SY, Wang QJ, Ji YB. Effect of solanine on the membrane po-
tential of mitochondria in HepG2 cells and [Ca21]i in the cells.
World J Gastroenterol 2006;12(21):335967.
9. Rietjens IM, Martena MJ, Boersma MG, et al. Molecular mecha-
nisms of toxicity of important food-borne phytotoxins. Mol Nutr
Food Res 2005;49(2):13158.
10. 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
[letter].
11. Neilson J, Burren V. Intoxication of two dogs by fruit of Brunfelsia
australis. Aust Vet J 1983;60(12):37980.
12. Banton MI, Jowett PL, Renegar KR, et al. Brunfelsia pauciora
(yesterday, to-day and tomorrow) poisoning in a dog. Vet Hum
Toxicol 1989;31(5):4967.
13. Singh M, Cowan S, Child G. Brunfelsia spp (yesterday, today, to-
morrow) toxicity in four dogs. Aust Vet J 2008;86(6):2148.
14. Norred WP, Nishie K, Osman SF. Excretion, distribution and met-
abolic fate of 3H-alpha-chaconine. Res Commun Chem Pathol
Pharmacol 1976;13(2):16171.
15. Dalvi RR, Bowie WC. Toxicology of solanine: an overview. Vet Hum
Toxicol 1983;25(1):135.
144 JAAHA | 48:2 Mar/Apr 2012
16. Burrows GE, Tyrl RJ. Toxic plants of North America. Ames (IA): Iowa
State University Press; 2001:1342.
17. Raintree Nutrition. Tropical Plant Database. Database le for:
Manac (Brunfelsia uniora). Available at: http://www.rain-tree.
com/manaca.htm. Accessed November 26, 2011.
18. United States Department of Agriculture. Natural Resources Con-
servation Service. PLANTS Database. Available at: http://plants.
usda.gov/. Accessed November 26, 2011.
19. Spainhour CB Jr, Fiske RA, Flory W, et al. A toxicological investi-
gation of the garden shrub Brunfelsia calcyina var. oribunda
(yesterday-today-and-tomorrow) in three species. J Vet Diagn Invest
1990;2(1):38.
20. Lloyd HA, Fales HM, Goldman ME, et al. Brunfelsamidine: A novel
convulsant from the medicinal plant Brunfelsia grandora. Tetra-
hedron Lett 1985;26:26234.
21. Oliveira EJ, Romero MA, Silva MS, et al. Intracellular calcium
mobilization as a target for the spasmolytic action of scopoletin.
Planta Med 2001;67(7):6058.
22. Hopkins J. The glycoalkaloids: naturally of interest (but a hot
potato?). Food Chem Toxicol 1995;33(4):3238.
23. Cantwell M. A review of important facts about potato glyco-
alkaloids. Perishables Handling Newsletter. August 1996:87;26.
24. Baker DC, Keeler RF, Gareld WP, Mechanism of death in Syrian
hamsters gavaged potato sprout material, Toxicol Pathol. 1988;16(3):
3339.
25. Baker DC, Keeler RF, Gafeld W, Pathology in hamsters adminis-
tered Solanum plant species that contain steroidal alkaloids, Toxicon.
1989;27(12):13317.
26. Langkilde S, Schrder M, Stewart D, et al. Acute toxicity of high
doses of the glycoalkaloids, alpha-solanine and alpha-chaconine, in
the Syrian Golden hamster. J Agric Food Chem 2008;56(18):875360.
27. Rayburn JR, Friedman M, Bantle JA, et al, Synergistic interaction of
glycoalkaloids a-chaconine and a-solanine on developmental
toxicity in Food and Chem Toxicol, Vol 33, Issue 12, Dec 1995:
10139.