0.0 OVERVIEW
0.1 LIFE SUPPORT
This overview assumes that basic life support measures
have been instituted.
0.2 CLINICAL EFFECTS
0.2.1 SUMMARY
A. There are several types of toxic substances found in
toads, including cardioactive agents, catecholamines,
indolealkylamines and non-cardiac sterols. These toxins
are located in the skin and parotid glands and may be
transferred by handling or ingesting a toad's skin.
0.2.3 HEENT
A. Secretions of the toad parotid glands will cause pain
and severe irritation when placed in eyes, nose, and
throat.
0.2.4 CARDIOVASCULAR
A. Dogs who have been poisoned with bufagins develop
ventricular fibrillation and symptoms resembling
digitalis poisoning. Vasoconstriction may also be seen.
0.2.5 RESPIRATORY
A. Dyspnea and weakened respirations may be seen.
0.2.6 NEUROLOGIC
A. Paralysis and seizures have been reported in both humans
and animals. Many bufagins have local anesthetic
actions, especially on the oral mucosa.
0.2.7 GASTROINTESTINAL
A. Salivation and vomiting were often seen in animals.
These toxins may cause numbness of the oral mucosa if
ingested.
0.2.14 HEMATOLOGIC
A. Cyanosis has been seen in poisoned dogs.
0.2.18 PSYCHIATRIC
A. HALLUCINATIONS: Drug users have been known to smoke the
chopped skins of toads for their hallucinogenic effect.
0.3 LABORATORY
A. No toxic levels have yet been established for any of the
bufagins. Since many of the other substances are
metabolized rapidly, laboratory analysis is impractical.
0.4 TREATMENT OVERVIEW
0.4.1 SUMMARY
A. There are three primary areas of toxicity, the first
involving cardiac glycoside effects, the second, the
pressor effects, and the third, the hallucinogenic
effects. Usually the cardiovascular effects are the
most prominent. Treatment is directed at prevention of
absorption, and monitoring for EKG effects and
hyperkalemia. Lidocaine, a transvenous pacemaker, and
cholestyramine have all been used to treat digitalis-
like poisonings. FAB fragments have not been reported
to be of use in toad poisoning.
B. Hemodialysis has been ineffective in removing cardiac
glycosides.
0.5 RANGE OF TOXICITY
A. The skin of one toad is sufficient to cause significant
symptoms and even death in both animals and humans.
Topic: TOAD TOXINS
B. No toxic serum or blood levels have yet been established.
1.0 SUBSTANCES INCLUDED
1.1 THERAPEUTIC/TOXIC CLASS
A. There are several types of toxic substances found in the
venom of toads.
1. CARDIOACTIVE SUBSTANCES: Bufagins (bufandienolides) are
cardioactive substances found in toad venom. They have
effects similar to the cardiac glycosides found in
plants. Bufotoxins are the conjugation products of the
specific bufagin with one molecule of suberylargine
(Chen & Kovarikova, 1967). Bufotoxins were originally
isolated from the parotoid glands of toads, but have
since been seen in various plants and mushrooms
(Siperstein et al, 1957; Lincoff & Mitchel, 1977; Kibmer
& Wichtl, 1986).
2. CATECHOLAMINES: There are also several catecholamines
in toad venom. Epinephrine has been found in as high a
concentration as 5% in the venom of several species.
Norepinephrine has also been found (Chen & Kovarikova,
1967).
3. INDOLEALKYLAMINES: Chemicals found include several
bufotenines. Bufotenines are organic bases containing
an indole ring and have primarily oxytocic actions and
often pressor actions (Palumbo et al, 1975). Specific
substances include bufothionine, serotonin,
cinobufotenine, bufotenine, and dehydrobufotenine (Chen
& Kovarikova, 1967). Bufotenine is the 5-hydroxy
derivative of N,N,dimethyltryptamine and is a
hallucinogen (Gilman et al, 1985).
4. NONCARDIAC STEROLS: The sterols found in toad venom
include cholesterol, provitamin D, gamma sitosteral, and
ergosterol. They do not appear to have a significant
role in toxicity (Chen & Kovarikova, 1967; Palumbo et
al, 1975).
1.3 DESCRIPTION
A. Toads known to contain toxins include:
1. Bufo alvarius
2. Bufo americanus
3. Bufo arenarum
4. Bufo asper
5. Bufo blombergi
6. Bufo bufo
7. Bufo bufo gargarizans
8. Bufo formosus
9. Bufo fowerii
10. Bufo marinus
11. Bufo melanostictus
12. Bufo peltocephalus
13. Bufo quercicus
14. Bufo regularis
15. Bufo valliceps
16. Bufo viridis
1.4 GEOGRAPHICAL LOCATION
A. Toads are found throughout the world, Bufo marinus having
one of the widest distributions.
Topic: TOAD TOXINS
2.0 CLINICAL EFFECTS
2.1 SUMMARY
A. Poisoning by toad toxins is primarily a problem with
animals and may be fatal (Perry & Bracegirdle, 1973).
There have been fatalities in Hawaii, Phillipines, and
Fiji occurring after eating the toads as food (Tyler,
1976; Palumbo et al, 1975). The toxins are located in
the skin and parotid glands and may be transferred by
handling a toad. A toad that sits in a dog's watering
dish for some time may leave enough toxin to make the pet
ill (Smith, 1982). The toxicity varies considerably by
the toad species and its geographic location. The death
rate for untreated animals exposed to Bufo marinus is
nearly 100% in Florida, is low in Texas, and only about
5% in Hawaii (Palumbo et al, 1975).
2.3 HEENT
2.3.2 EYES
A. IRRITATION: If the secretions of the toad parotid
glands come in contact with human eyes, pain and severe
irritation will result (Tyler, 1976; Smith, 1982).
2.3.4 NOSE
A. IRRITATION: Exposure of the nasal mucous membranes to
the toad toxins may produce severe irritation (Chen &
Kovarikova, 1967).
2.3.5 THROAT
A. The mouth and throat may become anesthetized if
bufotoxins have been ingested (Chen & Kovarikova, 1967).
2.4 CARDIOVASCULAR
A. VENTRICULAR FIBRILLATION: Dogs intentionally poisoned
with bufagins orally develop ventricular fibrillation and
if untreated - death (Palumbo et al, 1975). The symptoms
resemble digitalis poisoning.
B. VASOCONSTRICTION: Bufagins constrict arterial blood
vessels (Chen & Kovarikova, 1967). Bufotenine itself is
not hallucinogenic, but acts as a pressor rather than a
hallucinogen in humans (Kantoretal, 1980).
2.5 RESPIRATORY
A. DYSPNEA: Weakened respirations may be seen if toad
toxins have been ingested (Smith, 1982).
2.6 NEUROLOGIC
A. PARALYSIS: Paraplegia has been noted in toad poisonings
of dogs and cats. Incoordination and progressive
paralysis may be earlier symptoms (Perry & Bracegirdle,
1973; Smith, 1982).
B. SEIZURES: Have been reported in poisoned dogs and a few
cats (Palumbo et al, 1975; Chen & Kovarikova, 1967), as
well as a 5-year-old boy (Hitt & Ettinger, 1986). Onset
was within 5 minutes. The seizures continued unabated
for 60 minutes.
C. LOCAL ANESTHESIA: Many bufagins have local anesthetic
actions, especially on the oral mucosa (Chen &
Kovarikova, 1967).
2.7 GASTROINTESTINAL
A. SALIVATION: Intense salivation is usually seen in
poisoned cats and dogs (Perry & Bracegirdle, 1973), and
Topic: TOAD TOXINS
was seen in one 5-year-old boy (Hitt & Ettinger, 1986).
B. VOMITING: Is often present in animals (Perry &
Bracegirdle, 1973).
C. NUMBNESS: If ingested, the toxins cause numbness of the
oral mucosa (Smith, 1982; Chen & Kovarikova, 1967).
2.12 FLUID-ELECTROLYTE
A. HYPERKALEMIA: Similar to that seen with digitalis
poisoning, may be seen.
2.13 TEMPERATURE REGULATION
A. FEVER: Is a symptom common to ingestion of toads by cats
and dogs (Perry & Bracegirdle, 1973).
2.14 HEMATOLOGIC
A. CYANOSIS: Has been seen in dogs (Hitt & Ettinger, 1986).
2.15 DERMATOLOGIC
A. PERSPIRATION: Although handling toads is generally not
considered seriously injurious to humans, it is thought
to dramatically reduce perspiration (Smith, 1982).
2.18 PSYCHIATRIC
A. HALLUCINATIONS: In 1971, drug users in Queensland were
smoking the chopped skins of Bufo marinus for its
hallucinogenic effect (Tyler 1976). Toad skin has been
used for its hallucinogenic properties throughout the
world (Emboden, 1979), but Bufo alvarins is the only Bufo
species known to contain a hallucinogenic tryptamine
(McKenna & Towers, 1984).
3.0 LABORATORY
3.2 MONITORING PARAMETERS/LEVELS
3.2.1 SERUM/BLOOD
A. No toxic levels have yet been established for any of the
bufagins. Many of the other substances are metabolized
rapidly, and laboratory analysis would be impractical.
3.2.3 OTHER
A. EKG: Patients who have had significant exposures should
have a baseline EKG to observe for abnormalities.
Symptomatic patients should continue to have EKGs
performed.
B. A serum potassium level should be drawn to test for
hyperkalemia (Chen & Kovarikova, 1967).
4.0 CASE REPORTS
A. A typical animal case report involves a dog that finds a
slow hopping toad and mouths the animal playfully. The
animal usually experiences immediate salivation, and
irritation of the mucus membranes of the mouth and
throat. If the dog eats the toad, vomiting and paralysis
may lead to seizures and death. Animals who recover
usually do not have significant sequelae.
B. Although human deaths have been reported in the lay
literature, we were able to find only one case report of
a human death or serious intoxication in the medical
literature. This was a 5-year-old who had mouthed a Bufo
alvarius (Colorado River Toad) and developed status
epilepticus successfully treated with diazepam and
phenobarbital (Hitt & Ettinger, 1986).
5.0 TREATMENT
5.1 LIFE SUPPORT
Topic: TOAD TOXINS
Support respiratory and cardiovascular function.
5.2 SUMMARY
A. There are 3 primary areas of toxicity. The first
involves the cardiac glycoside-like effects of the
bufagins; the second is the pressor effects of the
catecholamines; and the third is the hallucinogenic
effect of the indolealkylamines. After a toad had been
ingested, it is difficult to evaluate which of these
effects will predominate. Usually, the cardiovascular
effects are the most prominent. The patient should be
observed for arrhythmias and for hallucinations. There
have been minimal human exposures, so clinical
presentation and course are difficult to predict.
5.3 ORAL/PARENTERAL EXPOSURE
5.3.1 PREVENTION OF ABSORPTION
A. EMESIS
1. Emesis may be indicated in substantial recent
ingestions unless the patient is obtunded, comatose or
convulsing or is at risk of doing so based on
ingestant. Emesis is most effective if initiated
within 30 minutes of ingestion. Dose of ipecac syrup:
ADULT OR CHILD OVER 90 TO 100 POUNDS (40 to 45
kilograms): 30 milliliters; CHILD 1 TO 12 YEARS: 15
milliliters; CHILD 6 TO 12 MONTHS (consider
administration in a health care facility): 5 to 10
milliliters. After the dose is given, encourage clear
fluids, 6 to 8 ounces in adults and 4 to 6 ounces in a
child. The dose may be repeated once if emesis does
not occur within 30 minutes.
2. If emesis is unsuccessful following 2 doses of ipecac,
the decision to lavage or otherwise attempt to
decontaminate the gut should be made on an individual
basis. This amount of ipecac poses little toxicity of
itself.
3. Refer to the IPECAC/TREATMENT management for further
information on administration and adverse reactions.
B. MULTIPLE DOSE ACTIVATED CHARCOAL/CATHARTIC
1. Cardiac glycosides and bufandienolides are adsorbed to
activated charcoal and enterohepatic circulation may be
decreased by multiple-dose activated charcoal (Balz &
Bader, 1974).
2. Repeated oral charcoal dose (every 2 to 6 hours) may
enhance total body clearance and elimination. A saline
cathartic or sorbitol may be given with the first
charcoal dose and repeated until charcoal appears in
the stools. Do not repeat charcoal if bowel sounds
absent.
3. Administer charcoal as slurry. The FDA suggests a
minimum of 240 milliliters of diluent per 30 grams
charcoal (Dose: Optimum dose of charcoal is not
established; usual INITIAL dose is 30 to 100 grams in
adults and 15 to 30 grams in children; some suggest
using 1 to 2 grams per kilogram as a rough guideline,
particularly in infants). REPEAT doses have ranged
from 20 to 50 grams in adults. Doses in children have
Topic: TOAD TOXINS
not been established, but one-half the initial dose is
recommended.
4. Administer a saline cathartic or sorbitol, with the
INITIAL charcoal dose, mixed with charcoal or
administered separately. Dose:
a. Magnesium or sodium sulfate (ADULT: 20 to 30 grams
per dose; CHILD: 250 milligrams per kilogram per
dose) OR magnesium citrate (ADULT AND CHILD: 4
milliliters per kilogram per dose up to 300
milliliters per dose).
b. Sorbitol (ADULT: 1 to 2 grams per kilogram per dose
to a maximum of 150 grams per dose; CHILD: (over 1
year of age): 1 to 1.5 grams per kilogram per dose
as a 35 percent solution to a maximum of 50 grams
per dose). Consider administration in a health care
facility, monitoring fluid-electrolyte status,
especially in children.
5. When used with multiple-dose charcoal regimens, the
safety of repeated cathartics has not been established.
Hypermagnesemia has been reported after repeated
administration of magnesium containing cathartics in
overdose patients with normal renal function. In young
children, cathartics should be repeated no more than 1
to 2 times per day. Administration of cathartics
should be stopped when a charcoal stool appears.
Cathartics should be used with extreme caution in
patients who have an ileus or absent bowel sounds.
Saline cathartics should be used with caution in
patients with impaired renal function.
6. Refer to the ACTIVATED CHARCOAL/TREATMENT management
for further information on administration and adverse
reactions.
C. One of the best first aid measures to prevent toxicity
in animals is to immediately flush the oral mucous
membranes of dogs, cats, and even people who have had
mucous membrane exposure to decrease absorption. Do not
swallow the rinse water.
5.3.2 TREATMENT
A. CARDIAC EFFECTS
1. MONITOR EKG CONTINUOUSLY: For abnormal cardiac rates
and rhythms. In patients with previously healthy
hearts, the most common manifestation is bradycardia
with or without varying degrees of AV block. Peaked T
waves, depressed ST segments, widened QRS, and
prolonged PR interval may also be noted.
2. HYPERKALEMIA: Hyperkalemia following acute overdose
may be life-threatening. The emergency management of
life-threatening hyperkalemia (potassium levels greater
than 6.5 mEq/L) includes the intravenous administration
of bicarbonate, glucose, and insulin. DOSE:
Administer 0.2 units/kg of regular insulin with 200 to
400 mg/kg glucose (IV dextrose 25% in water).
Concurrent administration of IV sodium bicarbonate
(approximately 1.0 mEq/kg up to 44 mEq per dose in an
adult) may be of additive value in rapidly lowering
Topic: TOAD TOXINS
serum potassium levels. Monitor the EKG while
administering the glucose, insulin, and sodium
bicarbonate. This therapy should lower the serum
potassium level for up to 12 hours.
3. ATROPINE: Atropine is useful in the management of
bradycardia, varying degrees of heart block and other
cardiac irregularities due to the digitalis-like
induced effects of enhanced vagal tone on the SA node
rhythmicity and on conduction through the AV node.
DOSE: Adult: 0.6 mg per dose IV; Child: 10 to 30
mcg/kg per dose up to 0.4 mg per dose (may be repeated
as needed to achieve desired effects). Monitor EKG
carefully while administering atropine.
4. PHENYTOIN: Phenytoin is useful in the management of
digitalis-like induced ventricular dysrhythmias and
improves conduction through the AV node. Low dose
phenytoin (Adult: 25 mg per dose IV at 1 to 2 hour
intervals; Child: 0.5 to 1.0 mg/kg per dose IV at 1 to
2 hour intervals) appears to improve AV conduction.
Larger doses are needed for the management of
ventricular dysrhythmias: Loading Dose for adults and
children: Administer 15 mg/kg up to 1.0 gram IV not to
exceed a rate of 0.5 mg/kg per minute. Maintenance
Dose: Adults - administer 2 mg/kg IV every 12 hours as
needed; Child - administer 2 mg/kg every 8 hours as
needed. Monitor serum phenytoin levels just prior to
initiating and during maintenance therapy to assure
therapeutic levels of 10 to 20 mcg/ml (39.64 to 79.28
nmol/L). Monitor EKG carefully.
5. LIDOCAINE
a. Lidocaine is useful in the management of ventricular
tachyarrhythmias, PVC's, and bigeminy. Lidocaine does
not improve conduction through the AV node.
b. ADULT: BOLUS: 50 to 100 milligrams (0.70 to 1.4
milligrams per kilogram) under EKG monitoring. Rate:
25 to 50 milligrams per minute (0.35 to 0.70
milligrams per kilogram per minute). A second bolus
may be injected in 5 minutes if desired response is
not obtained. No more than 200 to 300 milligrams
should be administered during a one hour period.
INFUSION: Following a bolus, an infusion at 1 to 4
milligrams per minute (0.014 to 0.057 milligram per
kilogram per minute) may be used. PEDIATRIC: BOLUS:
1 milligram per kilogram. INFUSION: 3 micrograms per
kilogram per minute.
6. TRANSVENOUS PACEMAKER: Insertion of a transvenous
pacemaker should be considered in those patients with
severe bradycardia and/or slow ventricular rate due to
second degree AV block who fail to respond to atropine
and/or phenytoin drug therapy.
7. FAB FRAGMENTS: Have not been documented to be of any
value in the treatment of bufagins. Cross reactivity
has not been proven.
8. CHOLESTYRAMINE: Digitoxin (and theoretically bufagins)
elimination appears to be enhanced by the serial
Topic: TOAD TOXINS
administration of cholestyramine, 4 grams orally every
6 hours. Cholestyramine appears to have minimal effect
on absorption and excretion of cardiac glycosides in
man.
9. One 5-year-old boy did well on high-dose hydrocortisone
sodium succinate and phenobarbital (Hitt & Ettinger,
1986).
B. ANIMALS (ESPECIALLY DOGS) (Palumbo et al, 1975):
1. ATROPINE: May be used to decrease secretions and block
vagal effects. It is not a specific antidote.
2. ANTIHISTAMINES OR CORTICOSTEROIDS: May reduce the
effects of bufotoxins on the mucous membranes of the
mouth and other organs, but have little direct action.
3. PENTOBARBITAL-INDUCED ANESTHESIA: Does increase canine
tolerance to toad venom intoxication.
4. PROPRANOLOL: Has been tried on canines, with some
success. The dose used was high: 5 mg/kg.
5.3.3 ENHANCED ELIMINATION
A. MULTIPLE DOSE ACTIVATED CHARCOAL: May be of some use.
It has been used after IV administration of methyl
proscillaridin (Belz & Bader, 1974).
B. HEMODIALYSIS: Has been ineffective in removing cardiac
glycosides but may assist in restoring potassium to
normal levels. It has yet to be tried on bufagins.
5.6 DERMAL EXPOSURE
5.6.1 DECONTAMINATION
A. Wash exposed area extremely thoroughly with soap and
water. A physician may need to examine the area if
irritation or pain persists after washing.
5.6.2 TREATMENT
A. Effects may be seen after dermal exposure. Treatment
should be as appropriate under the oral treatment
section.
6.0 RANGE OF TOXICITY
6.2 MINIMUM LETHAL EXPOSURE
A. The skin of one toad is sufficient to cause significant
symptoms and even death in both animals and humans.
6.4 TOXIC SERUM/BLOOD CONCENTRATIONS
A. No toxic serum or blood levels have yet been established.
6.6 LD50/LC50
A. TABLE I - BUFAGIN LETHAL DOSES IN CATS
NAME Mean (Geo.)
LD,, mg/kg
Arenobufagin 0.08
Bufotalin 0.13
Desacetylbufotalin 0.26
Cinobufagin 0.20
Acetylcinobufagin 0.59
Desacetylcinobufagin inactive
Cinobufotalin 0.20
Acetylcinobufotalin 0.18
Desactylcinobufotalin inactive
Marinobufagin 1.49
Acetylmarinobufagin 0.95
12Beta-Hydroxymarinobufagin 3.00
Topic: TOAD TOXINS
Bufotalidin (hellebrigenin) 0.08
Acetylbufotalidin 0.06
Resibufogenin inactive
Acetylresibufogenin inactive
12Beta-Hydroxyresibufogenin 4.16
Bufalin 0.14
Telocinobufagin 0.10
Bufotalinin 0.62
Artebufogenin inactive
Gamabufotalin 0.10
Vallicepobufagin 0.20
Quercicobufagin 0.10
Viridobufagin 0.11
Regularobufagin 0.15
Fowlerobufagin 0.22
B. TABLE II BUFOTOXIN LETHAL DOSES IN CATS
NAME Mean (Geo.)
LD, mg/kg
Viridobufotoxin 0.27
Vulgarobufotoxin 0.29
Cinobufotoxin 0.36
Gamabufotoxin 0.37
Arenobufotoxin 0.41
Marinobufotoxin 0.42
Regularobufotoxin 0.48
Alvarobufotoxin 0.76
Fowlerobufotoxin 0.79
C. REFERENCE: (Chen & Kovarikova, 1967).
6.8 OTHER
A. The structure of the cardioactive bufadienolides leads to
greater potency than the corresponding plant glycosides
thus the cardenolides of plants - digitoxigenin,
periplogenin, oleandrigenin, sarmentogenin, and
strophanthidin, corresponding to bufalin,
telocinobufagin, bufotalin, gamabufotalin, and
bufotalidin - have lower toxicities.
B. The toxicity of the cardioactive bufotoxins is lower than
those of the corresponding bufagins (bufadienolides)
(Chen & Kovarikova, 1967).
C. The skin of Bufo alvarius contains 5-methoxy-N,N-
dimethyltryptamine (5-MeO-DMT) at a concentration of 50
to 160 mg/g of skin (Daly & Witkop, 1971).
7.0 AVAILABLE FORMS/SOURCES
A. BUFOTOXINS: Is the name of a collection of compounds
found in the toad venom which may be secreted into toad
skin or found in 2 glands behind the eyes, called parotid
glands (Tyler, 1976). Bufotoxins may also be
specificially applied to the conjugates of a bufagin with
suberylargine.
B. Before digitalis was extracted from Digitalis purpura,
dried and powdered toad skins were used as a cardiac
medication (Burton, 1977). Other "folk" uses include
expectorant, diuretic, and remedy for toothaches,
sinusitis, and hemorrhage of the gums.
C. Toad skins have also been used for their hallucinogenic
Topic: TOAD TOXINS
effect (Emboden, 1979).
8.0 KINETICS
8.1 ABSORPTION
A. The oral absorption of the bufagins and bufotoxins is
generally poor. Less than 15% of cinobufagin is absorbed
orally in rats.
B. Other components of toad venom are rapidly absorbed via
mucous membranes and cause immediate symptoms in animals
(Smith, 1982).
8.4 EXCRETION
8.4.3 BILE
A. Little could be found concerning the excretion of these
compounds; similar cardenolides and substances such as
proscillaridin are excreted largely in the bile (Belz &
Bader, 1974).
9.0 PHARMACOLOGY/TOXICOLOGY
9.1 PHARMACOLOGIC MECHANISM
A. Most bufandienolides are cardiotonic sterols synthesized
by toads from cholesterol (Siperstein, 1957). The
lactone ring is 6-membered of an alpha pyrone type
attached to C17. They have a secondary hydroxy group at
C3 and are called bufagins - which corresponds to the
aglycones found in the cardiac glycosides in plants.
None of these bufandienolides conjugates with a
carbohydrate (as do the plants) to form glycosides, but
some do form bufotoxins by combining with suberylargine
(Chen & Kovarikova, 1967).
B. In the toad, some of these compounds (eg, resibufogenin)
are ouabain-like and increase the force of contraction of
heart muscle (Lichtstein et al, 1986).
C. The pharmacology of the catecholamines found in toad
venom is well known and need not be discussed here.
D. INDOLEALKYLAMINES: Pharmacology is also known. Besides
having some hallucinogenic effects, these compounds may
stimulate uterine and intestinal muscle (Chen &
Kovarikova, 1961).
9.2 TOXICOLOGIC MECHANISM
A. Bufagins and bufotoxins have been shown to inhibit
sodium, potassium, ATPase activity (Lichtstein et al,
1986). Their action is almost the same as that of the
digitalis glycosides (Palumbo et al, 1975).
12.0 REFERENCES
12.1 GENERAL REFERENCES
1. Belz GG & Bader H: Effect of oral charcoal on plasma
levels of intravenous methyl proscillaridin. Klin
Wochenschr 1974; 52:1134-1135.
2. Burton R: Venomous Animals: Colour Library International
Ltd. London, 1977.
3. Chen KK & Kovarikova A: Pharmacology and toxicology of
toad venom. J Pharm Sci 1967; 56:1535-1541.
4. Daly JW & Witkop B: Chemistry and pharmacology of frog
venoms. In: Bucherl W & Buckly EE (eds). Venomous
Animals and Their Venoms, vol 2, Academic Press, New York,
1971.
5. Emboden W: Narcotic Plants. MacMillan Publishing Company,
Topic: TOAD TOXINS
Inc, 1979.
6. Gilman AG, Goodman LS, Rall TW et al: The Pharmacological
Basis of Therapeutics, 7th ed. MacMillan Publishing
Company, 1985.
7. Gould L, Solomon F, Cherbakoff A et al: Clinical studies
on proscillaridin, a new squill glycoside. J Clin
Pharmacol 1971; 11:135-145.
8. Hitt M & Ettinger DD: Toad toxicity. N Engl J Med 1986;
314:1517.
9. Kantor RE, Dudlettes SD & Shulgin AT: 5-Methoxy-a-methyl-
tryptamine (a, O-dimethylserotonin), a hallucinogenic
homolog of serotonin. Biological Psychiatry 1980;
15:349-352.
10. Kibmer B & Wichtl M: Bufadienolide aus samen von
helleborus odorus. Planta Med 1986; 2:77-162.
11. Lichtstein P, Kachalsky S & Deutsch J: Identification of
a ouabain-like compound in toad skin and plasma as a
bufodienolide derivative. Life Sci 1986; 38:1261-1270.
12. Lincoff G & Mitchel DH: Toxic and Hallucinogenic Mushroom
Poisoning. Van Nostrand Reinhold Company, Dallas, 1977.
13. McKenna DJ & Towers GH: Biochemistry and pharmacology of
tryptamines and beta-carbolines, a minireview. J
Psychoactive Drugs 1984; 16:347-358.
14. Palumbo NE, Perri S & Read G: Experimental induction and
treatment of toad poisoning in the dog. J Am Vet Med
Assoc 1975; 167:1000-1005.
15. Perry BD & Bracegirdle JR: Toad poisoning in small
animals. Vet Rec 1973; 92:589-590.
16. Siperstein MD, Murray AW & Titus E: Biosynthesis of
cardiotonic sterols from cholesterol in the toad Bufo
marinus. Arch Biochem Biophys 1957; 67:154-160.
17. Smith RL: Venomous Animals of Arizona. Cooperative
Extension Service, College of Agriculture, Univ AZ,
Tucson, 1982.
18. Tyler MJ: Frogs. William Collins Ltd, Sydney, 1976.
13.0 AUTHOR INFORMATION
A. Written by: David G. Spoerke, M.S., RPh., 06/86
B. Reviewed by: Ken Kulig, M.D., 06/86
C. Specialty Board: Biologicals
D. In addition to standard revisions of this management
certain portions were updated with recent literature:
11/86.
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