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Toad Toxins
by David G. Spoerke
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.
B. No toxic serum or blood levels have yet been established.



1.0 SUBSTANCES INCLUDED
1.1 THERAPEUTIC/TOXIC CLASS
  1. 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
  1. 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
  1. Toads are found throughout the world, Bufo marinus having one of the widest distributions.


2.0 CLINICAL EFFECTS
2.1 SUMMARY
  1. 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
  1. 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
  1. IRRITATION: Exposure of the nasal mucous membranes to the toad toxins may produce severe irritation (Chen & Kovarikova, 1967).
2.3.5 THROAT
  1. The mouth and throat may become anesthetized if bufotoxins have been ingested (Chen & Kovarikova, 1967).
2.4 CARDIOVASCULAR
  1. VENTRICULAR FIBRILLATION: Dogs intentionally poisoned with bufagins orally develop ventricular fibrillation and if untreated - death (Palumbo et al, 1975). The symptoms resemble digitalis poisoning.
  2. 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
  1. DYSPNEA: Weakened respirations may be seen if toad toxins have been ingested (Smith, 1982).
2.6 NEUROLOGIC
  1. 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).
  2. 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.
  3. LOCAL ANESTHESIA: Many bufagins have local anesthetic actions, especially on the oral mucosa (Chen & Kovarikova, 1967).
2.7 GASTROINTESTINAL
  1. SALIVATION: Intense salivation is usually seen in poisoned cats and dogs (Perry & Bracegirdle, 1973), and was seen in one 5-year-old boy (Hitt & Ettinger, 1986).
  2. VOMITING: Is often present in animals (Perry & Bracegirdle, 1973).
  3. NUMBNESS: If ingested, the toxins cause numbness of the oral mucosa (Smith, 1982; Chen & Kovarikova, 1967).
2.12 FLUID-ELECTROLYTE
  1. HYPERKALEMIA: Similar to that seen with digitalis poisoning, may be seen.
2.13 TEMPERATURE REGULATION
  1. FEVER: Is a symptom common to ingestion of toads by cats and dogs (Perry & Bracegirdle, 1973).
2.14 HEMATOLOGIC
  1. CYANOSIS: Has been seen in dogs (Hitt & Ettinger, 1986).
2.15 DERMATOLOGIC
  1. PERSPIRATION: Although handling toads is generally not considered seriously injurious to humans, it is thought to dramatically reduce perspiration (Smith, 1982).
2.18 PSYCHIATRIC
  1. 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
  1. 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
  1. 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.
  2. B. A serum potassium level should be drawn to test for hyperkalemia (Chen & Kovarikova, 1967).

4.0 CASE REPORTS
  1. 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.
  2. 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
  1. Support respiratory and cardiovascular function.
5.2 SUMMARY
  1. 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
  1. 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.
  2. 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 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:
      1. 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).
      2. 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.
  3. 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
  1. 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 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
      1. Lidocaine is useful in the management of ventricular tachyarrhythmias, PVC's, and bigeminy. Lidocaine does not improve conduction through the AV node.
      2. 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 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).
  2. 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
  1. MULTIPLE DOSE ACTIVATED CHARCOAL: May be of some use. It has been used after IV administration of methyl proscillaridin (Belz & Bader, 1974).
  2. 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
  1. 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
  1. 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
  1. 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
  1. No toxic serum or blood levels have yet been established.
6.6 LD50/LC50
  1. 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
    	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
    	
  2. 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
    	
  3. REFERENCE: (Chen & Kovarikova, 1967).
6.8 OTHER
  1. 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.
  2. The toxicity of the cardioactive bufotoxins is lower than those of the corresponding bufagins (bufadienolides) (Chen & Kovarikova, 1967).
  3. 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
  1. 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.
  2. 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.
  3. Toad skins have also been used for their hallucinogenic effect (Emboden, 1979).

8.0 KINETICS
8.1 ABSORPTION
  1. The oral absorption of the bufagins and bufotoxins is generally poor. Less than 15% of cinobufagin is absorbed orally in rats.
  2. 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
  1. 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
  1. 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).
  2. 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).
  3. C. The pharmacology of the catecholamines found in toad venom is well known and need not be discussed here.
  4. 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
  1. 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, 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.