Human Poisoning by Toxic Frogs and Toads
![Omid Mehrpour](/_next/image?url=https%3A%2F%2Fd21vqf76ys4v7k.cloudfront.net%2Fimage%2Fprofile%2Fomid.png&w=96&q=75)
Omid Mehrpour
Post on 05 Feb 2025 . 10 min read.
Omid Mehrpour
Post on 05 Feb 2025 . 10 min read.
Poisonous frogs and toads secrete toxic substances from their skin or specialized glands, posing potential risks to humans through ingestion, skin contact, or exposure to mucous membranes. Unlike venomous animals that inject toxins through bites or stings, these amphibians cause intoxication via passive contact or ingestion.
Toad and frog toxins have been extensively studied due to their potent effects on the cardiovascular, neuromuscular, and gastrointestinal systems. Bufadienolides, found in many toad species, are steroidal cardiac glycosides structurally related to digoxin and ouabain. These compounds inhibit Na+/K+-ATPase, increasing intracellular calcium and potentially life-threatening cardiac toxicity. Some frog species, such as the Phyllobates genus, produce batrachotoxins, which interfere with sodium channel function and can be lethal.
This blog consolidates evidence from published research on the toxic effects of frog and toad secretions, clinical case reports, and the global impact of amphibian poisoning. Understanding the toxicological mechanisms and clinical manifestations of toad and frog poisoning is crucial for early diagnosis and appropriate management.
Related Blog: Deadly Delicacy: The Hidden Danger of Eating Sea Turtles
Poisonous Toxins in Frogs and Toads produce various toxins, which differ in composition, potency, and mechanism of action. These toxins are primarily secreted from the skin and parotid glands.
Bufadienolides are steroidal compounds with strong cardiotoxic effects. They are found in the secretions of Bufo and Rhinella species, such as the cane toad (Rhinella marina) and the Asiatic toad (Bufo gargarizans). These toxins inhibit Na+/K+-ATPase, increasing intracellular calcium and subsequent cardiac arrhythmias.
Effects: Bradycardia, ventricular arrhythmias, cardiac arrest.
Documented Cases: Several cases of bufadienolide poisoning in humans have been reported, particularly from ingestion of toad meat or eggs (Trakulsrichai et al., 2020; Kuo et al., 2009).
Batrachotoxins are potent neurotoxins found in frogs of the Phyllobates genus, particularly Phyllobates terribilis, Phyllobates aurotaenia, and Phyllobates bicolor. These toxins originate from dietary alkaloid precursors obtained from arthropods, such as melyrid beetles. These toxins irreversibly activate voltage-gated sodium channels, leading to paralysis and respiratory failure.
Effects: Muscle paralysis, respiratory arrest, seizures.
Toxicity: Batrachotoxins have an estimated lethal dose (LD50) of 2–7 µg/kg in animal models, suggesting that a few micrograms could be potentially fatal in humans. However, direct human toxicity data is limited.
Tetrodotoxin (TTX), a potent neurotoxin primarily associated with pufferfish and certain newts, has also been detected in select frog species, particularly Atelopus spp. However, documented cases of human tetrodotoxin poisoning from frogs remain exceedingly rare. It acts by blocking sodium channels, leading to paralysis and cardiac failure.
Effects: Numbness, paralysis, cardiac arrest.
Fatal Dose: The estimated lethal dose of tetrodotoxin in humans ranges from 1–2 mg, though individual sensitivity varies based on body weight and metabolism.
The severity of poisoning depends on the route of exposure (ingestion, dermal contact, inhalation) and the dose of toxins absorbed.
Bradycardia and Arrhythmias: Cases of toad poisoning commonly present with sinus bradycardia, hyperkalemia, and ventricular fibrillation (Trakulsrichai et al., 2020).
Cardiac Arrest: Several fatalities have been reported from ingesting toad meat or eggs, leading to irreversible cardiac dysrhythmias.
Electrocardiogram (ECG) abnormalities in bufadienolide poisoning include sinus bradycardia, atrioventricular (AV) block, ST-segment depression, and potentially life-threatening ventricular tachyarrhythmias.
Muscle Weakness and Paralysis: Neurotoxic toad and frog secretions cause flaccid paralysis due to sodium channel blockade or overactivation.
Seizures and Respiratory Failure: Severe cases, particularly with batrachotoxin exposure, can lead to asphyxiation due to diaphragm paralysis.
Nausea, Vomiting, and Abdominal Pain: Common in toad poisoning cases (Trakulsrichai et al., 2020).
Hyperkalemia: Occurs due to Na+/K+-ATPase inhibition by bufadienolides.
• Serum Digoxin Levels:
Elevated levels in patients with toad poisoning confirm digitalis-like toxicity. Given the structural similarity of bufadienolides to digoxin, measurement of serum digoxin levels using immunoassays may cross-react with these toxins, leading to falsely elevated results. However, chromatographic techniques such as high-performance liquid chromatography (HPLC) or mass spectrometry (MS) can provide more accurate toxin identification.
• Electrolyte Imbalance:
Hyperkalemia and acidosis are common due to bufadienolides' inhibition of Na+/K+-ATPase, which leads to intracellular sodium accumulation and extracellular potassium elevation. Severe hyperkalemia (>6.5 mmol/L) can precipitate life-threatening arrhythmias such as ventricular tachycardia or fibrillation. Additional laboratory findings may include elevated lactate levels, indicative of metabolic acidosis due to impaired tissue perfusion in severe cases.
• Additional Markers:
Elevated cardiac troponins may be observed in severe cases, suggesting myocardial injury secondary to bufadienolide toxicity. Monitoring renal function and creatinine levels is also crucial, as bufadienolide-induced toxicity may cause acute kidney injury (AKI) secondary to hemodynamic instability.
• Confirmatory Testing:
In cases of suspected toad poisoning, liquid chromatography-mass spectrometry (LC-MS) can be used to confirm the presence of bufadienolides in blood or tissue samples .
Continuous ECG monitoring is crucial in suspected cases of toad poisoning.
Frog and toad poisoning—most often resulting from exposure to cardiotoxic substances such as bufadienolides and bufotoxins—can cause life-threatening cardiac arrhythmias, neurological deficits, and gastrointestinal distress. Prompt recognition, stabilization, and targeted treatment are crucial to improving outcomes.
Airway and Breathing:
Airway Management: Secure the airway; consider intubation if there is respiratory compromise.
Oxygen Support: Administer supplemental oxygen as needed.
Circulatory Support:
Cardiac Monitoring: Initiate continuous ECG monitoring to detect and manage arrhythmias.
Fluid Therapy: Correct dehydration and electrolyte imbalances.
Gastrointestinal Decontamination:
If exposure is recent, consider gastric lavage, activated charcoal, or induced emesis to reduce toxin absorption (Yei & Deng, 1993).
Decontamination should occur after initial stabilization.
Digoxin-Specific Antibody Fragments (DsFab):
Indication: Used in severe bufadienolide toxicity cases.
Note: Calcium gluconate is generally avoided as it may worsen cardiac glycoside toxicity (Trakulsrichai et al., 2020).
Beta-Blockers:
Propranolol: Can counteract tachycardia and ventricular arrhythmias (Palumbo et al., 1975).
Combination Therapy: In veterinary cases, a regimen including propranolol, phenytoin, metoclopramide, and ranitidine has been successfully used (Varshney et al., 2011).
Other Antiarrhythmics and Cardiac Support:
Lidocaine: May be employed for arrhythmia control when appropriate.
Atropine: For severe bradyarrhythmias, intravenous atropine can restore heart rate; additional support with dopamine or pacing might be necessary (Sruamsiri, 2014).
Novel Antidotes:
Bezoar Bovis: This traditional Chinese medicine has demonstrated promise in animal models by reducing mortality and arrhythmias induced by toad venom (Ma et al., 2012).
Hyperkalemia:
Severely elevated serum potassium levels (≥7 mEq/L) are associated with poor outcomes and require aggressive intervention (Chi et al., 1998).
Timeliness of Antidote Administration:
Early use of DsFab or other effective antidotes is critical for improving survival rates.
Adherence to ACLS Protocols:
Management of cardiac arrhythmias should follow Advanced Cardiovascular Life Support guidelines.
In cases of refractory bradyarrhythmia, pacemaker placement may be considered.
Avoidance of Calcium in Hyperkalemia:
Calcium administration is contraindicated as it may exacerbate intracellular hypercalcemia and worsen dysrhythmias.
Support in Resource-Limited Settings:
Where Digoxin-specific Fab is unavailable, comprehensive supportive care remains essential (Trakulsrichai et al., 2020).
36 patients studied (2012–2016).
8.3% mortality rate due to cardiac arrest.
Common symptoms: Bradycardia, hyperkalemia, gastrointestinal distress.
Treatment: Supportive care, pacemakers, digoxin-specific antibody fragments.
A previously healthy woman developed severe bradyarrhythmia and cardiac arrest after ingesting toad eggs. She required emergency transvenous pacemaker placement and administration of digoxin-specific Fab fragments for stabilization.
Frogs and toads secrete highly toxic compounds that can cause severe cardiac, neurological, and gastrointestinal effects, necessitating urgent medical attention in cases of poisoning. Bufadienolide toxicity closely resembles digitalis toxicity, primarily affecting the cardiovascular system. Management focuses on prompt stabilization (airway, breathing, circulation), gastrointestinal decontamination when appropriate, and targeted pharmacologic interventions. Digoxin-specific antibody fragments (DsFab) remain the cornerstone of treatment, with additional therapies such as beta-blockers and emerging agents like Bezoar Bovis playing supportive roles. Early recognition, continuous cardiac monitoring, and adherence to ACLS protocols are critical in optimizing patient outcomes.
Answer:
Toad poisoning presents with cardiac, gastrointestinal, and neurological effects, depending on the species and level of exposure. Common symptoms include:
Cardiac symptoms: Bradycardia, arrhythmias (AV block, ventricular tachycardia, fibrillation), hypotension, and cardiac arrest.
Neurological effects: Convulsions, ataxia, stupor, paralysis, and in severe cases, coma.
Gastrointestinal effects: Nausea, vomiting, diarrhea, and abdominal pain.
Additional symptoms: Hypersalivation, dizziness, anxiety, and muscle weakness.
Death may occur within 15 minutes in severe cases due to cardiac arrest.
Answer:
Poison dart frog toxins (Batrachotoxins): Keep sodium channels open, leading to sustained depolarization, paralysis, respiratory failure, and death .
Bufadienolides (Toad toxins): Cause digitalis-like toxicity, cardiac arrhythmias, hyperkalemia, and cardiac arrest .
Tetrodotoxin (TTX) in some frogs: Blocks sodium channels, leading to paralysis, numbness, and respiratory arrest .
Answer:
Most poisonous frogs secrete alkaloid toxins through their skin, which can cause numbness, tingling, and irritation upon contact.
In highly toxic species like the golden poison dart frog (Phyllobates terribilis), even a single microgram of toxin can be lethal if absorbed through wounds or mucous membranes (Dumbacher et al., 2004).
Handling without gloves is strongly discouraged due to the potential dermal absorption of toxins.
Answer:
Yes. Frogs can transmit bacterial and parasitic infections:
Salmonella infection: Frogs are known carriers of Salmonella, which can cause diarrhea, fever, and vomiting in humans.
Zoonotic parasites: Frogs can harbor Sparganosis (Spirometra species), Mycobacterium spp., and Aeromonas hydrophila, which may cause skin infections, intestinal issues, and severe systemic illness.
Answer:
Toad venom contains 5-MeO-DMT, a psychedelic compound extracted primarily from the Colorado River toad (Incilius alvarius). It is known for inducing intense hallucinations and mystical experiences but can cause severe tachycardia, nausea, vomiting, and even death in overdoses.
Answer:
Toad toxins are typically thick, creamy, white secretions produced by the parotid glands behind their eyes.
These secretions contain bufadienolides, epinephrine, and serotonin, which contribute to their toxic and hallucinogenic effects (Merck Veterinary Manual, 2024).
Answer:
Licking a toxic frog or toad can cause severe poisoning, as the toxins are rapidly absorbed through the mucous membranes.
Symptoms include numbness, hallucinations, nausea, seizures, arrhythmias, and cardiac arrest.
Answer:
If batrachotoxin enters the bloodstream, it irreversibly opens sodium channels, leading to paralysis and death within minutes to hours.
There is no known antidote; supportive treatment includes mechanical ventilation and cardiac monitoring.
Answer:
The golden poison dart frog (Phyllobates terribilis) is the most toxic frog species. Just 2 micrograms of its batrachotoxin can kill a human.
Answer:
Tetrodotoxin (TTX) blocks sodium channels, preventing nerve impulses and causing numbness, respiratory failure, and cardiac arrest.
There is no antidote, but rapid mechanical ventilation and supportive care can increase survival chances.
Answer:
Wash your hands immediately with soap and water to remove potential toxins.
Avoid touching your eyes, mouth, or open wounds to prevent absorption of bufotoxins.
If symptoms such as tingling, dizziness, or nausea develop, seek medical attention immediately.
Answer: Toad poisoning has no specific antidote. However, supportive and symptomatic treatments can be effective:
Digoxin-Specific Antibody Fragments (DsFab): Used in bufadienolide poisoning to bind and neutralize cardiac toxins.
Activated charcoal: Helps bind and limit toxin absorption when administered early.
IV fluids and vasopressors: Used to stabilize hypotension and arrhythmias.
ECG and electrolyte monitoring are critical in severe cases.
© All copyright of this material is absolute to Medical toxicology
Dr. Omid Mehrpour is a distinguished medical toxicologist known for his extensive clinical and research expertise. He focuses on understanding and treating toxic exposures. Renowned for his ability to diagnose and manage poisoning cases, Dr. Mehrpour has authored numerous impactful publications and is dedicated to educating future medical toxicologists. His innovative approach and commitment to patient care make him a leading figure in medical toxicology.
Bressman, M., Repplinger, D., Slater, W., & Patt, M. (2016). Electrophysiologic similarities of overdose between digoxin and bufadienolides found in a Chinese aphrodisiac. Journal of Arrhythmia, 33, 76 - 78. https://doi.org/10.1016/j.joa.2016.05.004.
Brubacher, J., Lachmanen, D., Ravikumar, P., & Hoffman, R. (1999). Efficacy of digoxin specific Fab fragments (Digibind) in the treatment of toad venom poisoning. Toxicon : official journal of the International Society on Toxinology, 37 6, 931-42 . https://doi.org/10.1016/S0041-0101(98)00224-4.
Brubacher JR, Ravikumar PR, Bania T, Heller MB, Hoffman RS. Treatment of toad venom poisoning with digoxin-specific Fab fragments. Chest. 1996 Nov;110(5):1282-8. doi: 10.1378/chest.110.5.1282
Chen, Z., Yu, Q., Chen, J., Yu, X., Cao, J., Zhai, Y., Tan, Y., Zhan, Z., Li, W., Zou, X., Guo, X., Xie, J., Huang, W., Zhang, Z., & Tian, H. (2024). Bufadienolide-Fatty Acid Conjugates from the Fertilized Eggs of Toad Bufo gargarizans: Isolation, Characterization, Toxicity, and Antiproliferative Evaluation.. Journal of agricultural and food chemistry. https://doi.org/10.1021/acs.jafc.4c03184.
Chi, H., Hung, D., Hu, W., & Yang, D. (1998). Prognostic implications of hyperkalemia in toad toxin intoxication. Human and Experimental Toxicology, 17, 343 - 346. https://doi.org/10.1177/096032719801700610.
Daly, J., Gusovsky, F., Myers, C., Yotsu-Yamashita, M., & Yasumoto, T. (1994). First occurrence of tetrodotoxin in a dendrobatid frog (Colostethus inguinalis), with further reports for the bufonid genus Atelopus.. Toxicon : official journal of the International Society on Toxinology, 32 3, 279-85 . https://doi.org/10.1016/0041-0101(94)90081-7.
Ma H, Zhou J, Jiang J, Duan J, Xu H, Tang Y, Lv G, Zhang J, Zhan Z, Ding A. The novel antidote Bezoar Bovis prevents the cardiotoxicity of Toad (Bufo bufo gargarizans Canto) Venom in mice. Exp Toxicol Pathol. 2012 Jul;64(5):417-23. https://doi.org/10.1016/j.etp.2010.10.007.
Pierach, C. (1996). Digoxinlike toxicity and death from a purported aphrodisiac.. JAMA, 275 13, 988 . https://doi.org/10.1001/JAMA.1996.03530370026023.
Palumbo, N., Perri, S., & Read, G. (1975). Experimental induction and treatment of toad poisoning in the dog. Journal of the American Veterinary Medical Association, 167 11, 1000-5 .
Kuo, H., Hsu, C., Chen, J., Wu, Y., & Shen, Y. (2009). Life-threatening episode after ingestion of toad eggs: a case report with literature review. BMJ Case Reports, 2009. https://doi.org/10.1136/bcr.11.2008.1241.
Trakulsrichai S, Chumvanichaya K, Sriapha C, Tongpoo A, Wananukul W. Toad Poisoning: Clinical Characteristics and Outcomes. Ther Clin Risk Manag. 2020 Dec 16;16:1235-1241. doi: 10.2147/TCRM.S272863
Yei, C., & Deng, J. (1993). [Toad or toad cake intoxication in Taiwan: report of four cases]. Journal of the Formosan Medical Association = Taiwan yi zhi, 92 Suppl 3, S135-9 .