Toad poisoning (toxicosis) can occur when dogs or cats bite, ingest, or mouth toads, although serious reaction or death generally occurs only after exposure to large toads such as Rhinella marina (marine toad) or Incilius alvarius (Colorado river toad). Clinical signs of toxicosis include hypersalivation, gagging or retching, vomiting, weakness, cyanosis, dyspnea, and seizures; hyperkalemia and cardiac arrhythmias can occur in severe cases. Treatment is generally supportive, although digoxin-specific Fab (a life-saving antidote to treat severe digoxin toxicosis) can be considered in cases of severe arrhythmias and/or hyperkalemia refractory to supportive care.
Dogs and, less frequently, cats can develop clinical signs of toxicosis (poisoning) after oral exposure (biting, ingesting, or mouthing) to many types of toads. Severity varies greatly, depending on the extent of contact and type of toad.
Etiology and Pathogenesis of Toad Poisoning in Dogs and Cats
Toxins are produced by all toads; however, potency varies with species and even between geographical areas for the same species (1). Toad toxin, a defensive mechanism, is secreted by large glands located dorsal and caudal to the eyes and by small glands distributed throughout the skin.
The toxin, a thick, creamy white, highly irritating substance, can be expelled quickly by contraction of periglandular muscles in the skin. Its many components include bufagenins, which have digitalis-like effects, and bufotoxins, which block sodium channels in nerves via a mechanism similar to that of local anesthetics, catecholamines, and serotonin.
The most toxic species of toad in the US is the giant or marine toad, Rhinella marina (formerly Bufo marinus), an introduced species that is established in Florida, Hawaii, and Texas. R marina is also known as the cane toad in Australia, where its range extends across the northeastern half of the continent.
The Colorado River toad, Incillus (formerly Bufo) alvarius, found in the southwestern US and northern Mexico, is another toad of sufficient size to have potentially lethal amounts of toxins in its skin secretions.
Clinical Findings of Toad Poisoning in Dogs and Cats
Encounters with toads are most common in warm or mild weather.
Clinical signs of toxicosis are variable and range from local mouth/throat irritation to seizures and death. Severity depends on patient state of health, extent of exposure, length of time since exposure, and species of toad.
Exposure to smaller toads generally elicits milder clinical signs; however, in animals with preexisting health issues, especially cardiac disease, clinical signs can be more severe, especially if the toad is ingested.
Local effects (profuse, sometimes frothy salivation, accompanied by vigorous head shaking, pawing at the mouth, and retching) are immediate, because the toxin is extremely irritating. Vomiting is not unusual, especially in severe cases, and although it can persist for several hours, often no further clinical signs develop in poisoning by common indigenous toads.
Other reported clinical effects include hyperemic mucous membranes, tachypnea, pulmonary edema, ataxia, recumbency, stupor, or coma. With Rhinella marina or Incillus alvarius, cardiac arrhythmias, dyspnea, cyanosis, and seizures are characteristic. Cardiac and CNS involvement can be life-threatening.
Diagnosis of Toad Poisoning in Dogs and Cats
History and clinical findings
Serum biochemical analysis
Measurement of serum digoxin concentration
Diagnosis of toad poisoning might be suspected on the basis of history and compatible clinical findings. Ingestion or mouthing a toad might be reported.
Abnormalities on serum biochemical analysis are not specific. Hyperkalemia is a possible finding, because of the digitalis-like effects of bufagenins; however, it is not always present.
Specific bufotoxin measurement is not valuable for diagnosis. In cases of toad poisoning, positive serum digoxin concentrations have been reported, attributable to the cross-reaction between toad toxins and digoxin (2). However, measurement of serum digoxin concentration, while possibly aiding in confirming exposure, is not likely to indicate severity of exposure.
Cardiac arrhythmias should be identified.
Differential diagnoses include other cardiac glycoside toxicoses (eg, digoxin, lily of the valley, oleander).
Treatment of Toad Poisoning in Dogs and Cats
Copious flushing of oral mucous membranes
Supportive care
A specific antidote for toad toxins is not available.
Treatment is directed at minimizing toxin absorption and controlling associated clinical signs. Minimal treatment might be required after exposure to toxins in geographical areas where less toxic toads are found.
The patient's mouth should be immediately and thoroughly lavaged with copious amounts of water. Affected animals should be prevented from inhaling aerosols of saliva or water that contain toad toxin.
Induction of emesis is not recommended because of the potential for rapid onset of neurological signs. Atropine can decrease the volume of saliva and the risk of aspiration; however, it should not be used until cardiovascular status is assessed. More severely affected animals need more extensive treatment.
Pearls & Pitfalls
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Cardiac arrhythmias should be treated with standard protocols. If bradyarrhythmias exist, atropine or dopamine should be considered; tachyarrhythmias should be treated with lidocaine, phenytoin, propranolol, or procainamide hydrochloride.
Digoxin-specific Fab (a life-saving antidote to treat severe digoxin toxicosis) can be considered in cases of severe arrhythmias or hyperkalemia refractory to standard treatment; however, the cost of digoxin-specific Fab often prohibits its use in veterinary patients.
CNS excitation or seizures, if present, should be controlled by benzodiazepines, barbiturates, or a combination of the two. Anesthetics that predispose to ventricular fibrillation (eg, halothane) should be avoided. Supplemental oxygen and mechanical ventilation might also be needed if cyanosis and dyspnea are severe.
Key Points
Serious or life-threatening toad intoxication can result from exposure to large toads such as marine toads (cane toads) or Colorado river toads.
Clinical signs include hypersalivation, vomiting, lethargy, cyanosis, dyspnea, cardiac arrhythmias, seizures, or coma.
Treatment is largely supportive; in patients with severe cardiac effects refractory to standard treatment, digoxin-specific Fab can be considered.
For More Information
Wilkins A, Cagle L, Wells R, Granfone M. Clinical review of Colorado river toad (Incilius alvarius) intoxication in dogs in Arizona: clinical signs, treatments, and outcomes. J Am Vet Med Assoc. 2026;264(6):1-4.
Vieira dos Santos C, Kerkhoff J, Aparecida Tomazelli C, et al. Vasoconstrictor and hemodynamic effects of a methanolic extract from Rhinella marina toad poison. Toxicon. 2022;218:57-65.
Rose'Meyer RB, Wilson JC, Grice ID, et al. The chemical profile and cardiovascular effects of Rhinella marina cane toad skin secretion on murine heart. Toxin Rev. 2025;45(1):15-28.
Smit A. Toads. In Hovda LR, Brutlag AG, Poppenga RH, Epstein SE, eds. Blackwell's Five-Minute Veterinary Consult Clinical Companion: Small Animal Toxicology. 3rd ed. Wiley Blackwell; 2024.
Johnnides S, Green T, Eubig P. Toad intoxication in the dog by Rhinella marina: the clinical syndrome and current treatment recommendations. J Am Anim Hosp Assoc. 2016;52(4):205-211.
Also see pet owner content regarding toad poisoning.
References
Hudson CM, Brown GP, Blennerhassett RA, Shine R. Variation in size and shape of toxin glands among cane toads from native-range and invasive populations. Sci Rep. 2021;11(1):936. doi:10.1038/s41598-020-80191-7
Gowda RM, Cohen RA, Khan IA. Toad venom poisoning: resemblance to digoxin toxicity and therapeutic implications. Heart. 2003;89(4):e14. doi:10.1136/heart.89.4.e14
