Toad poisoning (toxicosis) can occur when dogs or cats bite or ingest toads, although serious disease or death generally occurs only after exposure to large toads such as the 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 F(ab) may be considered in cases of severe arrhythmias and/or hyperkalemia refractory to supportive care.
Dogs and, less frequently, cats may develop signs of toxicosis (poisoning) after oral exposure to many types of toads. Severity varies greatly, depending on the extent of contact and type of toad. Toxins are produced by all toads; however, potency varies with species and apparently even between geographic areas for the same species. 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 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 levels of toxins in its skin secretions. Exposure to smaller toads generally elicits milder clinical signs; however, in animals with preexisting health issues, especially cardiac disease, clinical signs may be more severe, especially if the toad is ingested.
Clinical Findings and Diagnosis of Toad Poisoning in Dogs and Cats
Clinical evaluation
Serum biochemical analysis to detect hyperkalemia and measurement of serum digoxin concentration
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 convulsions and death. Severity depends on patient state of health, extent of exposure, length of time since exposure, and species of toad. 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 may persist for several hours, no further signs may develop in poisoning by common indigenous toads.
Other reported clinical effects include hyperemic mucous membranes, tachypnea, pulmonary edema, ataxia, recumbency, stupor, or coma. With R marina or I alvarius, cardiac arrhythmias, dyspnea, cyanosis, and seizures are characteristic. Cardiac and CNS involvement can be life-threatening. Hyperkalemia, due to digitalis-like effects of bufagenins, may be present, and digoxin may be detectable in serum due to cross-reaction between toad toxins and digoxin. However, serum digoxin concentration, while aiding in confirming exposure, is not likely to indicate severity of exposure.
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 may be required after exposure to toxins in geographic 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 neurologic signs. Atropine may reduce 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.
Cardiac arrhythmias should be identified and 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 F(ab) may be considered in cases of severe arrhythmias or hyperkalemia refractory to standard treatment; however, cost of F(ab) 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 may also be needed if cyanosis and dyspnea are severe.
Key Points
Serious or life-threatening toad intoxication is generally the result of exposure to large toads such as marine toads or Colorado river toads.
Clinical signs include hypersalivation, vomiting, lethargy, cyanosis, dyspnea, cardiac arrhythmias, convulsions, or coma.
Treatment is largely supportive; in patients with severe cardiac effects refractory to standard treatment, digoxin-specific F(ab) may be considered.
For More Information
Also see pet health content regarding toad poisoning.
