Dogs and, less frequently, cats may be poisoned by oral exposure to many types of toads. Severity varies greatly, depending on extent of contact and type of toad. Venom is produced by all toads, but its potency varies with species and apparently between geographic locations within individual species. Toad venom, a defensive mechanism, is secreted by glands located dorsal and posterior to the eyes and by other dermal structures, including warts. The venom, a thick, creamy white, highly irritating substance, can be expelled quickly by the contraction of periglandular muscles in the skin. Its many components include bufagins, which have digitalis-like effects, catecholamines, and serotonin. The most toxic species in the USA appears to be the giant or marine toad, Bufo marinus, an introduced species that is established in Florida, Hawaii, and Texas. Mortality is 20–100% in untreated cases, depending on venom potency.
Clinical Findings and Diagnosis
Encounters with toads are most common in warm or mild weather. Signs of poisoning are variable and range from local effects to convulsions and death. Severity depends on host factors, 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, probably because the venom 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. With more severe intoxication, as from B marinus, cardiac arrhythmias, dyspnea, cyanosis, and seizures are characteristic. Both cardiac and CNS involvement are life-threatening.
A specific antidote for the toxins in toad venom is not available. Therapy is directed at minimizing absorption of the venom and controlling the associated clinical signs. Minimal treatment may be required after exposure to venom in areas where less toxic toads are found. The mouth should be immediately and thoroughly flushed with copious amounts of water. The victim should be prevented from inhaling aerosols of saliva or water that contain toad venom. Atropine may reduce the volume of saliva and the risk of aspiration. More severely affected animals require more extensive therapy. Cardiac arrhythmias should be identified and controlled using standard treatment protocols (also see Arrhythmias). If bradyarrhythmias exist, atropine or dopamine should be considered; tachyarrhythmias should be treated with lidocaine, phenytoin, propranolol, or procainamide hydrochloride. CNS excitation, if present, should be controlled by pentobarbital anesthesia, diazepam, or a combination of the two. Thiamylal, halothane, and other forms of anesthesia may be contraindicated because they may predispose to ventricular fibrillation. Supplemental oxygen and mechanical ventilation may also be needed if cyanosis and dyspnea are prominent.
Last full review/revision March 2012 by Keith A. Clark, DVM, PhD