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. Toxins are produced by all toads, but potency varies with species and apparently between geographic locations within individual species. Toad toxin, a defensive mechanism, is secreted by large glands located dorsal and posterior to the eyes and by smaller glands distributed throughout the skin. The toxin, a thick, creamy white, highly irritating substance, can be expelled quickly by the 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 similar to the actions of local anesthetics, catecholamines, and serotonin. The most toxic species in the USA is the giant or marine toad, Rhinella marina (formerlyBufo 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. Mortality ranges from 20%–100% in untreated cases, depending on exposure circumstances. The Colorado River toad, Incillus (formerly Bufo) alvarius, found in the southwestern USA and northern Mexico, is another toad of sufficient size to have potentially lethal levels of toxins in its skin secretions.
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 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. With more severe intoxication, as from R marina or I alvarius, cardiac arrhythmias, dyspnea, cyanosis, and seizures are characteristic. Cardiac and CNS involvement can be life-threatening.
A specific antidote for toad toxins is not available. Therapy is directed at minimizing toxin absorption and controlling associated clinical signs. Minimal treatment may be required after exposure to toxins in areas where less toxic toads are found. The mouth should be immediately and thoroughly flushed with copious amounts of water. Affected animals should be prevented from inhaling aerosols of saliva or water that contain toad toxin. Atropine may reduce the volume of saliva and the risk of aspiration but should not be used until cardiovascular status is assessed. 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. Digoxin-specific Fab may be considered in cases of severe arrhythmias refractory to standard antiarrhythmic therapy. CNS excitation, 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 prominent.
Last full review/revision May 2014 by Sharon M. Gwaltney-Brant, DVM, PhD, DABVT, DABT