Clinical and electrocardiographic evaluation during experimental toad poisoning in dogs

Abstract

Accidents involving toad poisoning are frequent and dogs are the most common victims; they become poisoned by biting or ingesting a toad. When released in the organism, the venom is absorbed by both the oral mucosa and the digestive tract, initiating its toxic action. The aim of this work was to evaluate the clinical and electrocardiographic aspects of dogs subjected to experimental toad poisoning, as well as their response to treatment with propranolol. Twenty dogs were divided into two groups, a control group (n = 5) and a poisoned group (n = 15). After general anesthesia, the control group received a placebo, while the poisoned group received a venom aliquot through an orogastric tube. Results were tested through multivariate analysis (p < 0.05). The animals in the poisoned group had gastrointestinal symptoms including emesis, intense salivation, hyperemic or congested oral mucosa and pasty diarrhea. Non-responsive mydriasis, nystagmus, depression, stupor, tachypnea, opisthotonus and ataxia were also manifested by 100% of the poisoned animals. Affected dogs had an increase in blood pressure, statistically significant throughout study. Five poisoned animals developed ventricular tachycardia and were treated with propranolol (0.5 mg/kg IV). All propranolol-treated animals returned to normal sinus rhythm, which evidences the efficacy of this drug to treat ventricular arrhythmias caused by toad venom.

A Fatal Case of Toad (Buffo Melanostictus) Intoxication in a German Shepherd Dog and Review of Literature

“…The major active substances of the venom can be classified into two groups including biogenic amines and steroid derivatives (Peterson and Roberts, 2006). Bufotenines (serotonin and 5-hydroxytryptophan), bufotyonines, dihydro-butenines and catecholamines (dopamine, epinephrine and norepinephrine) can be highlighted under the category of biogenic amines owing to their toxic relevance (Peterson and Roberts, 2006;Reeves, 2004 Kuo et al, 2009;Camplesi et al, 2010). Additionally the decreased level of Hb, PCV, RBC, serum Na + and Cl + are in consistent with the findings of Palumbo (1975).…”

“…Several factors including toad's specie, victim's age and body weight, habitat, concurrent disease and exposure time are incriminated to forecast the clinical outcome (Sakate, 2001;Barbosa et al, 2009;Camplesi et al, 2010). Smaller patients are often presented with sever clinical signs of toxicosis.…”

Toad Intoxication in the Dog by Rhinella marina: The Clinical Syndrome and Current Treatment Recommendations

“…2 Neurologic signs can vary in both length and severity. 10,11 Initially, mydriasis, altered mentation, or abnormal gait may be present. Signs may progress to extensor rigidity, opisthotonos, seizures, and coma in the most severe of cases.…”

“…With early, appropriate treatment, the outcome of R. marina toxicosis is considered excellent, with a marked resolution of signs typically occurring within the first 12-24 hr, even for severely affected patients. 2,3,10,11,13 Although early reports suggest a high mortality rate, more recent reports suggest at least 96% survival with early supportive and symptomatic therapy. 2,3 In one case series, the dogs that died developed seizures in addition to other neurologic abnormalities, but seizures do not necessarily indicate a poor prognosis since only 18% of dogs that developed seizures died.…”

“…marina toxicosis is influenced by the amount of toxin ingested, the size of the dog, and the administration of proper, prompt and appropriate medical treatment 2,3,10,11,13. Conclusion In the United States, R. marina toads are found in southern Florida, the southern tip of Texas, and Hawaii.…”