Toads (order: Anura; family: Bufonidae; genus: Bufo) are distributed throughout the world, but more species are found in areas of tropical and humid temperate climates. Although toads do not have a venom inoculation system, they are venomous animals because the glands covering the whole surface of their bodies secrete a milk-like venom of which composition is not yet completely known. Some of these glands are the bilateral glands located in post-orbital position. These glands, which are somewhat diamond-shaped and can be seen by the naked eye, are known as parotids. Toad envenoming in dogs may cause local and systemic alterations and may cause death by cardiac ventricular fibrillation. The electrocardiographic alterations observed consist of gradual deterioration of the normal standards with progressive appearance of negative ventricular deflections that can result in ventricular fibrillation and death if the envenomed dog is not promptly treated. Traditional therapy consists mainly of administration of atropine and propranolol; the latter used to prevent ventricular fibrillation
ABSTRACT:Toad poisoning is frequent in dogs, but has been infrequently addressed in published case reports and review articles. Dogs can be poisoned when they bite a toad or otherwise ingest the venom. The venom effects manifest soon after the accident, since the toxin is rapidly absorbed by the mucous membrane of the digestive system. Hospital records of three dogs, diagnosed with toad poisoning, were retrospectively reviewed from January 2005 to July 2007. Poisoned dogs may present only local irritation or systemic signs in the gastrointestinal, cardiac and neurological systems. All three cases presented herein had clinical signs of gastrointestinal alterations including vomiting, sialorrhea and diarrhea. Two dogs developed abnormal cardiac rhythm and two exhibited neurological signs. A poisoned animal requires emergency care and symptomatic therapy with intense monitoring of its clinical parameters. Although there have been reports on the low mortality of dogs poisoned by toads, one animal died even after appropriate therapy. The severity of clinical signs and the risk of death must be considered by the veterinarian.KEY WORDS: veterinary emergency, poisoning, toad venom, bufotoxin, Bufo sp., dog.
The effects of amitraz, a formamidine derivative, on motor function were studied in rats. Behavioural and neurochemical studies were performed. Results show that amitraz was able: 1) to decrease locomotion and rearing frequencies of rats and to increase their immobility time in an open-field; 2) to displace to the left the control dose-response curve constructed to apomorphine-induced stereotyped behavior; 3) to potentiate both pentobarbital sleeping time and amphetamine effects on open-field behaviour of rats and 4) to increase not only the whole brain levels of noradrenaline but also the striatal levels of dopamine. In relation to control animals, the pesticide also induced 5) a decrease in the striatal levels of homovanillic acid, 6) pesticide effects on open-field behaviour of rats were not antagonized by yohimbine administration, and 7) metoclopramide administration on amitraz pretreated rats antagonized not only amphetamine effects on open-field behaviour, but also apomorphine-induced stereotypy. These results are discussed in the light of the actions of amitraz on biogenic amines. It is suggested that the pesticide effects on motor function are consequences of the inhibitory effects on MAO activity, most probably through the increases produced on catecholamine levels within the central nervous system.
Toad envenoming in dogs can cause death by cardiac fibrilation (CVF). Traditional therapy consists mainly of atropine and propranolol, the last one used to prevent the CVF, that is preceded by negative ventricular deflections (NVDs) in the QRS complex of the electrocardiogram. This study intended to verify, comparatively, the lidocaine, propranolol, amiodarone, and verapamil abilities to prevent CVF in experimentally envenomed dogs. Thirty-six dogs were divided into 6 groups (GL, GP, GA, GV, GST, and GSV) with n=6; the dogs were submitted to volatile anaesthesia. The animals of the groups GL, GP, GA, and GV received 0.38g of toad venom through oro-gastric catheter and were treated with the following drugs respectively: lidocaine (4mg/Kg), propranolol (0.1mg/Kg), amiodarone (8mg/Kg), and verapamil (2mg/Kg). These drugs were repeated if NVDs reappeared with cardiac frequency >150, GST was not treated and GSV was just anaesthetized. The following results were obtained: GL, NVDs present in 4 animals, 100% recuperation with 3.66 doses/animal; GP, NVDs present in 2 animals, 100% recuperation with 1.66 dose/animal, with bradycardia at the anaesthetic return; GA, NVDs present in 3 animals, 33.33% recuperation with 1.5 dose/animal; GV, NVDs present in 4 animals, 100% recuperation with 2.16 doses/animal; GST, NVD present in 6 animals, 100% death and GSV, NVDs absent, 100% recuperation. As a conclusion, the anaesthetic proceedings used, did not cause NVDs, the envenoming that was not treated was lethal, and among the antiarrhythmics drugs used, verapamil was the most efficient, as it did not cause any serious bradycardia at the anaesthetic return and did not require repeated administrations. For lidocaine, it was efficient but required various administrations; amiodarone could not prevent the death of 4 animals; propranolol was efficient in relation to NVDs control, but caused serious bradycardia at the anaesthetic return
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.
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