Toad venom toxicity and its clinical occurrence in small animals in the United Kingdom

Bedford, P. G. C.

doi:10.1136/vr.94.26.613

Cited by 23 publications

(12 citation statements)

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“…Moderate cases includes, in addition to oral mucosa irritation and sialorrhea, emesis, depression, weakness, ataxia and neurological signs like walking in circles, cardiac rhythm abnormalities, spontaneous evacuation and urination. Severe cases can also comprise diarrhea, abdominal pain, sternal decubitus, pupils not responsive to light, seizures, pulmonary edema, and cyanosis, possibly evolving to death (8,9,(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

Clinical and electrocardiographic evaluation during experimental toad poisoning in dogs

Camplesi¹,

Sakate²,

Simão³

et al. 2010

J. Venom. Anim. Toxins incl. Trop. Dis

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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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Section: Introductionmentioning

confidence: 99%

Clinical and electrocardiographic evaluation during experimental toad poisoning in dogs

Camplesi¹,

Sakate²,

Simão³

et al. 2010

J. Venom. Anim. Toxins incl. Trop. Dis

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“…Existem várias espécies no Brasil, como B. ictericus, B. schneideri, B. rufus e B. marinus (Zelnik 1965, Bedford 1974. Os cães são as vítimas mais comuns desse tipo de envenenamento, pois são atraídos pelos movimentos lentos dos sapos, principalmente no período noturno (MacDonald 1990).…”

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“…Em casos graves, pode haver ainda diarréia, dor abdominal, midríase não-responsiva, convulsões, edema pulmonar e cianose. As alterações eletrocardiográficas observadas são arritmias, que podem evoluir para taquicardia ventricular multiforme e, se o cão não for tratado, para fibrilação ventricular e morte (Knowles 1968, Otani et al 1969, Bedford 1974, Palumbo et al 1975, Russel 1979, Palumbo & Perry 1983, Oliveira 1998, McFarland 1999, Sakate & Oliveira 2000, 2001.…”

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Dosagem de marcadores cardíacos CK-MB e TnIc e eletrólitos no envenenamento experimental por veneno de sapo em cães

et al. 2009

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INTRODUÇÃOMuitas espécies de anfíbios possuem glândulas secretoras cutâneas que previnem o ressecamento da pele e os pro- Among the systemic signs of toad venom (bufotoxin) poisoning in dogs, the cardiotoxic effects are one of the most important. Thus, the objective of this experiment was to evaluate potential changes in the cardiac muscle in dogs poisoned experimentally by toad venom and to observe the eletrolyte alterations which may occur in this condition. Twenty dogs divided into control group (n=5) and poisoned group (n=15) were utilized. The toad venom was extracted by manual compression of the paratoidic glands. After general anesthesia, dogs in the control group received placebo and dogs in the poisoned group received the venom by orogastric catheter. Samples for dosage were collected 6 hours and 24 hours after poisoning and 0, 2, 4, 6 and 12 hours after poisoning for electrolytes dosage. The Man-Withney test was used for statistical analysis (P<0.05). The poisoned dogs showed (saline) elevated levels of cardiac markers CK-MB and TnIc, confirming the cardiotoxic effect of the bufotoxin. Hypokalemia and hypocalcemia were also observed.INDEX TERMS: Toad venom poisoning, bufotoxin, cardiac markers, electrolyte, dogs.

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“…Irrigation of the mouth or eyes with clean water and gastrointestinal decontamination as first-aid treatment are recommended. 13 Sympatholytics, acting on both a-and b-adrenergic receptors, have proven effective in the treatment of toad poisoning. 14 Atropine, propanolol, diphenylhydantoin, and calcium gluconate have also been used.…”

Section: Long-term Prophylaxis and Immune Parameters In Haemophiliamentioning

confidence: 99%

Letter. Upper airway obstruction in an HIV-1 infected child with acute Epstein-Barr virus infection

Weber¹,

R²,

Mf³

et al. 1999

Journal of Tropical Pediatrics

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Toad venom toxicity and its clinical occurrence in small animals in the United Kingdom

Cited by 23 publications

References 0 publications

Clinical and electrocardiographic evaluation during experimental toad poisoning in dogs

Clinical and electrocardiographic evaluation during experimental toad poisoning in dogs

Dosagem de marcadores cardíacos CK-MB e TnIc e eletrólitos no envenenamento experimental por veneno de sapo em cães

Letter. Upper airway obstruction in an HIV-1 infected child with acute Epstein-Barr virus infection

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