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Bromethalin was developed and released in 1985 to combat a world-wide problem of rodent resistance   to   warfarin-like   anticoagulant rodenticides.Bromethalin is not an anticoagulant but is a highly potent rodenticide that provides a lethal dose to rodents in a single feeding. Death occurs within 24 to 36 hours after ingestion. It is a pale, odorless, crystalline solid compound in the diphenylamine family. Its mechanism of action is to uncouple oxidativephosphorylation in the mitochondria of the central nervous system. This leads to a decreased production of ATP. Low levels of ATP inhibit the activity of the Na/K ATPase and lead to a subsequent buildup of cerebral spinal fluid and vacuolization of myelin. The increased CSF results in high intracranial pressure, causing damage to nerve axons, inhibiting neural transmission and leading to paralysis, convulsions and death.

The LDso of pure bromethalin for dogs is 4.7 ing/kg body weight and 1.8 mg/kg for cats. Minimum lethal doses of bait are 25 g/kg in the dog and 4.5 g/kg in the cat. A typical package contains 21 grams of 0.01% bromethalin. Thus, a five kg dog would have to consume five to six packages to reach toxic levels and a five kg cat would have to consume one to two packages to reach toxic levels.  Signs of a sub-lethal dose include hind limb ataxia, depression, extensor rigidity, opisthotonus, lateral recumbency and vomiting. High doses may bring about severe muscle fasiculations, hind limb hyper-reflexia, seizures, hyperthennia, depression and death.

There are no antemortem tests available, although through clinical signs, a history of exposure,    irregular   electroencephalographic measurements and cerebral edema (fundic exam) may lead to an antemortem diagnosis. There is no specific antidote for bromethalin poisoning. Therefore, prevention of absorption is of the utmost importance. Treatment is most successful in dogs and cats when emesis is induced and activated charcoal with a saline cathartic are given immediately after ingestion.   Treatments with osmotic diuretics and steroids have been utilized but are not as successful as removal of the toxin from the gastrointestinal tract.

The gross lesions seen on post-mortem examination are limited to those caused by cerebral edema which include narrowing of suici and flattening of gyri. Mild pulmonary congestion may be seen in some cases.    The predominant histological change is seen in the brain. There is diffuse spongiform degeneration of the white matter and vacuolization of myelin such as occurs in the optic nerve. There can be microgliosis of the cerebellum and cerebrum.

Bromethalin or its metabolitedesmethy-bromethalin can be detected in liver, fat, kidney, and brain. Samples should be submitted frozen and kept in the dark (wrap in aluminum foil). Bromethalintoxicosis must be considered as a potential differential diagnosis for neurologic Syndromes and may resemble toxicity from lead, strychnine and organophosphate compounds. Bromethalintoxicosis must also be differentiated from syndromes producing seizures, such as epilepsy and paralytic syndromes, such as trauma, larval migration and neoplasia.

- by Paul Klausen, Class of 1997

- edited by Stephen Hooser, DVM, PhD


Dorman,DC, Simon,J,Harlin,KA, Buck, WB.Diagnosis of BromethalinToxicosis in the Dog.     Journal  of Veterinary Diagnostic Investigation. 1990, 2: 123-128.

Dorman,DC, Parker,AJ, Buck, WB.BromethalinToxicosis in the Dog.Journal of the AmericanAnimalHospital Association. 1990, 26:589-598.

Dorman, DC. Anticoagulant,Cholecalciferol, and Bromethalin based rodenticides.Veterinary Clinics of North America, Small Animal Practice. 1990,20: 339-352.

Dreikom,B.,O'Dorherty, GO. The Discovery and Development of Bromethalin, an Acute Rodenticide with a Unique Mode of Action. American Chemical Society. 1984, 45-63.

Jackson, WB. BROMETHALIN-A PROMIS­ING NEW RODENTICIDE.Proceedings Tenth Vertebrate Pest Conference.    R.E.MarshUniversity of CaliforniaDavis. 1982,10-14



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