Page 651 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

616 SECTION | VIII Rodenticides

VetBooks.ir including dogs and cats. Signs of bromethalin appear within Diagnosis
In field cases, most often, poisoning occurs in pets,
Diagnosis of bromethalin poisoning is based on history of
10 h to several days after exposure, and may last up to 12
days. In most cases, the poisoning is acute in nature, char- exposure to bromethalin bait, clinical signs, and identifica-
tion of bromethalin in bait, GI content, brain, and visceral
acterized by cerebral edema and paralysis of the hind limbs.
organs. Residue of bromethalin, or its major metabolite
In general, clinical signs in pets include severe muscle tre-
(desmethyl bromethalin), can be quantified using GC cou-
mors, hyperexcitability, hyperesthesia (hypersensitivity to
pled with electron capture detector (Dorman et al., 1990c)
touch), and seizures. Symptoms with mild exposure to bro-
or high-performance liquid chromatography (HPLC), cou-
methalin occur with slow progress in several days, and they
pled with ultraviolet detector or with negative-ion
include loss of ability to bark, loss of appetite, vomiting,
atmospheric pressure chemical ionization mass spectro-
depression, lethargy, tremors, paralysis, lateral recumbency,
metric detector (Mesmer and Flurer, 2001). The highest
coma, and death. Following exposure to a large dose of bro-
concentrations of bromethalin are found in the fat, liver,
methalin, animals can show signs of muscle tremors and
kidney, and brain. Differential diagnosis should rule out
seizures, hyperexcitability, ataxia and paddling, hyperther-
lead, ethylene glycol, organophosphates, strychnine, met-
mia, potential loss of vocalization, loss of tactile sensation,
aldehyde, zinc phosphide, and tremorgenic mycotoxins.
forelimb extensor rigidity (Schiff Sherrington posture),
and death occurs within 2 4 days. Death can occur with a
low or high dose, and is usually caused by respiratory paral- Treatment
ysis. Poisoned dogs show the signs of tremors, ataxia,
depression, tachypnea, hyperreflexia of the hind limbs, loss There is no specific antidote for bromethalin poisoning
of vocalization, recumbency, anorexia, vomiting, and death (Coppock, 2013). Symptoms can be treated with corticos-
(Dorman et al., 1990a). Poisoned cats exhibit the signs of teroids, but clinical studies indicate that symptoms return
ataxia, seizures, vocalization, rigidity, decreased propriocep- as soon as the corticosteroids are discontinued. Emesis
tion, abdominal distension, recumbency, depression, and should be induced using apomorphine or 3% hydrogen
death (Dorman et al., 1990b, 1992). Other signs of poison- peroxide if the animal is not exhibiting signs of convul-
ing include generalized seizures, head pressing, hyperesthe- sions and seizures. Alternatively, perform gastric lavage
sia, coma, hyperexcitability, ataxia, extensor rigidity, and give activated charcoal with saline cathartic.
nystagmus, hyperthermia, cyanosis, miosis, and drooling Activated charcoal needs to be repeated if the dog or cat
(Moorman, 2003). Overall, cats are much more sensitive is exposed to a large dose of bromethalin. The animal
than dogs to bromethalin. needs to be monitored and treated for cerebral edema.
Histopathological changes have been described in dogs Intravenous fluids can be administered with great caution
receiving a single oral dose of bromethalin (6.25 mg/kg). so as not to worsen cerebral edema. The seizures in dogs
Histologic lesions included diffuse white matter spongiosis, can be somewhat refractory to diazepam; thus, a barbitu-
mild microgliosis, optic nerve vacuolization, mild thicken- rate can be given to control seizures.
ing of Bowman’s capsule, and occasional splenic megakar-
yocytes. Ultramicroscopic examination of the mid brain Conclusion
stem revealed occasional swollen axons, intramyelinic
vacuolization, and myelin splitting at the intraperiod line Bromethalin is a commonly used rodenticide that is
(Dorman et al., 1990c). Dorman et al. (1992) also reported encountered in poisoning in dogs and cats. Bromethalin
histopathological changes in cats induced by bromethalin. exerts toxicity by uncoupling oxidative phosphorylation in
In brief, ultrastructural changes include separation of myelin mitochondria, thereby decreasing ATP synthesis. The CNS
lamellae at the interperiod lines, with the formation of intra- is the target organ, and toxicity is characterized by cerebral
myelinic vacuoles (intramyelinic edema), rupture and coa- edema, convulsions, and paralysis. There is no specific
lescence of intramyelinic vacuoles into larger extracellular antidote, so treatment is symptomatic and supportive.
spaces (spongy change), and pronounced cytosolic edema
of astrocytes and oligodendroglial cells. Histopathology of
the brain and spinal cord of rodents receiving multiple low CHOLECALCIFEROL
or sublethal doses of bromethalin revealed a spongy degen- Introduction
eration of the white matter that was shown upon ultramicro-
scopic examination to be intramyelinic edema (Van Lier Cholecalciferol is a form of vitamin D, also called vitamin
and Cherry, 1988). D 3 , that is commonly used as rodenticide. Vitamin D 3 is a
According to the World Health Organization and the secosteroid, and structurally similar to other steroids, such
US Environmental Protection Agency, bromethalin is as cholesterol, testosterone, and cortisol. It has chemical
considered carcinogenic. formula C 27 H 44 O, with a molecular weight of 384.64. Its