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718 Organophosphate and Carbamate Insecticide Toxicosis

Recommended Monitoring PEARLS & CONSIDERATIONS Client Education
Weekly or bimonthly re-examination for Comments • Consult a veterinarian as soon as an alteration
VetBooks.ir PROGNOSIS & OUTCOME Orbital disease should be investigated in a • Relapses can occur with myositis or when
in position of the eye(s) is noted.
inflammatory diseases
an orbital foreign body persists.
timely fashion to alleviate discomfort and
• Favorable with orbital abscess if treated potentially preserve vision. SUGGESTED READING
adequately Technician Tips Betbeze C: Management of orbital diseases. Top
• Guarded with myositis Check the intraocular pressure on all dogs with Companion Anim Med 30:107, 2015.
• Poor with orbital neoplasia orbital disease as glaucoma can have a similar
appearance. AUTHOR: Chantale L. Pinard, DVM, MSc, DACVO
EDITOR: Diane V. H. Hendrix, DVM, DACVO

Organophosphate and Carbamate Insecticide Toxicosis Client Education
Sheet

BASIC INFORMATION • Tremors, muscle weakness, ataxia, seizures; new enzyme. Inhibition of AChE by the OPs
acute death possible tends to be irreversible, whereas inhibition
Definition • Cats may not show typical OP toxicosis signs by the carbamates is reversible, which allows
Organophosphate (OP) and carbamate from chlorpyrifos intoxication. Clinical signs, a spontaneous regeneration of the enzyme.
insecticides are used for controlling insects which begin 1-5 days after exposure, can Both carbamates and OPs respond initially
in agriculture, around the home, and on or consist of anorexia, depression, vomiting, to atropine, but only carbamates continue
around animals (e.g., controlling fleas and tremors, salivation, ataxia, seizures, and to do so. OPs become refractory to atropine
ticks). Toxicosis results from dermal or oral ventroflexion of the neck. treatment.
exposure and is characterized by any combina- • Atropine blocks the effects of the excess ACh
tion of increased salivation, lacrimation, urinary PHYSICAL EXAM FINDINGS at the neuromuscular junction. Atropine can
incontinence, diarrhea, dyspnea, and emesis • Muscarinic signs: SLUDDE, miosis, and control only the muscarinic signs, not the
(SLUDDE), bradycardia, tremors, shaking, bradycardia nicotinic signs.
ataxia, seizures, and/or sudden death. • Nicotinic signs: muscle tremors, weakness, • Death occurs secondary to respiratory failure
and paresis progressing to paralysis from excessive bronchial secretions, bron-
Synonyms • Central nervous system (CNS) signs: hyper- chiolar constriction, paralysis of intercostal
Acetylcholinesterase (AChE) inhibitors, activity, depressed respiration, and seizures muscles or diaphragm, or respiratory paralysis
cholinesterase inhibitors • Muscarinic signs may be overridden by (CNS effects).
sympathetic stimulation, resulting in opposite
Epidemiology effects (e.g., mydriasis, tachycardia).
SPECIES, AGE, SEX DIAGNOSIS
• All breeds and both sexes Etiology and Pathophysiology Diagnostic Overview
• Very young, elderly, or debilitated animals Source: A tentative diagnosis is based on history of
are more susceptible. • Organophosphates (OPs) are aliphatic carbon, exposure (recent use of pesticide on the animal
• Cats are particularly sensitive to chlorpyrifos; cyclic, or heterocyclic phosphate esters. or in the environment) and presence of one or
the onset of clinical signs is usually delayed ○ Commonly used OPs are disulfoton, several SLUDDE signs. Serum AChE levels are
(1-5 days) after exposure, and signs can last acephate, terbufos, phorate, parathion, the clinical confirmatory test of choice, but
2-4 weeks. chlorpyrifos (Dursban), fenthion, diazi- treatment generally needs to be initiated before
non, and malathion. availability of results.
RISK FACTORS • Carbamates are cyclic or aliphatic derivatives
Exposure to other AChE inhibitors of carbamic acid. Differential Diagnosis
○ Commonly used carbamates are aldicarb, • Some Solanaceae family plants; anatoxin-a(s)
GEOGRAPHY AND SEASONALITY carbofuran, methomyl, propoxur, and found in some blue-green algae
Toxicosis is more common in summer months carbaryl (Sevin). • Muscarinic signs: muscarinic mushrooms,
(insecticide use). Mechanism of toxicosis: tremorgenic mycotoxins
• OPs and carbamates competitively inhibit • Nicotinic signs: nicotine, pyrethrins/
Clinical Presentation AChE by binding to its esteric site. pyrethroids, organochlorine-type pesticides,
HISTORY, CHIEF COMPLAINT Acetylcholine (ACh) then accumulates in caffeine, strychnine, sodium fluoroacetate
• Known dermal or oral exposure to an OP the synapse and causes excessive synaptic (compound 1080), 4-aminopyridine, met-
or carbamate neurotransmitter activity, leading to musca- aldehyde, zinc phosphide, lead
• Recent history (usually within 24 hours rinic, nicotinic, or CNS effects. Competitive • CNS signs: any disorder that can cause
before onset of clinical signs) of using an inhibition of AChE explains the result of seizures (p. 903)
OP or carbamate insecticide in the yard/ confirmatory testing with OP or carbamate
house toxicosis (low blood AChE level). Initial Database
• Rapid onset of clinical signs (typically • Some OPs undergo aging, rendering the • CBC, urinalysis (usually normal)
minutes to hours after exposure) phosphorylated (inactivated) cholinesterase • Serum biochemistry profile: possible mild
• Salivation, vomiting, diarrhea, lacrimation, enzyme very stable so that recovery of AChE increase in liver and pancreatic enzymes with
dyspnea activity occurs only through the synthesis of some OPs (disulfoton)

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