Carbamates (Shokry) Flashcards
What are the uses of carbamate pesticides?
Generally used to organophosphates
- Animal and plant insecticides
- Insecticides synergists
- Anthelmintics
- Antiglaucoma
- Soil nematocides
- Fungicides
- Herbicides
- Rodenticides
- Insect repellants
What are the sources of carbamate poisoning?
- Widely used
- Contaminated feed or drinking water
- Empty pesticide containers used for feeding or watering animals
- Dusting or spraying animals or animal premises
- Overdosing
What are some examples of carbamates pesticides?
Most of the names contain “carb”
- Carbaryl
- Aldricard
- Bendiocarb
What are the properties of carbamate pesticides?
No storage activation
Describe the toxicity of carbamates and who is more sensitive.
Young animals are more sensitive
- Occurs when the rate of carbamylation of acetylcholinesterase exceeds the rate of hydrolysis of carbamate by the enzyme
What are the toxicokinetics of carbamates?
- Don’t require enzymatic activation
- More toxic to young animals or those deficient in liver enzymes
- Metabolized very rapidly
What is the MOA of carbamates?
- Acetylcholinesterase can hydrolyze carbamate insecticides but at a slower rate than ACh (acetylcholine)
- Cause reversible inhibition of acetylcholinesterase
What causes the clinical signs of carbamate toxicosis?
Due to accumulation of ACh (as in organophosphate)
What may be the exception to the carbamate mechanism of action with clinical signs?
Leg paralysis of chickens, muscular degeneration/necrosis and cerebral edema in swine caused by large doses of carbaryl may NOT be due to inhibition of cholinesterases
What are some clinical signs associated with carbamates?
Generally similar to organophosphates but less severe or shorter duration
- Acute: muscarinic stimulation (salivation, lacrimation, coughing, vomiting, colic, diarrhea), nicotinic stimulation (muscle fasciculations, tremors, stiff gait), CNS signs (anxiety, hyperactivity, clonic/clonic-tonic convulsions [small animals, horses]), nicotinic blockage (muscle paralysis), CNS depression (death from respiratory failure)
- Delayed: neurotoxic reaction (muscle weakness, rear limb ataxia, paralysis), myopathy lameness, weight loss, secondary bacterial or viral infection
What are the lesions associated with carbamate toxicity?
Same as organophosphates
- None in animals that die quickly
- Few nonspecific (pulmonary edema/congestion, cyanosis, hemorrhages, congestion/edema of brain, patches and necrosis in skeletal muscle)
- In delayed neurotoxicity, degeneration and demyelination of peripheral and spinal motor neurons
What laboratory tests diagnose carbamate toxicosis?
- Refrigerated, undiluted blood samples analyzed ASAP using a rapid method
- May not be detectable in tissues, blood, or secretions (rapidly destroyed)
How do you diagnose carbamate toxicosis?
Depends on history, clinical signs, lesions (or their absence) and atropine therapy response
How do you treat carbamate toxicosis?
As in organophosphate toxicosis treatment
- Atropine sulfate (1/4 dose IV, remainder IM or SQ)
- Drugs that depress respiration contraindicated
- 2-PAM ineffective
- Diphenhydramine (antagonize nicotinic effects in small animals)
- Oxygen therapy (dyspnea, cyanosis)
- Remove pesticide source (ativated charcoal, mineral oil, wash skin w/ soap and water)
- Supportive therapy (fluids, electrolytes, acidosis treatment, vitamins)
How do you treat the neurotoxic effects of carbamate poisoning?
No specific treatment for neurotoxic effects (degeneration and demyelination)
