BASICS
- Toxicosis caused by exposure to AChE-inhibiting OP or carbamate compounds
- These compounds are active ingredients in many animal oral and topical parasiticides, as well as in numerous household and agricultural pesticide products. There are dozens of different, but structurally similar, OP and carbamate compounds with hundreds of different formulations, containing varying concentrations of active ingredient
- The toxicity among individual compounds varies tremendously
- Oral ingestion is the most common form of exposure in horses, either from ingesting pasture grass or hay where pesticide spills or drift have occurred or from overdosing with oral parasiticide products. Inhalation or dermal exposure leading to poisoning is not common but can occur
- Be careful—not all pesticides labeled as “carbamates” inhibit AChE
- Most OP and carbamate pesticides are rapidly absorbed by the respiratory and GI systems and dermally
- Some are direct-acting compounds; others require metabolic activation by the liver to a toxic metabolite. The underlying biochemical change responsible for the clinical syndrome is an inhibition of AChE activity in the nervous system, resulting in accumulation of acetylcholine at synapses and myoneural junctions. Inhibition of the enzyme by OPs is considered irreversible, particularly once covalent bonding or aging has occurred
- Inhibition of the enzyme by carbamates is reversible. In order to restore AChE activity following pesticide exposure, the enzyme must either be reactivated or synthesized
- Nervous and musculoskeletal—excess acetylcholine at synapses and myoneural junctions initially excites, then paralyzes, transmission in cholinergic synapses found in the CNS and at parasympathetic and a few sympathetic nerve endings (muscarinic effects) and somatic nerves and ganglionic synapses of autonomic ganglia (nicotinic effects)
- Respiratory—build-up of secretions from the muscarinic effects can lead to respiratory difficulties, perfusion problems, and secondary bacterial invaders
Poisonings with these compounds in horses seem to be not as common as observed in other species. However, most cases occur in the spring and summer when agricultural and household pesticide use is highest. Poisonings can occur from eating hay that was baled several months previously; any pesticide spilled or drifted onto the hay and then baled will have a slower rate of degradation, and some pesticides have been known to persist in baled hay for up to 6 months.
There is considerable variation in clinical signs between different species of animals despite the fact that the mechanism of action is the same. In the horse, GI signs predominate and nervous signs may be absent altogether. The severity of the clinical syndrome and time to onset depend on exposure dose, route of exposure, and formulation of the pesticide product. Clinical signs can be immediate, following inhalation or oral exposure, or may be delayed by several hours (oral or dermal route).
- Abdominal pain, accompanied by restlessness, anxiety, and sweating
- Markedly increased intestinal sounds
- Watery diarrhea
- Weakness and depression
- Mild to severe muscle tremors (seizures uncommon)
- Tachycardia or bradycardia
- Miosis or mydriasis
- Dyspnea
- Excessive salivation can occur
Most cases of poisoning occur via ingestion of pesticide-contaminated grass or hay or from overdosing of oral parasiticide products. Horses also can be poisoned by accidental access to spilled or improperly used, stored, or discarded pesticides. Dermal and inhalation exposure can also occur.
DIAGNOSIS
TREATMENT
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS