Organophosphate and Carbamate Insecticide
Poisoning
Organophosphate and carbamate insecticides are commonly
used for small animals as flea and tick powders, sprays, foggers,
shampoos and dips, flea collars, and formerly, as systemic
insecticides. They are also frequently used as household,
garden, and farm insecticides. Chlorpyrifos, parathion, diazinon,
famphur, phorate, terbufos, and malathion are examples of
organophosphates while carbofuran, aldicarb, and carbaryl,
are carbamates. They are all marketed under a wide variety
of trade names.
Both organophosphate and carbamates are highly toxic to
all animals, including pets, livestock, and humans although
some are far more toxic than others. All OP/Carbamate insecticides
are fat soluble and therefore are easily absorbed through
the skin and then transported throughout the body. These chemicals
kill insects and cause poisoning in animals by inhibiting
the enzyme, acetylcholinesterase (AChE) which normally functions
to degrade acetylcholine in nerve synapses. Inhibition of
AChE in the nerves results in a buildup of acetylcholine (ACh)
and overstimulation of ACh receptors. Since all organophosphate
and carbamate insecticides have the same mechanism of action
and can be long-lasting, the effects of multiple exposures
(for example: flea dip, flea powder, flea collar, and home
and lawn flea treatment) are additive. There are two types
of ACh receptors, muscarinic and nicotinic. Overstimulation
of muscarinic receptors gives rise to the characteristic SLUDD
signs of OP/Carbamate poisoning: salivation, lacrimation,
urination, defecation, and dyspnea (due to increased bronchial
secretions and bronchoconstriction), plus bradycardia and
miosis. Overstimulation of nicotinic ACh receptors produces
muscular fasiculations and tremors initially followed by flaccid
paralysis. Death in acute poisonings is frequently due to
respiratory failure resulting from inhibition of central (medullary)
respiratory drive, excessive bronchial secretions, and bronchospasms
coupled with depolarizing blockade at neuromuscular junctions
(diaphragm and intercostals).
The diagnosis of OP/Carbamate poisoning is made based
on:
- (1) History of exposure to one or more OP/Carbamates.
- Signs:
- Muscarinic signs: SLUDD + bradycardia and miosis.
- Nicotinic signs: muscle stiffness, muscle fasiculations,
tremors, weakness, flaccid paralysis.
- CNS signs: restlessness, hyperactivity, seizures.
- Animals often found dead.
NOTE: Not all animals read the book and can present with
any combination of the signs listed above.
- Blood ACh activity: usually less than 25% of normal
with OP/Carbamate exposure. Whole blood must be submitted
with an anticoagulant such as EDTA or heparin.
- Clinical Pathology: Some organophosphates have
been associated with an increase in CPK and AST.
- Necropsy: There are no definitive gross or histological
lesions in acute poisonings. Brain cholinesterase is significantly
decreased. Stomach contents and liver are frequently used
to diagnose OP/Carbamate poisoning and identify which chemical
was responsible for the poisoning.
If OP/Caramate poisoning is suspected, the samples which
should be taken and submitted for diagnosis are:
- Whole, unclotted blood, refrigerated as quickly as possible.
Do not freeze.
- Frozen brain (one half of the brain frozen as quickly
as possible.).
- Vomitus or stomach contents, frozen. This is often the
best sample to positively identify which chemical is responsible
for the poisoning.
- Liver, 25g, frozen.
- Eyeball for retinal cholinesterase activity. Remove and
freeze as soon as possible. (Used primarily in large animal
cases when no other samples are available.)
- Skin is not routinely tested, but can sometimes be used
if exposure was dermal and no other samples are available.
- NOTE: A full necropsy should always be performed and a
full set of tissues submitted for histology to rule out
other causes of death, particularly if legal action is a
possibility.
Organophosphate and carbamate poisoning is relatively
common in pets and livestock. Animals can present with any
combination of the muscarinic and/or nicotinic signs listed
above or are frequently found dead. Diagnosis in live animals
is based on a history of appropriate clinical signs, depressed
blood acetylcholinesterase activity, and the identification
of an OP/Carbamate in vomitus or stomach contents, if available.
Diagnosis at necropsy is based on history, depressed brain
or retinal acetylcholinesterase activity, and the identification
of a specific OP/Carbamate in stomach contents and/or liver.
- by Jennifer Harms, B.S.
Christina Wilson, B.S.
Robert Everson, PhD
Stephen Hooser, DVM, PhD
|
