Insecticides and other pesticides (Proceedings)
The U.S Environmental Protection Agency (EPA) defines a pesticide as "any substance or mixture of substances intended for preventing, destroying, repelling, or lessening the damage of any pest".
The U.S Environmental Protection Agency (EPA) defines a pesticide as "any substance or mixture of substances intended for preventing, destroying, repelling, or lessening the damage of any pest". The EPA regulates all pesticides except those which might be regulated by the US Food and Drug Administration (FDA) such as anthelmintics, heartworm preparations and some pour-on insecticides. It should be noticed that extra-label use of pesticides regulated by the EPA is prohibited.
·Organophosphate and Carbamate insecticides act by inactivating or inhibiting by noncompetitive inhibition, cholinesterases, specifically acetylcholinesterase, to prevent the biotransformation of acetylcholine (ACH) and prolong its action. Organophosphates tend to be irreversible whereas the carbamates are reversible inhibitors of cholinesterases. Although carbamates as a group are considered quite safe, some of the available carbamate insecticides (Aldicarb - TEMIK® Aldicarb - TEMIK®TEMIK® ) are more toxic than many of the more potent organophosphate insecticides and may be as toxic as some of the war gasses such as Sarin and Tabun.
The clinical signs in animals with an acute cholinergic crisis (due to build up of acetylcholine) are divided into 3 categories, muscarinic, nicotinic and central nervous signs (CNS). The muscarinic signs include the “SLUD” signs: salivation, lacrimation, urination and defication. Meiosis may or may not be present. The nicotinic signs commonly seen include: skeletal muscles with initial stimulation proceeding to fasiculations, weakness and paralysis. The CNS signs include: convulsions, ataxia and respiratory center depression. The cause of death is respiratory failure.
The treatment regimen is as follows. The animal should be respirated signs of hypoxia exist. Administer Atropine at a dosage rate of 0.2 - 0.4 mg/kg, give 1/2 the dose IV and the remainder sub Q or IM. If bradycardia and hypoxia both exist, be sure to ventilate prior to administering atropine IV. (It should be noted that this dose of atropine is ten (10) times the pre-anesthetic dose.) Administer 2-PAM, 20 mg/kg, IV over a 2 hour period, slowly, repeat every 12 hours. Be careful about administering 2-PAM in cases of carbamate intoxications since it is contraindicated in cases of Sevin® Sevin® intoxication. The animal should be bathed if the exposure was dermal and the clinician/technician should wear personal protective equipment (PPE) to prevent exposure. It is important not to attempt to control all signs since intoxications with atropine and 2-pam can be induced.
·Amitraz (a formamidine) is a parasiticide for dogs most commonly known as Mitaban Mitaban®. Amitraz is also used on cattle, pits and agricultural crops. The mode of action is as a alpha2 -adrenergic agonist (similar in action as xylazine) and a weak monamine oxidase (MAO) inhibitor. The animals affected include dogs, cats and horses. The clinical signs in affected animals include: hypotension hypotension, mydriasis mydriasis, hypotension hypotension, bradycardia bradycardia, hypoperistalsis, ataxia, sedation, vasoconstriction, vomiting, and diarrhea.
Amitraz also induces a profound hyperglycemia in some animals. Treatment of affected animals should include remove the animal from the source. Dose with activated charcoal in the case of small animals, and mineral oil in the case of horses. Intravenous fluids are necessary for the hypotension. Specific antidotes are Yohimbine yohimbine (0.1 to 0.2 mg/kg, IV) or atipamezole at a dose of 50 µg/kg, IM.
·Pyrethrins Pyrethrum is extracted from the flowers of a chrysanthemum grown in Kenya and Ecuador. It is one of the oldest and safest insecticides available.The products generally have a very quick "Knock down" but are rapidly metabolized by insects. Piperonyl butoxide is used as a synergist because it inhibits the insects from metabolizing the pyrethrins.
The pyrethroid products labeled for dogs do not produce significant toxic effects but when the dog-labeled products are used on cats, significant toxicities occur. The clinical signs in intoxicated animals may be minor and self-limiting or may progress to more severe manifestations. Some animals may exhibit increased sensitivity to external stimuli and show fine tremors progressing to gross tremors, and finally prostration. Muscle twitching and seizures are common and ventroflexion of head/neck may occur (especially in cats).
Generalized weakness may resemble the nicotinic signs seen in organophosphate and carbamate intoxications. Some cats may also exhibit aggression and vocalizing/crying in addition to the above signs. Animals may exhibit salivation. emesis and/or diarrhea. The general treatment for intoxicated animals should be bathing and general supportive care. Diazepam (Valium®) and atropine may help control the excessive salivation. Early, aggressive therapy is often successful, but delayed treatment may result in the animal dying.
·Fipronil( Fiproles)(Regent®, Icon®, Frontline®) is the only insecticide in this new class. Fipronil blocks the (g-aminobutyric acid- (GABA) regulated chloride channel in neurons, thus antagonizing the "calming" effects of GABA. There is limited available information on adverse effects in dogs or cats.
The other botanicals pyrethrum, rotenone and limonene or d-limonene. Pyrethrum was discussed above. Rotenone or rotenoids are produced in the roots of two genera of the legume family: Derris and Lonchocarpus (also called cubé) grown in South America.. Rotenone is practically non-toxic to animals, but fish are very sensitive to it. Rotenone is currently used to kill fish in lakes and ponds to return the habitat to game fish. It is not toxic to the fish food organisms. The clinical signs might include vomiting due to gastric irritation, incoordination, muscle tremors, clonic convulsions, and respiratory failure. Treatment would be general and supportive.
Most of the available fungicides are generally non-toxic under conditions of use. There are some herbicides which are classified as carbamates, but they do not inhibit acetylcholilneesterase. Pentachlorophenol (PCP - not to be confused with phencyclidine) is a product which has been called an uncoupler of oxidative phosphorylation but in reality, keeps the mithchondria from storing energy by producing high energy phosphate bonds.
Since the energy cannot be stored, it is released in animals as heat resulting in hyperthermia. Removal of the affected animal from the source and supportive therapy should result in a favorable outcome. Years ago, there was an injectable product on the market, DNP (diisonitrophenol) which was marketed as a treatment for hook worms in dogs and cats. Over dosage with this product produced similar effects in dogs and cats.
Many herbicides are non-hazardous under conditions of use in and around the house and garden. In fact, one of the most popular herbicides, glyphosate (Roundup®) is practically non-toxic and safe around the house. However, there is a group of herbicides designated as the paraquat group which are exceedingly toxic when ingested. When used according to the manufacturer's instructions this group of compounds should not cause a problem as once it gets on plant material it is rapidly biotransformed by the plant and degrades in the environment. This group of agents, when ingested produce a fibrogenic pneumonia and have deleterious effects on the liver and kidney. There is no good treatment for paraquat intoxication and the prognosis for intoxicated animals is very poor.
The most commonly used molluscicide is MOLLUSCICIDES metaldehyde ( m-acetaldehyde)(CH2-CHO)4)Metaldehyde: m-acetaldehyde ((CH2-CHO)4) . It is marketed as a liquid or meal preparation of 3.5% as a snail or slug killer. Some baits look and taste like cat or dog food.. It is also available as a fuel for food warmers or camping stoves. The toxic oral dose of metaldehyde for most species is from 60 - 500 mg/kg. Metaldehyde toxicosis has not been reported in cats. The onset of clinical signs may be rapid or take up to 3 hours to develop.
In dogs, the clinical signs include: emesis (odor of acetaldehyde), incoordination, increase in respiratory and pulse rates, hypersalivation, hyperesthesia, opisthotonus and often continuous convulsions. There may be an apparent recovery following therapy but death may occur from secondary liver damage in several days or 1 - 2 weeks. There is no specific antidote but control of the CNS hyperactivity by diazepam or pentobarbital is generally successful. Appropriate GI decontamination and supportive care is necessary. Appropriate liver supportive measures should be instituted. The primary differential diagnosis is strychnine intoxication.
·Zinc phosphide is considered a rodenticide (Mouscon®, Kilrat®, Rumetan®, Mr. Rat Guard®.) and a grain fumigant (Fumitoxin®,PHOSFUME®). The compound is grayish black powder, insoluble in water with a faint phosphine or acetylene (carbide) odor, especially when wet. Stable in bait for about 2 weeks. The toxicity is due to the liberation of phosphine PH3 in the stomach. Phosphine is a general intracellular poison and can affect all tissues.
Clinical signs induced include: anorexia and lethargy, vomiting dark blood, abdominal pain, colic, profuse and sweating in horses. Respiration is rapid, deep, wheezy and the animals exhibit ataxia, weakness, recumbency. hyperesthesia, struggling, and convulsions. There is terminal hypoxia, gasping, and death can occur in 3-48 hours. At times, convulsions may resemble strychnine convulsions. There is no good treatment.
·Anticoagulant rodenticides are used extensively by the lay public and professional exterminators. The oral anticoagulants act by inhibiting the Vitamin K epoxide reductase enzyme which prevents the reduction of Vitamin K epoxide to Vitamin K. Depending upon the species of animal involved and the respective half-life of the clotting factors involved, defects in blood coagulation may not occur for 2 - 5 days following oral ingestion of the Vitamin K competitive inhibitors.
The clotting factors affected are II, VII., IX, and X. An interesting finding is that a small quantity fed for several days is more toxic than a single dose of a larger quantity, i.e., rats may survive single doses of 50 mg/kg, but are killed by repeated dosing for five successive days with 1 mg/kg. Because of the deficiency of prothrombin and the interference with the clotting mechanism, clinical signs are manifested by internal and external hemorrhages resulting in a severe anemia. The signs will depend upon where the hemorrhaging is occurring . A prolongation of any clotting test should raise the index of suspicion about exposure. Therapeutic measures may include the administration of fresh whole blood or fresh frozen plasma. Fresh products retain almost all of the clotting factors.
Specific therapy is directed toward the administration of Vitamin K1, orally along with a fatty meal to enhance absorption. The usual dose is 1.5 to 2.5 mg/kg, twice daily. If bleeding has started, the dose should be 5.0 mg/kg and increased as required based on PT results. Most dogs and cats should be treated for approximately 28 days. The PT should be checked at 48 hours following the last dose. Clinical signs may occur at this time if the treatment is stopped too soon. These requiring retreatment may become more difficult cases.
·Bromethalin is marketed as a single feeding rodenticide active against anticoagulant resistant rodents. Rodent deaths are delayed for 3 - 5 days, and no bait shyness has been reported. The mechanism of action of this product is similar to the DNP fungicides. Most animals start exhibiting clinical signs within 4 hours of ingestion but may be as long as 18 hours. High dose bromethalin exposure cases exhibit incoordination, tremors, convulsions or respiratory distress, hyperthermia, extreme hyperexcitability, and focal motor or generalized convulsions. Hind leg ataxia and paresis develop in the beginning progressing to hind-limb paralysis.
Therapy designed to abolish seizures is indicated. This would include phenobarbital (administered at 5 - 10 mg/kg, IV, to effect) or diazepam (5 - 10 mg, IV, as needed). The clinician must remember that phenobarbital has a 10 to 15 minute latent period before exhibiting full control of seizures so over dosing may happen. Treatments for cerebral edema using mannitol, dexamethasone and furosemide have proven inconclusive. Hypertonic saline (7.5% NaCl) solutions have also given variable results. Cool water enemas and baths may be indicated if the rectal temperature is above 104? F (40? C).
·Cholecalciferol is a very active form of Vitamin D3. It is reported by pest control personnel as safe around pets and this understates the toxicity of cholecalciferol. The mechanism of action is the compound mobilizes calcium from bones into the blood causing a "calcium-like" toxicity to the heart. The clinical signs most commonly associated with cholecalciferol-induced hypercalcemia are rather non-specific. The signs will generally develop within 18 - 36 hours postexposure and include: anorexia, lethargy, nausea, weakness, vomiting (+ blood), diarrhea (+ blood), polyuria, polydipsia, and rarely neurological disturbances (e.g., seizures).
Clinical signs become more severe as serum calcium levels increase. Hypercalcemia can result in EKG changes including shortened Q-T interval and prolonged P-R interval. Vasoconstriction and hypertension may occur. Lesions in the acute disease is a strongly contracted heart. In chronic exposures, calcium deposits often occur in soft tissues, aorta, tendons, and muscle. There is no good treatment for cholecalciferol intoxication. The decision to initiate therapy depends upon the severity of the condition.
Normal emergency procedures should be followed if the ingestion was recent. The intoxicated animal should be placed on a low calcium-containing diet such as s/d, u/d/, or k/d, and kept out of the sunlight..Fluid therapy should include normal saline IV and furosemide as a diuretic. Thiazide diuretics are contraindicated. Corticosteroids have several beneficial effects and should be used. Also, calcitonin can be administered in microgram quantities (4-6 IU/kg) SQ every 2-3 hours initially. Treatment with diuretics and cortisone should continue until serum calcium remains normal. Check the serum calcium level 24 hours after treatment is stopped. Long term therapy, for two weeks or more, may be required.
·Strychnine is used primarily for small mammals and coyotes, today as a restricted use pesticide. In most states it is available as an 0.5% bait for gophers in small quantities as an unrestricted pesticide. Malicious poisonings still occur, primarily in canine, although intentional poisonings in horses have occurred. Strychnine is a spinal convulsant, blocking the glycine receptors in the spinal cord and medulla, and is not considered a central convulsant.
Affected animals may present initially as exhibiting anxiety, restlessness, and increased respiratory rates. This progresses to constant panting, muscle tremors and finally muscle groups contract antagonistically. Clonic-tonic seizures may occur spontaneously or with touch, light, or noise stimuli. The severity and duration of convulsions are not prognostic. Death is generally from asphyxia due to prolonged paralysis of the respiratory muscles. Death may be as sudden as 5 - 10 minutes or as long as 2 hours after the beginning of the convulsions. Dead animals present with non-specific lesions and the rapid development of rigor mortis with petechial hemorrhages and traumatic lesions . The stomach is generally filled with ingesta.
Differential diagnoses include sodium fluoroacetate (1080) intoxication, Metaldehyde and Brunfelsia spp. (Yesterday, today and tomorrow plant).Therapy is directed towards controlling the seizures and protecting the dog. After onset of signs, control the convulsions and give respiratory support. Pentobarbital sodium, given to effect is the best therapeutic measure, however the patient may have to be taken almost to respiratory depression before the signs can be controlled. The animal should have an endotracheal tube. Once the convulsions are controlled, a gastric lavage should be performed to empty the stomach. The patient should be place in dark, quiet room, temperature maintained and turned periodically. Central acting skeletal muscle relaxants may be used, but require a constant rate infusion for 2 or more days.
·Sodium fluoroacetate(Compound 1080 ) is a chemical which inhibits the Krebs cycle in the mitochondria causing an energy shortage. It is a severely restricted rodenticide. The clinical signs in dogs and cats are convulsive in nature with attempts to vomit and defecate. The animals will die 30 minutes to 4 hours after clinical signs begin. There is no treatment for this intoxication. In contrast to strychnine poisoning, the stomach is empty in animals dying from sodium fluoroacetate