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Small Animal Toxicoses - Insecticides

Tina Wismer, DVM
Veterinary Poison Information Specialist
ASPCA Animal Poison Control Center



Permethrin is approved for small animal flea control, large animal topical fly control, crops, ornamental plants and human use. Permethrin is found in shampoos, dips, foggers, spot-ons, and sprays for small animal use. Permethrin is a synthetic type I pyrethrin. Type I pyrethrins bind to the sodium channels on nerves and alter the voltage-dependent gating kinetics. This causes reversible prolongation of sodium conductance in the nerve axons and results in repetitive nerve discharges. (Valentine, 1990; Casida, 1983) This effect is enhanced in hypothermic mammals and in cold-blooded animals.

Oral absorption of permethrin is rapid for all species, but dermal absorption of permethrin varies. Rat skin absorbs significantly more permethrin than monkey skin. (Sidon, 1988) Permethrin is highly lipid soluble and concentrates in nervous tissue at 1.5 - 7.5 times the plasma concentration. (Anadon, 1991) Permethrins are broken down in the liver and are excreted in the urine. (Tomlin, 1994)

Permethrins appear to be relatively safe in dogs. Smaller dogs seem to have a greater risk of toxicity and any animal can have a dermal hypersensitivity reaction to a spot-on. These dermal hypersensitivity reactions may be to the active ingredient or to the carriers. Skin reactions can be treated with bathing +/- antihistamines or steroids.

Cats are more likely than dogs to develop pyrethroid toxicosis. This is due to the feline liver being inefficient at glucuronide conjugation. Glucuronide conjugation is needed to metabolize permethrin. The low concentration products approved for cats contain 0.05-0.1% of permethrin and do not seem to cause the signs that the concentrated (45-65% permethrin) canine spot-ons do. (MacDonald, 1995) Permethrin toxicity usually occurs when the owner applies the dog spot-on product to the cat; however, cats which actively groom or engage in close physical contact with recently treated dogs may also be at risk of toxic exposure. The severity of permethrin toxicity varies with each individual. Some cats develop signs when only “one drop” is applied, while others show no clinical signs after an entire vial is used.

Onset of clinical signs is usually within a few hours of exposure but may be delayed up to 24 hours. The most common clinical signs of permethrin toxicity in cats are muscle tremors and seizures. Hypersalivation, depression, vomiting, anorexia and even death may also be seen. Methocarbamol (50-150mg/kg IV bolus, titrate up as needed, but do not exceed 330mg/kg/d) works best to control the tremors. If no injectable methocarbamol is available, the oral form may be dissolved in water and given rectally. If the cat is actively seizuring, barbiturates, propofol or inhalant anesthesia can be used. Valium does not seem to work as well to control permethrin induced tremors and seizures. Once stabilized, a bath with liquid dish washing detergent should be given. Permethrins appear to have no direct action on the liver or kidneys, but fluids may be needed to help protect kidneys from myoglobin break-down products in actively tremoring cats. Prognosis for mildly tremoring cats is usually good, but treatment may last 24-48 hours. Uncontrollable seizures or extended duration of seizure activity despite aggressive treatment efforts worsens the prognosis.

For definitive confirmation of permethrin toxicosis, urine and plasma can be analyzed for permethrin using liquid chromatography. (Anadon, 1991; Sidon, 1991) Although not a routine analysis, necropsy samples of liver, fat, brain, and/or CSF fluid can also be used to confirm exposure.


Chlorpyrifos (Brodan, Detmol UA, Dowco 179, Dursban, Empire, Eradex, Lorsban, Paqeant, Piridane, Scout, Stipend) is one of the most widely used organophosphates. Chlorpyrifos is effective in controlling cutworms, corn rootworms, cockroaches, grubs, fleas, ticks, beetles, flies, termites, fire ants, and lice. It is used as an insecticide on crops, lawns, ornamental plants, several species of animals and in dwellings. Except for flea collars, chlorpyrifos is not approved for use on cats.

Chlorpyrifos is undergoing a phase out in “around the home” use products in both the US and Canada due to concerns about neurological effects in children. Sales of chlorpyrifos containing products will continue until existing stocks are depleted, with retail sales occurring until December 31, 2001.

Chlorpyrifos is readily absorbed following oral, inhalation, or dermal exposure. (NLM, 1995) It is metabolized and then eliminated primarily through the kidneys. (NLM, 1995) Chlorpyrifos is different from most organophosphates, as it is more lipid-soluble: therefore, residues persist longer. The chlorpyrifos is redistributed to adipose tissue, which forms a depot for slow release. Chlorpyrifos undergos "aging", rendering the phosphorylated enzyme very stable so that recovery of AChE activity occurs only through the synthesis of new enzyme. (Osweiler, 1996) When chlorpyrifos (Dursban) was fed to cows, unchanged pesticide was found in the feces, but not in the urine or milk. (EPA, 1984) However, it was detected in the milk of cows for 4 days following spray dipping with a 0.15% emulsion. The maximum concentration in the milk was 0.304 ppm. (Gallo, 1991)

Sensitivity to chlorpyrifos varies with species.
Species LD50 (mg/kg) Route
Cat 10-40 Oral
Rat 95-270 2000 Oral Dermal
Mouse 60 Oral
Rabbit 1000 1000-2000 Oral Dermal
Chicken 32 Oral
Guinea pig 500-504 Oral
Sheep 800 Oral
(Fikes, 1992; Gallo, 1991; Kidd, 1991; Gosselin 1984; Dow 1986)

Chlorpyrifos is highly toxic to birds, fish, aquatic invertebrates, and honeybees. (Kidd, 1991; EPA, 1989; EPA, 1984)

Signs of cholinesterase inhibition occurred at 1 mg/kg/day, however, plasma cholinesterase levels are decreased for up to 28 days even at doses of 0.1mg/kg. (Hooser, 1988) Animals with respiratory ailments, recent exposure to cholinesterase inhibitors, cholinesterase impairment, or liver disease are at increased risk from exposure to chlorpyrifos.

Animals exposed to chlorpyrifos may present with typical muscarinic SLUDDE signs (salivation, lacrimation, urination, defecation, dyspnea, emesis) and bradycardia. Very large exposures may result in tremors, coma, seizures and death. Chlorpyrifos is also reported to cause a delayed neuropathy syndrome that can be seen 18-20 days post exposure and is characterized by ataxia, hypermetria, and hindlimb CP deficits. (Fikes, 1992) Chlorpyrifos causes non-typical signs in cats. With acute toxicity, predominant neurologic signs are tremors, (especially of the back, top of head, and neck), ataxia, depression, and seizures. Other signs include anorexia, ventroflexion of neck, change in personality, hyperesthesia, and hyperactivity. Mydriasis and miosis occur with the same frequency. Depression, anorexia, and tremors can persist for 2-4 weeks. (Fikes, 1992) Cats may also have delayed signs 1 to 5 days post topical exposure. These cats are anorectic, depressed, hypokalemic, and need to be force fed. Signs can last for 10-14 days.

If the animal is orally exposed to a toxic amount and is still asymptomatic, induce emesis and give activated charcoal. If the animal is dermally exposed, wash with a liquid dish soap. Due to dermal absorption, activated charcoal might still be beneficial even after a dermal only exposure. (Fikes, 1990) Treatment of symptomatic patients consists of stabilizing the animal and controling seizures (with diazepam, methocarbamol, or barbiturates) before proceeding with other treatments. Provide oxygen and ventilatory support as needed for animals in respiratory distress. Atropine is a specific antagonist and may be given (0.1-0.2 mg/kg for dogs, cats, birds, horses; 0.5 mg/kg for cattle) to control the muscarinic signs (atropine does not control nicotinic signs, ie. tremors, seizures, ataxia). Give 1/4th of the initial dose IV and the rest IM or SQ. The dose can be repeated as needed, but do not over-atropinize the animal. Animals do not die from constricted pupils or hypersalivation; the primary goal of atropine use is to control bradycardia and bronchial secretions. (Fikes, 1990) Atropine does not affect the AChE-insecticide bond, but blocks the effects of accumulated acetylcholine at the synapse. Pralidoxime chloride (2-PAM; Protopam) may also be used. 2-PAM interacts with the insecticide-AChE combination with the result of freeing the AChE and forming a complex with the insecticide that is excretable in the urine. Pralidoxime is used to control the nicotinic signs and the initial dose is 20 mg/kg IM BID for small animals. If no response after 3 doses, discontinue treatment. 2-PAM is ineffective once "aging" occurs. However, the time of "aging" varies with the compound and so 2-PAM may be effective even days after exposure.

Since muscarinic signs can be seen with many conditions, a test dose of atropine can be given to determine whether or not the signs are caused by an anticholinesterase insecticide. Give a preanesthetic dose of atropine (0.02 mg/kg IV for dogs and cats) and monitor the response. If the heart rate increases and mydriasis occurs, then the muscarinic signs are probably not due to an OP or carbamate insecticide because it usually takes roughly 10X the preanesthetic dose to resolve signs caused by acetylcholinesterase inhibitors.

AChE activity testing is a diagnostic indicator and will not indicate which insecticide or how much an animal was exposed to. A definitive diagnosis of OP toxicosis is based on clinical signs, AChE activity, and history of exposure or by finding an anticholinesterase insecticide with diagnostic testing. AChE levels can be checked using serum, plasma, or whole blood. Liver, kidney, GI contents, and source material should be collected (and frozen) so that insecticide panels can be done to identify which insecticide has caused the toxicosis. AChE activity results cannot be interpreted without a normal reference from the lab that ran the sample because there are several different methods of testing AChE activity (all of which have different reference ranges) and because AChE activity varies widely among the different species of animals. If using a human hospital, also send a blood sample from an animal that has not been exposed to an anticholinesterase for at least 8 weeks (human labs will not have established animal reference ranges). Generally, an AChE activity that is <50% of normal indicates significant exposure while an AChE activity <25% of normal indicates toxicosis. (Fikes, 1990) However, blood AChE does not always correlate well with clinical signs. AChE activity can remain depressed for 6-8 weeks after exposure. On necropsy, AChE activity can be checked in brain or retina. Half of the brain should be submitted to the lab as AChE activity varies among regions of the brain (the lab will homogenize the half-brain before testing). (Plumlee, 1997) Insecticide screens can also be checked on tissue samples and GI contents. Animals that die rapidly (in a few hours) are less likely to have depressed brain AChE activity than animals that live longer before dying. However, the blood AChE will probably be depressed. This may have something to do with the blood-brain barrier. (from discussion on Vettox List, 1994-95) Samples that are to be shipped or that have to wait longer than 24 hours for testing should be frozen.

Prognosis for acute toxicity is good unless the animal suffers from respiratory distress or seizures. A guarded prognosis should be given for chlorpyrifos cats that have stopped eating due to the risk of developing fatty liver disease.


Disulfoton (Bay S276, Disyston, Disystox, Dithiodemeton, Dithiosystox, Frumin AL, Solvigram, Solvirex) is a selective, systemic organophosphate insecticide and acaricide that is especially effective against sucking insects. It is used to control aphids, leafhoppers, thrips, beet flies, spider mites, and coffeeleaf miners. Disulfoton products are approved for use on cotton, tobacco, sugar beets, cole crops, corn, peanuts, wheat, ornamentals, cereal grains, and potatoes. When applied to the soil, disulfoton is actively taken up by plant roots and is translocated to all parts of the plant. (Gallo, 1991) This systemic distribution is effective against sucking insects, while predators and pollinating insects are not destroyed.

Disulfoton is very highly toxic to all mammals by all routes of exposure. Disulfoton is rapidly absorbed by the gastrointestinal tract, metabolized in the liver, and excreted via urine. Dogs are usually exposed to disulfoton after the owner mixes systemic rose products with bone or blood meal to fertilize their roses. Disulfoton is moderately toxic to birds and bees and is highly toxic to fish, crab, and shrimp. (NLM, 1995; Kidd, 1991)

Onset of clinical signs is 2-8 hours post ingestion and signs can last for several days (it is believed that there is some enterohepatic recirculation). (Osweiler, 1996) Not only can these animals present with the typical SLUDDE signs, but they can also have hemorrhagic diarrhea plus liver and pancreas enzyme elevations.

With disulfoton, do not induce emesis at home if exposure was possibly longer than ˝ hour earlier because of the possibility of acute onset of seizures. If the animal is still asymptomatic, activated charcoal with a cathartic may be given. If symptomatic, atropine may be given to control the muscarinic signs (atropine does not control nicotinic signs). The dose will probably need to be repeated, but do not over-atropinize the animal. Pralidoxime chloride (2-PAM; Protopam) may also be used. Use valium, barbiturates or methocarbamol to control seizures and tremors. Provide IV fluids and supportive care as needed. If large amounts of dirt or bone meal are ingested and if the animal does not yet have diarrhea, an enema may help to increase excretion of the product.

Prognosis is good to guarded depending on the severity of the signs. Complete recovery from acute effects may take several days, but blood cholinesterase levels may take up to 3 months to return to normal. (NLM, 1995) Due to the continued AChE depression, these recovered animals should not be exposed to any other organophosphate or carbamate insecticides for several months.


Tetrachlorvinphos (Rabon®) is a low toxicity organophosphate available in collars, powders, dips, sprays, and feed additives. Dogs fed 2000 ppm per day (2 g/kg of food) had decreased plasma cholinesterase activity (normal erythrocyte and brain cholinesterase activity) but no other clinical effects. There have been no reports of delayed neurotoxic effects with tetrachlorvinphos. (Rabon, 1984)

Cats have shown some depression, ataxia and salivation when saturated with the tetrachlorvinphos sprays, but this may be due to the alcohol content and the taste of the product. Quick recovery is seen after bathing and supportive care.


Carbamates are acetylcholinesterase (AChE) inhibitors derived from carbamic acid. Like organophophates, carbamates competitively inhibit AChE by binding to its esteric site. However, this is a reversible inhibition of acetylcholinesterase.


Methomyl (Golden Malrin) is a “hot” carbamate insecticide. It is found in fly baits. These baits contain large amounts of sugar that make it very palatable to dogs and other animals.

Methomyl is quickly absorbed through the skin, lungs, and gastrointestinal tract and is broken down in the liver. Metabolites are readily excreted through respiration and urine. (Kidd, 1991) Although methomyl does not appear to accumulate in any particular body tissue, it may alter many other enzymes besides cholinesterase. (NLM, 1995)

Species Oral LD50 (mg/kg)
Dog 17
Rat 17-24
Mouse 10
Guinea pig 15
Mule deer 11-22
(Tucker, 1970; Baron, 1991; RTECS, 2000; Kidd, 1991)

Methomyl is also highly toxic to birds, fish, aquatic invertebrates and bees. (EPA, 1987)

Clinical signs can be seen within 30 minutes of ingestion. Symptoms of methomyl exposure are similar to those caused by other carbamates and cholinesterase inhibitors. (Baron, 1991) Vomiting, seizures and death are the most common clinical signs.

Do not instruct owners to induce emesis at home due to the quick onset of signs and the possibility for seizures. Treatment consists of atropine, and supportive care to control the seizures. If seizures can be controlled, prognosis is good.


Organochlorines are chlorinated hydrocarbons that inhibit GABA.


Lindane is an organochlorine insecticide which acts by competitive inhibition of the binding of GABA at its receptor. Lindane can no longer be manufactured in the U.S. (since July 1999), but products containing lindane can still be sold until gone. It will take several years before all lindane containing products are removed from the shelves. Lindane is presently found in lotions, creams, and shampoos for the control of lice and mites (scabies) in humans along with dips for dogs. Lindane is approved for use on dogs for fleas, ticks, and sarcoptic mange.

Animal studies show that lindane is readily absorbed through the gastrointestinal tract, skin, and lungs. (Smith, 1991) Metabolism of lindane includes conjugation with sulfates or glucuronides and then excretion through the urine. (Smith, 1991) Since part of lindane’s metabolism requires glucuronidation, lindane is extremely toxic to cats and has never been approved for use in this species

Species LD50 (mg/kg) Route
Cat 25 Oral
Dog 40 Oral
Rat 88-190 500-1000 Oral Dermal
Mouse 59-562 300 Oral Dermal
Guinea pig 100-127 400 Oral Dermal
Rabbit 200 300 Oral Dermal
Mallard duck 2000 Oral
(Smith, 1991; Kidd, 1991; RTECS, 2000; Hill, 1986)

Lindane is highly toxic to fish, aquatic invertebrates and bees. (Kidd, 1991)

Clinical signs of lindane toxicity can develop within 1 hour and include hypersensitivity, muscle fasiculations (esp. head, neck, and shoulders), tremors, seizures and death. Treatment for dermal exposure is bathing with liquid dish washing detergent (avoid human exposure by the use of heavy-gauge rubber gloves). For recent oral exposures, an emetic may be used only if presented very early and if the animal is asymptomatic. Activated charcoal and a cathartic may be given (weigh risk of aspiration). Seizure control with diazepam or barbiturates is usually necessary for 24 hours, and sometimes longer.

Other Insecticides


Fipronil is a phenylpyrazole insecticide. It is found in spot-ons and sprays (Frontline®) for pets, along with roach traps. It is also licensed for food crops in 30 countries and for use on golf courses in the US. Fipronil works by binding to the GABA receptors of insects and blocking chloride passage. By being a GABA antagonist, fipronil causes excitation of the nervous system in insects. (Cole, 1993) Its neurotoxicity is selective, because the configuration of GABA receptors in mammals is different from insects. The activity of fipronil is opposite to that of ivermectin.

Fipronil is not systemically absorbed. (Weil, 1997) Fipronil is detected on the hair shafts but is never detected in the dermis and adipose tissue, suggesting that it is absorbed and accumulated in the sebaceous glands, from which it is slowly released via follicular ducts.

Fipronil is a safe insecticide. It has been tested and can be used in kittens and puppies as young as 8 weeks of age. It is easily removed by bathing in the first 48 hours after application before it is absorbed into the sebaceous glands. (Weil, 1997) In toxicity studies, the application of Frontline® spray to dogs and cats at a dose five times higher than recommended for 6 months did not cause any clinical, biochemical, hematological, or cutaneous abnormalities. (Consalvi, 1996) Oral doses equal to 87 pipettes in dogs and 20 pipettes in cats showed no adverse reactions beyond drooling and occasional vomiting. A few skin hypersensitivity reactions have been reported, most likely to the carrier. Fipronil, used off-label, has been reported anectodally to cause seizures in rabbits. (Webster, 1999)

There have been reports of benign thyroid tumors in rats exposed to fipronil and concern was expressed about the potential for carcinogenicity. These rat thyroid tumors were caused by suppression of thyroxin (T4) and a subsequent increase in thyrotropin stimulation hormone production leading to thyroid gland hyperplasia. Feeding studies in mice did not find any evidence of carcinogenicity and in addition, studies in dogs exposed to fipronil showed no effect on T4 or thyroid stimulation hormone concentrations. (Keister, 1996) Based on these findings, it was concluded that the carcinogenicity was limited to rats.


Imidacloprid is a chloronicotinyl nitroguanide insecticide. It is used for crop, fruit and vegetable pest control, termite control, and flea control in dogs and cats (Advantage, Admire, Condifor, Gaucho, Premier, Premise, Provado, and Marathon). It works by binding to the acetylcholine receptor on the postsynaptic portion of insect nerve cells, preventing acetylcholine from binding. (Bai, 1991; Lui, 1993) This prevents transmission of impulses, resulting in paralysis and death of the insect. Imidacloprid is not degraded by the enzyme acetylcholinesterase and atropine is not antidotal. It has been recently hypothesized that there are two binding sites with different affinities for imidacloprid and that this compound may have both agonistic and antagonistic effects on the nicotinic acetylcholine receptor channels. (Nagata, 1998)

Imidacloprid is quickly and almost completely absorbed from the gastrointestinal tract, and eliminated via urine and feces (70-80% and 20-30%, respectively, of the 96% of the parent compound administered within 48 hours). The most important metabolic steps include the degradation to 6-chloronicotinic acid, a compound that acts on the nervous system as described above. This compound may be conjugated with glycine and eliminated, or reduced to guanidine. (Kidd, 1991)

Imidacloprid is a safe insecticide. It has low toxicity in mammals as there is a much lower concentration of nicotinic acetylcholine receptors in mammalian nervous tissue as compared to insects. Imidacloprid also has a higher binding affinity for insect receptors. (Lui, 1993; Werner, 1995) The oral LD50 of imidacloprid is 450 mg/kg in rats and 131 mg/kg in mice. (Meister, 1994; Kidd, 1991) The 24-hour dermal LD50 in rats is >5,000 mg/kg. Results of a chronic feeding study revealed no adverse effects in dogs given imidacloprid at a dose of 15 mg/kg daily for 1 year. (Griffin, 1997) Topical application on dogs and cats at a dose of 50 mg/kg also caused no adverse effects. (Griffin, 1997) No adverse effects were seen in pregnant and lactating dogs at three times the recommended dose or in pregnant queens at four times the recommended dose. (Griffin, 1997) Additionally, 20 times the recommended dose was safe in puppies. (Griffin, 1997) Imidacloprid is approved for use in puppies as young as 7 weeks of age and in kittens as young as 8 weeks of age. With oral exposure, salivation or vomiting is occasionally seen and dilution with milk or water is recommended. Imidacloprid is very toxic to aquatic invertebrates, toxic to upland game birds, and of low toxicity to fish.

Due to the large safety margin of imidacloprid, signs are rarely seen. Signs of toxicity would be expected to be similar to nicotinic signs and symptoms, including lethargy, muscle fasiculations, tremors, and muscle weakness. (Doull, 1991)


Selamectin (Revolution®) is a novel, semi-synthetic avermectin. Selamectin works by inducing neuromuscular paralysis of the parasite by increasing chloride permeability.

Selamectin is rapidly absorbed from the skin into the bloodstream where it kills heartworm microfilaria. Selamectin is excreted into the intestinal tract where it kills intestinal parasites. Finally, selamectin is selectively distributed from the bloodstream into the sebaceous glands of the skin, forming reservoirs that provide persistent efficacy against fleas, ear mites and sarcoptic mites. (Selamectin, 1999)

Selamectin is safe in collies and heartworm positive dogs and cats. It has also been used in breeding, pregnant and lactating animals without any adverse effects. Selamectin has been given to six week old puppies and kittens at ten times the normal dose with no problems. (Thomas, 1999) With oral dosing, some salivation and vomiting has been seen, most likely due to the isopropyl alcohol in the carrier. In the clinical setting, diarrhea has been reported 24 hours after dosing and is believed to be from the die off of intestinal parasites.


Hydramethylnon (Amdro, Maxforce, Combat, Blatex, Cyaforce, Cyclon, Impact, Matox, Pyramdron, Seige, Wipeout) is a trifluoromethyl aminohydrazone insecticide used in baits to control fire ants, leafcutter ants, harvester ants, big-headed ants, and cockroaches in both indoor and outdoor applications. (Farm Chemicals Handbook, 1996). It is available as a 0.73% granular bait (utilizing soybean oil as the attractant on inert corn carriers), a 0.88% granular bait, and as a 1.65% gel bait or bait stations for cockroaches.

Hydramethylnon inhibits the formation of ATP by uncoupling oxidative phosphorylation. Hydramethylnon is poorly absorbed orally by mammals and greater than 95% is excreted unchanged in the feces. (Prod Info, 1986) Rats dosed orally with hydramethylnon eliminate 72% of the dose in 24 hours and 92% in 9 days. (Tech Info, 1988)

Hydramethylnon appears to be quite safe in mammals as the oral rat LD50 is 1100 to 1300 mg/kg. (Kidd, 1991) Dermal LD50s are greater than 5000 mg/kg in both the rat and rabbit. (Sine, 1987; Kidd, 1991) In a 26-week study in dogs, doses of up to 3.0 mg/kg/day resulted in increased liver weights and increased liver:body weight ratios. No other effects were observable in either the structure of tissues examined, the chemistry and consistency of the blood, or the chemistry of other bodily fluids. In dogs, 6 mg/kg/day caused decreased food consumption, decreased weight gain and caused testicular atrophy in a 90-day feeding study. (EPA, 1995) Chronic studies in several animals have shown the testis as a target organ. Hydramethylnon is highly toxic to fish and nontoxic to birds and honey bees. (NLM, 1995). Grazing animals fed 10x the recommended field application amount did not develop any problems. No residues were detectable in the milk or tissues of goats at a dietary dose of 0.2 ppm in the daily diet for 8 days. (NLM, 1995) No residues were found in the milk or tissues of cows at a dietary dose of 0.05 ppm for 21 consecutive days. (Kidd, 1991) Leukopenia and eosinopenia developed as early as 14 days after giving calves 1.3 to 1.5 g/kg/day of Amdro(R) and appeared to selectively affect production of immunocompetent T and B cells in a 50 day feeding trial. (Evans et al, 1984). A possible effect on the immune system of horses fed AMDRO has been suggested (Miller et al, 1984). Ponies fed AMDRO-treated grits (1/100th to 1/150th the calculated LD50) for 30 days (Miller et al, 1984) had leukopenia and eosinopenia and AMDRO-fed animals had increased severity of upper respiratory disease and an increased incidence of diarrhea as compared to controls.

Vomiting and gagging are the most common signs reported in dogs with oral ingestions of hydramethylnon. Emesis would only be necessary if large amounts (greater than 1 ounce of bait/kg) were ingested. According to the manufacturer of Combat® Roach Control System (1.65% hydramethylnon) a medium-sized (20 kg) dog would experience adverse effects from the bait itself only after eating an amount equivalent to 250 trays. Mechanical obstruction may be seen if the dog ingests the control system (plastic).

Hydramethylnon residues can be detected by using chromatography or mass spectrometry. (Stout et al, 1985). Any tissue, blood, milk, or feed may be tested for the presence of hydramethylnon.


Sulfluramid (perfluorooctanesulfonamide or N-ethylperfluorooctane sulfonamide) is a unique polyfluorinated insecticide found in ant and roach baits. Sulfluramid has been shown to be able to uncouple oxidative phosphorylation (no ATP production) in the mitochondria. Disruption of energy metabolism results in a slowly developing toxicity and leads to lethargy, paralysis and death in the insect. Fortunately, this compound appears to be very safe in dogs and cats.

The oral LD50 in the rat is 543 mg/kg. (RTECS, 2000)


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