A Neonicotinoid Insecticide

Imidacloprid is an active ingredient found in flea drops (Bayer Advantage). It kills 100% of fleas on animals, lasting 4 weeks before reapplication is needed. Most exposed fleas die within 20 minutes of treatment. It’s highly selective towards insects, resulting in a good safety profile for mammals.

History Efficacy Mode of Action Toxicity

bayer advantix II imidacloprid flea drops for dogs bayer advantage II imidacloprid flea drops for cats bayer seresto imidacloprid flea collar for dogs bayer seresto imidacloprid flea collar for cats
Product Name K9 Advantix II Bayer Advantage II Bayer Seresto Bayer Seresto
Price $45 $40 $45 $45
Size 4 tubes 4 tubes 1 collar 1 collar
Application Squeeze-On Squeeze-On Collar Collar
Use On Dogs Cats Dogs Cats
Kills Eggs
Active Ingredients Imidacloprid
A.I. Concentration 8.80%
Duration 4 months 4 months 8 months 8 months
Product Label
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  • Prices are approximations based off of prices at the time of publishing.
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What is Imidacloprid

Imidacloprid (IMI) belongs to a class of synthetic insecticides called neonicotinoids. It’s used to control a variety of agricultural and veterinary pests. Neonicotinoids are similar to nicotine, but more effective and safer.

Imidacloprid is the active ingredient in Bayer Advantage flea treatments for dogs and cats, where it’s found in concentrations of around 9%. Advantage gets applied to an animal’s skin at the base of their skull. Within 24 hours, it spreads all over the animal’s body. Fleas die within 24 hours of treatment, most dying sooner. One treatment stops new infestations for four weeks. To broaden its spectrum of activity, imidacloprid is often combined with moxidectin, ivermectin, permethrin, or pyriproxyfen.

Chemical Overview

Chemical type Neonicotinoid Insecticide
Developer Bayer
Developed in 1985
Common name Imidacloprid (IMI)
Trade names Advantage®, Admire®, Merit®, Gaucho® & Hachikusan®
IUPAC names N-[1-[(6-chloropyridin-3-yl)methyl]-4,5-dihydroimidazol-2-yl]nitramide
CA name 2-Imidazolidinimine, 1-[(6-chloro-3-pyridinyl)methyl]-N-nitro-
CAS No. 138261-41-3
Molecular formula C9H10CIN5O2
Molecular mass 255.7 g/mol
Physical state Liquid
Odor Mild odor
Color Clear or slightly yellow
Molecular Structure imidacloprid molecular structure


Initial Research into Neonicotinoids

In recent history, insecticide research has been motivated by a high demand for replacements to traditional compounds (e.g. organophosphates). Chemists searched for insecticides with versatile uses and favorable toxicological and environmental profiles.

In the early 1970s, Shell’s former Biological Research Center developed new compounds called nitromethylene heterocycles. One showed unexpected insecticidal properties. Soon after, it’s molecular structure was altered to achieve higher insecticide activity. Molecular design eventually led to identifying nithiazine, the first neonicotinoid prototype.

Nithiazine was an effective insecticide with low mammalian toxicity. Unfortunately, it degraded rapidly in sunlight or water. Thus, it was impractical for use in agriculture and couldn’t be stored easily. Still, in 1997, nithiazine was commercialized in a fly trap for animal shelters.

The Development of Imidacloprid

In 1979, Bayer CropScience began synthesizing molecules based off of nithiazine. They employed a new screening processes for testing compounds against leafhoppers. In 1984, a chemical with 100 times more activity than nithiazine was discovered. But it still wasn’t photostable, so they continued searching for a stable compound. In February 1985, after screening 2000 candidates, imidacloprid was found. Imidacloprid’s insecticidal activity is 3000 to 10000 times greater than that of nicotine, and 125-fold more effective than nithiazine.

Although neonicotinoids are related to nicotine in action and structure, they weren’t modeled after the tobacco toxin. The new compounds originated from Bayer’s screening process.

In 1991, IMI became commercially available. It was introduced to the Japanese market in 1992, the UK in 1993, and the US in 1994. Bayer Advantage, the most well-known IMI product, has been available since 1996. As the first commercialized neonicotinoid, IMI soon became one of the most important insecticides in the world.


The term ‘neonicotinoid’ was proposed to differentiate the new compounds from classical nicotinoid insecticides. Neonicotinoids and nicotinoids have common structural features and modes of action. However, there are significant differences. Specifically, nicotinoids (e.g. nicotine) are ionized and target mammalian nicotinic acetylcholine receptors (nAChR). Neonicotinoids, conversely, aren’t ionized and are selective for insect nAChRs. As a result, neonicotinoids have a wide safety margin for mammals.

The success of IMI led to chemical companies synthesizing other neonicotinoid compounds. Some of these include thiacloprid, thiamethoxam, nitenpyram, acetamiprid, clothianidin, and dinotefuran. Still, IMI remains the principal neonicotinoid.

Current Status

Imidacloprid’s development and market introduction initiated the era of neonicotinoids. It was a milestone in insecticide research and modern agriculture. Neonicotinoids became the fastest growing class of insecticides since pyrethroids. In 2006, neonicotinoids accounted for worldwide annual sales of $1.56 billion, nearly 17% of the global insecticide market.

Neonicotinoids quickly replaced pyrethroids, chlorinated hydrocarbons, organophosphates and carbamates. Their success is thanks to a broad-spectrum of activity, low application rates, selectivity towards insects, a good safety profile, and versatile uses. In addation, their unique mode of action meant there wasn’t cross-resistance to conventional insecticides. Neonicotinoids also benefited from the increased regulations and subsequent withdrawal of older compounds from the market.

In 2006, IMI became generic in many countries and was used even more widely. In the future, other neonicotinoids will run out of patent protection and increasing number of generics will have a strong impact on the global insecticide market.

Imidacloprid is the most successful and best-selling neonicotinoid in the world. It’s been approved in over 120 countries, for use on over 140 crops. Along with crops, IMI is used on pets, seed treatments, turfs and soils, and in homes. It’s sold under various Bayer brand names including Premise, Admire, Grub-ex and Advantage.


Imidacloprid’s efficacy as an insecticide is superior or comparable to classic compounds like phosphorus esters, carbamates, cyclic ureas, and pyrethroids.

Target Insects

IMI is a broad spectrum insecticide, capable of affecting a large variety of insects. It even works against insects that are notoriously difficult to control, such as plant-hoppers, leaf-hoppers, rice leaf beetles, and rice root weevils.

In agriculture, IMI is used to control numerous vegetable and fruit pests. Since it doesn’t penetrate insect cuticle easily, it’s most effective against plant-feeders (hemipterian insects), such as aphids, which quickly die after ingesting the chemical.

In veterinary practice, imidacloprid is used to combat fleas on pets. However, unlike fipronil, imidacloprid isn’t effective against ticks.

Imidacloprid can protect homes and buildings against chewing insects like termites and carpenter ants. It’s also commonly used against turf and soil pests, such as grubs.

On-Animal Flea Treatments

Modern flea control has three goals: Kill fleas on pets, eliminate environmental stages, and provide lasting protection. To a large extent, spot-on treatments of imidacloprid fulfill these objectives. Adults are rapidly killed, IMI residue accumulates where pets sleep to kill pre-adult stages, and there’s lasting activity.

Imidacloprid is approved for both dogs and cats. It’s applied to skin and protects against fleas for four weeks. Carefully timed monthly treatments prevent re-infestation by ensuring most, if not all, newly acquired fleas die before they can reproduce.

In addition to dogs and cats, imidacloprid can be used to treat ferrets and rabbits. In fact, it’s the only flea product authorized for use on rabbits. Studies show that it’s safe and effective at the recommended doses. For ferrets, the lowest effective dose (10 mg/kg) is used. Rabbits are dosed using the same schedule as cats.

Speed of Kill

Imidacloprid kills 100% of fleas on pets shortly after treatment. Adults and larvae often die within 20 minutes of exposure. The fleas stop feeding within 3-5 minutes and their movements slow down until they become motionless. Then rhythmic leg trembling and abdomen pumping begins. 10-25 minutes after the trembling, all movement ceases as the fleas die. 100% of fleas die after an hour of exposure. The fast kill prevents feeding and laying egg, and decreases the risk of disease transmission.

Fig 1 Percentage of fleas killed (y-axis) on dogs treated with imidacloprid recorded at four times after treatment (x-axis).

Some studies show IMI taking slightly longer to kill fleas on animals. In one, efficacy was measured 3 and 8 hours after treatment. On cats, the efficacy was 26.9% and 82.8%, respectively. On dogs, efficacy was 22.2% and 95.7%, respectively. Another study measured efficacy at 6, 12, 24 and 36 hours after initial treatment. The percentage of fleas killed was 86.6%, 96.7%, 97.6%, and 98.9%, respectively (see Fig 1). Two additional studies showed that fleas on dogs were completely eradicated 12 hours after treatment.

Repellent Effect

While IMI is lethal to fleas, it doesn’t have a repellent or anti-feeding effect. The fleas will continue to bite prior to succumbing to the chemical.

Residual Activity

Spot-on treatments of imidacloprid protect pets for at least 4 weeks. A high level of efficacy (over 90%) lasted for 41 days in one study. Another study showed 100% efficacy on day two, and remained over 90% for three weeks. In one study, efficacy on days 1 and 2 was 100%. Cats were then re-infested at day 7, and no fleas survived 24 hours later. A single dose resulted in over 95% efficacy for four weeks (see Fig 2).

Fig 2 Percent efficacy (y-axis) of imidacloprid on cats measured 2 days after initial treatment or 2 days after re-infestation, across 6 weeks (x-axis). 60 fleas were placed on each cat every week.

In a 56 day study, beagles were treated with imidacloprid + pyriproxyfen on days 0 and 28. Each dog was re-infested with 5 fleas weekly. On days 0-28, efficacy was 95-98%. Following the second treatment, flea counts fell to zero for the remainder of the study.

In a three month study, infested dogs and cats in 20 Florida homes were given monthly spot-on treatments of imidacloprid. During the first month, over 95% of on-animal flea populations were reduced. After three monthly applications, flea burdens on pets were reduced by 99.5%. The residual activity is remarkable considering the original flea burden and reinfestation pressure in the study.

Fig 3 Percent efficacy (y-axis) of three flea treatments on dogs across 150 days (x-axis), with treatment re-administered every 30 days.

In a five month study, dogs were treated with topical imidacloprid every 30 days. 14 days after initial treatment, flea counts were reduced by 97.5-99.1%. After the second monthly dose, flea burdens were reduced 99.7-100% to the end of the study (see Fig 3).

One study administered imidacloprid to cats monthly for six months, while also reinfesting the cats with ten fleas monthly. Control efficacy was 99.9% for the entire six month duration. When cats were reinfested, flea mortality commenced within a few hours. A similar study showed that 98% of newly acquired fleas die within 6 hours.

Environmental Transference

When pets are treated with IMI, trace amounts of the insecticide will transfer to the environment, especially in areas where animals rest. This residue can significantly reduce populations of immature flea stages living in the environment. The active environment kills the larvae before they mature, accelerating the progress of control. Outdoor cats sometimes share resting sites with other animals. Under these circumstances, environmental transfer can protect them against fleas developing from untreated animals.

Imidacloprid kills the fleas in the environment as larvae. They never reach the pupal stage. The larvae die almost immediately upon contact. Even when hair from a treated dog is introduced into their environment, larvae die within six hours. Skin debris from treated dogs also has a profound larvicidal effect.

Over time, flea numbers in home environments get reduced by 99% when pets are treated with imidacloprid. During the first 2-3 weeks, the decline of emerging populations is minimal. However, by day 28 there’s a reduction of 94.7%.

In one study, imidacloprid-treated cats were caged for 6-hour periods over 2 to 4 weeks. Fleece blankets were taken from their cages, and then flea eggs were incubated on them. On day 26, a near 100% reduction in adult emergence was observed. Even after the blankets were stored for 18 weeks, there was a 95% reduction in flea emergence. The residual activity was removed by normal laundry procedures.

In a similar study, treated cats were caged 6 hours a day, for 5 consecutive days a week, for 4 weeks. A new blanket was placed in the cages every week. Flea eggs were then incubated on the blankets. Adult flea emergence was reduced by 100% in the 1st week, and by 84%, 60% and 74% in the subsequent three weeks.

1 hour exposures
6 hour exposures

Fig 4: Percent efficacy in reducing emerging flea populations (y-axis) from carpets exposed to imidacloprid-treated cats across 6 weeks (x-axis). Cats were exposed to carpets for 1 or 6 hours, once every 2 weeks.

In one experiment, treated cats were exposed to carpets for either 1 or 6 hours, every two weeks, for six weeks. During the first two weeks, for both exposure periods, over 80% of fleas were prevented from developing in the carpeting. Efficacy steadily decreased with time (see Fig 4).

In natural conditions outside of laboratories, the environmental effect of IMI would likely be stronger. Treated animals would be exposed to carpets/bedding for much longer periods of time. Pet bedding is usually changed and washed infrequently. There are also habitual resting sites in homes don’t get cleaned often.

Fig 5: Percent efficacy in reducing emerging flea populations (y-axis) from blankets exposed to imidacloprid-treated cats across 4 weeks (x-axis). Cats were exposed to blankets for 6 hours day, for 5 consecutive days each week. Blankets were replaced every week.

In homes, most fleas fully develop in 21 to 28 days. Any emergence after 28 days indicates less than 100% control. It’s not uncommon for fleas to appear after the infestation seems to be completely eradicated. In one study, treated cats showed no signs of fleas for months. Untreated “tracer cats” were introduced to the cages 180 days after the original cats were treated. The tracers acquired 1 to 3 fleas of unknown origin. It’s likely they came from delayed emergence pupae. Regardless, this experiment emphasizes the difficulty in totally eradicating infestations.

Spot-on animal treatments by themselves can control a flea infestation. However, adult flea will continue emerging form carpets for at least 21 days. To speed up the eradication, it may be prudent to also apply insect growth regulators (IGR) to the environment, especially in extreme infestations or when pets have flea allergies. Additionally, using a combination of adulticide and IGR (such as Advantage) on pets is more effective than an adulticide alone.


Synergists, such as piperonyl butoxide, are sometimes used to boost the activity of insecticides. However, with imidacloprid, potency is only increased at temperatures of 78.8°F (26°C). At 95°F (35°C), the average fur temperature of cats and dogs, there’s no increased effect. Thus, using synergists with on-pet treatments of IMI is ineffective. However, they may be useful in premise sprays.


Cases of resistance to imidacloprid have been manageable and geographically localized. Still, some crops insects display strong resistance, demonstrating the potential of pests to adapt to neonicotinoids. For instance, insects which feed on tobacco have tolerance to nicotine. Some pests also have pre-existing resistance from being exposed to other insecticides. However, the greatest concern is resistance occurring from natural selection to IMI and other neonicotinoids. Resistance will inevitably occur as these products are used. However, currently, metabolic or target site resistance hasn’t developed.

Imidacloprid’s mode of action is unique. Neonicotinoids comprise a distinct, single mode of action group as defined by the Insecticide Resistance Action Committee for resistance-management purposes. As a result, there’s little to no cross-resistance to older insecticides.

Resistance in Fleas

Since its introduction to the United States in 1996, there have been no documented cases of fleas developing resistance to imidacloprid. Multiple studies have confirmed that cat fleas remain susceptible to imidacloprid. 1,347 flea isolates from the field were tested against imidacloprid with no reports of reduced efficacy of spot-on applications.

Though IMI resistance hasn’t been detected, it may exist in untested flea strains. There are significant differences in flea strain susceptibility to insecticides. For example, the KS1 strain of C. felis, which has been maintained in a laboratory since 1990, has documented resistance or natural reduced susceptibility to many insecticides, including imidacloprid.

It’s difficult, if not impossible, to determine if a particular product failed because of resistance. Presumed resistance to the newer flea control agents is usually unfounded or supported by limited research. In the majority of cases, product failures are likely related to pet owner compliance issues. Still, at least some control failures are probably due to resistance. Selection for resistance is inevitable when relying on a single insecticide to control fleas. To delay the onset of resistance, it’s best to use a combination of control methods with completely different modes of action.

Mode of Action

Translocation on Animals

When applied to an animal’s skin, imidacloprid incorporates into the lipid layer (oils produced by sebaceous glands) and into hair follicles. It doesn’t penetrate the skin or enter the bloodstream. Since it resides in the lipid layer, body oil eventually spreads the compound all over the animal’s body. Translocation across a pet’s body occurs within 12 hours. Treatments are sometimes applied on multiple locations of larger dogs in order to cover the greater surface area more rapidly.

Imidacloprid becomes water-resistant after it’s included into the body’s oil and hairs. Treatments aren’t easily removed by rain, swimming or bathing, because the lipid layer is always present. Efficacy remains high for four weeks, despite any contact with water.

Routes of Exposure

Imidacloprid is a contact insecticide, acting exclusively through direct exposure. With fleas, it’s taken up through thin, smooth, non-sclerotized membranes between body segments. It’s can’t pass through the sclerotized cuticle, which comprises most of the insect body. The route from the intersegmental membranes to the ganglia and muscles is short, thus the onset of the killing occurs very quickly.

Unlike other compounds, imidacloprid doesn’t absorb through skin. It doesn’t enter an animals blood or act systemically. If imidacloprid is removed from the skin of a treated dog with alcohol, fleas won’t be affected by consuming the animal’s blood. Likewise, larvae aren’t affected by consuming blood feces from treated adult fleas.

Fleas are typically affected after contacting treated host skin, or, to a lesser extent, hair and debris from a treated pet. Imidacloprid isn’t ionized once it enters an insect’s body. Thus, it’s easily transferred to the central nervous system and strongly interacts with the target site. In contrast, nicotine ionizes upon entering the body resulting in limited access to the target site and weak insecticidal activity.

Acetylcholine Receptors

In the central nervous system of insects, nerve cells communicate to target cells through chemical substances. Acetylcholine (ACh) is the predominant neurotransmitter of insects. It’s produced endogenously and is released from depolarized nerve endings.

There are two classes of acetylcholine receptors: nicotinic and muscarinic. Imidacloprid acts on nAChR subtypes, and is ineffective on muscarinic receptors. The richest source of nAChRs in the animal kingdom occurs in insect nervous tissue. And in insects, the receptors are located exclusively within the central nervous system. Thus, many insecticidal molecules are active at these receptors.

Imidacloprid competitively binds to the receptors within the ganglia and skeletal muscles. As a result, it blocks endogenous acetylcholine from binding and transmitting information.

Normally, acetylcholine briefly connects to the receptors, which causes a muscle contraction. It’s then released and gets rapidly broken down by an esterase (acetylcholinesterase). Imidacloprid’s receptor binding is stronger and the compound can’t be broken down by acetylcholinesterase. Thus, it constantly activates the muscle cells, which destroys the mitochondria, damages the nerve cells, and disintegrates the muscles. Hyperexcitation symptoms occur, seen as tremors, seizures, convulsions and death of the insect.

Lethal Affect to Fleas

Like other insects, imidacloprid acts on the central nervous system of fleas, causing strong excitation symptoms and eventually leading to death. After exposure, a flea’s legs begin trembling. Abdomen pumping occurs shortly after. These muscle contractions ultimately lead to complete separation of the muscle fibers and dysfunction of the ganglia’s nerve cells. The flea remains motionless as the nerves and muscles are constantly and irreversibly destroyed due to hyperactivity. Damage is limited to the ganglia and radiating muscles. Other cell types are unaffected (e.g. intestinal cells, respiratory system, and sexual organs).


Imidacloprid selectively targets insects. As a result, there’s a relatively low toxicity to avian, fish and mammalian species. Generally, neonicotinoids are safe and ecologically acceptable because they rapidly degrade in water and sunlight. Technical grade, 94% imidacloprid, carries the word “warning”, which is associated with moderate toxicity. All veterinary, agricultural, and end-use products are labeled “caution”, which means they’re of low toxicity.

Toxicity Data

I = Highly Toxic
II = Moderately Toxic
III = Slightly Toxic
IV = Practically Non-Toxic
Acute Dermal Exposure IV NPIC Fact Sheet
Acute Oral Exposure II FAO/WHO Fact Sheet
Acute Inhalation Exposure IV USDA Forest Service Report
Primary Skin Irritation IV MSDS
Primary Eye Irritation IV
Dermal Sensitizer no
Carcinogen no
Fish III
Aquatic Invertebrates I
Birds I

Insects vs. Mammals

The toxicity of imidacloprid to mammals is 1000-fold lower than to insects. This is due to differences between insect and vertebrate nAChRs. In insects, nAChRs are present only in the central nervous system. In vertebrates, nAChRs are present in the central and peripheral nervous systems, and very low concentrations are found in the brain. In addition, IMI poorly penetrates the blood-brain barrier in mammals. IMI can activate vertebrate nicotinic receptors, but it’s a weak agonist with 1–4% of the response to acetylcholine.

Acute Toxicity

Imidacloprid is practically non-toxic when inhaled, or exposed to skin or eyes. However, it’s moderately toxic when ingested. IMI isn’t an irritant or dermal sensitizer.

Fate in the Body

Imidacloprid doesn’t penetrate skin, which further enhances its safety. It has a safety factor of over 10,000 for skin application. When consumed orally, the compound is widely distributed in the body within an hour. It’s then metabolized by the liver into 6-chloronicotinic acids, which may join with glycine to get eliminated or be reduced to guanidine. About 70–80% of the dose gets excreted in urine and 20–30% is expelled through feces. It rapidly metabolizes and gets completely excreted within 48 hours. There’s no evidence of cumulative toxicity.

Carcinogenicity & Mutagenicity

Imidacloprid isn’t carcinogenic. The EPA (Environmental Protection Agency) has classified IMI as a “group E” compound, meaning there’s no evidence of carcinogenicity to humans. The EPA also found no evidence of mutagenicity. However, newer tests indicate it may be weakly mutagenic.

Developmental & Reproductive Toxicity

Imidacloprid isn’t a primary embryotoxicant and isn’t teratogenic. There are no effects on reproduction or development at any dietary level.


Neuropathology isn’t evident even at the highest dose level.

Chronic Exposure

Imidacloprid residues remain on an animals’s coat for up to 4 weeks. They can be transferred to human skin after contacting a treated dog or cat, especially in the first 12 to 24 hours after treatment. This may pose a health risk for people who contact numerous treated dogs per day over a long period of time (e.g. veterinarians or dog caretakers). However, it’s difficult to accurately determine the risk since skin penetration is so low.

Chronic dietary exposure is believed to be similar to toxicity from nicotine. Symptoms include fatigue, twitching, cramps and muscle weakness. In rats, there’s a decrease in weight gain and an increase in thyroid lesions. In dogs, there’s an increase in cholesterol levels.

Adverse Reactions

Typically, imidacloprid doesn’t cause any adverse symptoms when pets are treated. However, there’s one case of a cat with thymoma developing a skin reaction after treatment. Clinical effects from Advantage treatments are expected to be mild, and caused by the carrier or inert ingredients, not imidacloprid. Oral exposure, especially in self-grooming cats, may result in short-lasting drooling or retching.

Poisoning Cases

Occasionally, accidental or intentional cases of imidacloprid intoxication occur. Though IMI’s toxicity is low in mammals, high concentrations in the body can be lethal. Moderate to high doses of imidacloprid cause central nervous system activation similar to nicotine, including tremors, impaired papillary function, and hypothermia. The majority of human poisoning cases are suicides, where a person purposefully and rapidly consumes a large amount of insecticide.

Toxicity begins approximately 1 hour after ingestion. Signs of imidacloprid poisoning include severe vomiting, hypertension, drowsiness, disorientation, dizziness, cough, fever, abnormal breathing, rapid heart rate, dilated pupils with sluggish reaction to light, leukocytosis, hypernatremia, hypokalemia, loss of consciousness, coma, and damage to the mouth and esophagus. In severe cases, toxicity can lead to a slow heart rate, slow breathing, cardiopulmonary arrest and death. There’s no specific antidote for imidacloprid. Treatment is symptomatic and supportive.

Environmental Fate

Neonicotinoid insecticides are non-ionized and moderately soluble in water. They’re biodegradable and don’t accumulate in mammals or through food chains. IMI is persistent in soil, where it’s translocated to crops. On plants, it dissipates with a half-life of 3 to 5 days. Imidacloprid is safe in regards to crop protection and environmental contamination aspects.


Imidacloprid has a low toxicity towards fish.

Aquatic Organisms

Imidacloprid is highly toxic to many aquatic organisms. However, it’s more toxic to insect larvae (mosquito) than to crustaceans. Generally, imidacloprid can be used with reasonable environmental safety toward non-target aquatic crustaceans.


Imidacloprid’s toxicity to birds varies among species. It’s highly toxic to house sparrows, quail, canaries and pigeons. Birds species it isn’t highly toxic to still show adverse symptoms, such as diarrhea, lack of responsiveness, in-coordination and inability to fly. IMI also causes eggshell thinning and reduced fecundity.


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