1) Fipronil is ……. Insecticidal Mode of Action The mechanism by A. Trade name which insecticides kill B. Common name 0% 0% 0%
me me C. Chemical name a a n name n e l ad ica m Tr e h Common C
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Insecticides 1) Mode of Action is… Active ingredients + Inert ingredients
A. The insecticide class Active ingredient chemical name: 5-amino-1-(2,6 dichloro-4-(trifluoromethyl) B. Where the phenyl)-4-((1,R,S)-(trifluoromethyl) sulfinyl)- insecticide acts 1-H-pyrazole-3-carbonitrile C. The way the 0% 0% 0%
pesticide causes ss la c acts us.. ca Common name: fipronil de ci insecticide esti physiological insecticide p e the h The t ay w Where disruption at the The Trade names: Termidor SC, TopChoice target site granular, MaxForce FC Professional Insect Response Counter Control Ant Killer Bait Gel, etc.
1 Active ingredient chemicals are grouped into Insecticides that Target the Insect insecticide classes with similar Nervous System - neurotoxins characteristics Multi-lobed brain, in Human: spinal cord the head and nerve located dorsally - central The chemical structure of the active cord nervous system ingredient usually defines its mode of action Chemical and physical Insects: nerves ventrally nature of both systems located - decentralized Target site - the physical location within an is the same organism where the insecticide acts
Mode of action - the way in which it causes physiological disruption at the target site
Nervous System – interconnected cells Chemical MOA Target Site Route of Group Entry carrying an electrical impulse driven by Insecticides that Target the Insect Nervous System charged sodium, potassium, and chloride Pyrethrins / Sodium Channel Axon of Nerve Contact ions Pyrethroids Modulation Oxadiazines Sodium Channel Axon of Nerve Oral Blockage Semicarbazones Sodium Channel Axon of Nerve Contact & Oral Blockage OPs / Carbamates Acetyl cholinesterase Nerve Synapse Contact Inhibition Neonicotinoids Acetylcholine Receptor Nerve Post‐synapse Contact & Oral Stimulation Spinosyns Acetylcholine Receptor Nerve Post‐synapse Oral Important neurotransmitters include Stimulation acetylcholine (Ach), gamma amino butyric Phenylpyrazoles GABA Receptor Nerve Post‐synapse Contact & Oral Blockage acid (GABA), and glutamate Avermectins Glutamate Receptor Nerve Post‐synapse Oral Stimulation
2 Pyrethrins and Pyrethroids (natural vs. synthetic) Pyrethrins, bifenthrin, permethrin, cyfluthrin, beta- cyfluthrin, deltamethrin, cypermethrin, resmethrin, d- phenothrin, lambda-cyhalothrin Inhibit the on/off switch of nerve cells, called sodium channels, by delaying close, causing uncontrolled, uninterrupted nerve firing
sodium channels
Oxadiazines Semicarbazones Deltamethrin Indoxacarb Metaflumizone
Indoxacarb is broken down into a metabolite (activation), both indoxacarb and metaflumizone target sodium channels completely blocking ion flow into nerve cells, insect paralysis
Permethrin
sodium channels
3 Organophosphates (OPs) / Carbamates Chlorpyrifos, dichlorvos (DDVP), malathion, carbaryl, propoxur Inhibit the acetylcholinesterase (AchE) which normally removes the neurotransmitter acetylcholine from receptor sites, nerve overstimulation Indoxacarb
AchE
Metaflumizone Human system is very similar
Neonicotinoids Imidacloprid, dinotefuran, thiamethoxam, clothianidin, acetamiprid Synthetic “nicotine-like” chemical binds tightly to the acetylcholine receptor site on the post- synapse nerve cell, nerve overstimulation Neonicotinoids
Propoxur Chlorpyrifos Dichlorvos
4 Pyrethroid plus neonicotinoid – dual MOA Temprid: ß-cyfluthrin + imidacloprid Transport: bifenthrin + acetamiprid Tandem: thiamethoxam and Lambda- Cyhalothrin
Imidacloprid Dinotefuran
Imidacloprid Tau-luvalinate Tebuconazole Thiamethoxam
LD50s and Neonicotinoids Spinosyns Spinosad - Naturalytes
Imidacloprid 450 Chemicals produced by the soil bacterium Saccharopolyspora spinosa and bind to acetylcholine receptor site on the post-synapse Acetamiprid 217 nerve cell, nerve overstimulation Spinosyns Clothianidin >5000
Thiamethoxam 1563
Dinotefuran >2000
5 Phenylpyrazoles
Fipronil Binds to and blocks the GABA receptor on the post-synapse nerve cell, rapid, uncontrolled nerve Spinosad firing
Phenylpyrazoles
Fipronil LD50s
Spinosad (synaptic stimulation nicotinic acetycholine sites) Spinosads 3783-5000
Phenylpyrazoles (GABA receptor disruption) Fipronil 97
Spinosads are Category IV insecticides (practically non- toxic)
Fipronil, while quite toxic, is used at very, very low rates
6 Avermectins Abamectin, emamectin benzoate, ivermectin Chemicals originally isolated from the soil bacterium Streptomyces stimulate the chloride channels that are regulated by the neurotransmitter glutamate causing paralysis Avermectins
Abamectin
Chemical Group MOA Target Site Route of Diamides Entry Insecticides that Do Not Target the Insect Nervous System Chlorantraniliprole Diamides Muscle Stimulation Muscular Calcium Oral Bind to and stimulate muscular calcium Channel channels, causing uncontrolled calcium release Juvenile Hormone Mimic Juvenile JH Degradative Enzymes Contact & Oral Analogs Hormone Action / Receptor and resultant muscle contractions Chitin Synthesis Block Chitin Exoskeleton Oral Inhibitors Formation Amidinohydrazones Inhibit Energy Mitochondria within Oral Production Cells Pyrroles Inhibit Energy Mitochondria within Contact Production Cells Fumigant (sulfuryl Inhibit Energy Citric Acid / Glycolysis Inhalation fluoride) Production Cycles in Cells Borates Non‐Specific Cells Oral Metabolic Disruption Dehydrating Dusts Adsorption of Exoskeleton Contact Cuticular Wax Layer
7 Insect Growth Regulators (S)-Hydroprene Juvenile Hormone Analogs Hydroprene, methoprene, pyriproxyfen, fenoxycarb Juvenile hormones in immature insects keeps them from becoming adults – chemicals may bind to juvenile hormone-degrading enzymes, the juvenile hormone receptor itself, or a combination of both
Imidacloprid, Permethrin, Pyriproxyfen
Insect Growth Regulators Amidinohydrazone Chitin Synthesis Inhibitors Hydramethylnon Diflubenzuron, hexaflumuron, noviflumuron, lufenuron Cellular poison disrupting energy production by mitochondria During molting, chitin is synthesized and incorporated into the insect’s exoskeleton - chitin synthesis inhibitors block chitin synthase
8 Pyrrole Fumigant Chlorfenapyr Sulfuryl fluoride Must be converted by enzymes within the insect Inhibits energy production in cells – non-specific to an active form (activation) metabolic inhibitor
The metabolite form is insecticidal and toxic to Warning agent chloropicrin (tear gas) mammals, but, mammals lack the activation enzymes
It disrupts energy production by mitochondria
Borates Dehydrating Dusts Borax, boric acid, disodium octaborate Silica gels, diatomaceous earth tetrahydrate Silica gels are synthetically produced, Boron is an essential micronutrient for plants and diatomaceous earth is the fossilized remains of animals - at higher concentrations can be toxic diatoms
Evidence suggests that high levels of boron acts Adsorb the thin wax layer on the insect as a general cellular toxin or non-specific exoskeleton that prevents metabolic disruptor insects from losing water and desiccating
9 DDT copper acetoarsenite Amorphous silica gel Cyanide
1927 newspaper ad
10 1970’s
BENIGN PAROXYSMAL POSITIONAL VERTIGO
11 1) Fipronil is ……. 1) Mode of Action is…
A. The insecticide class A. Trade name B. Where the insecticide acts B. Common name C. The way the C. Chemical name pesticide causes 0% 0% 0% 0% 0% 0% ss la c acts us.. physiological ca e e de m m ci name na l na on a insecticide esti ic insecticide p Trade m m e The the th Com Che disruption at the y a w Where target site The
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Resources
•Suiter, D. R. and Scharf, M. E. 2015 Insecticide Basics for the Pest Management Professional. UGA Bulletin 1352.
•Insecticide Resistance Action Committee http://www.irac‐online.org/modes‐of‐action/
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