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Re-publish Scharf Insecticide MOA session with updated deliverables

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Co-Authored-By: Claude Opus 4.6 (1M context) <noreply@anthropic.com>
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# Reference Compendium — Insecticide Basics # Insecticide Mode of Action — Quick Reference Compendium
## Extracted from Dr. Michael Scharf's GTBOP Presentation (October 18, 2017)
> **Placeholder** — Paste your Stage 6 reference compendium here. **Prepared by:** Rich Braman, UGA Cooperative Extension / Center for Urban Agriculture
**For:** Dr. Dan Suiter & Dr. Michael Scharf — Bulletin revision reference
**Source:** GTBOP_ProseTranscript_2017-10-18_InsecticideMOA.md
--- ---
*Source: Dr. Michael Scharf, GTBOP Structural — October 18, 2017* ## Purpose
*Processed for UGA Center for Urban Agriculture / GTBOP Archives*
This document consolidates every insecticide class, target site, product name, and relationship mentioned in Dr. Scharf's presentation into reference tables. These can serve as:
- Quick-check references during the writing process
- Source material for bulletin tables and figures
- Verification that all content is accounted for in the revised bulletin
All content below is derived exclusively from the presentation transcript. Items marked with ⚠️ may benefit from updating with current information.
---
## TABLE 1: Master Classification — All Nine Insecticide Classes
### Neurotoxic Insecticides (5 classes)
| # | Class | Target Site | Location on Neuron | Mode of Action | Effect on Insect | Representative Products |
|---|-------|-------------|-------------------|----------------|-----------------|------------------------|
| 1 | Pyrethroids / Pyrethrins / DDT | Sodium channels | Axon | Stimulation (modulation) | Excitation → knockdown, incoordination | Pyrethroids (various), pyrethrins |
| 2a | Oxadiazines | Sodium channels | Axon | Blockage | Inhibition → paralysis ("on switch stuck off") | Indoxacarb |
| 2b | Semicarbazones | Sodium channels | Axon | Blockage | Inhibition → paralysis | Metaflumizone |
| 3a | Phenylpyrazoles | Chloride channels (GABA receptor) | Post-synaptic | Blockage | Excitation (blocks mellowing effect) | Fipronil |
| 3b | Isoxazolines | Chloride channels | Post-synaptic | Blockage | Excitation | Fluralaner, sarolaner |
| 3c | Avermectins | Chloride channels (glutamate receptor) | Post-synaptic | Stimulation | Inhibition → paralysis (opposite of fipronil) | Abamectin |
| 4a | Neonicotinoids / Nicotinoids | Acetylcholine receptor | Post-synaptic (synapse) | Stimulation | Excitation | Imidacloprid (nicotinoid), clothianidin (neonicotinoid) |
| 4b | Sulfoximines | Acetylcholine receptor | Post-synaptic (synapse) | Stimulation | Excitation | Sulfoxaflor |
| 4c | Spinosyns | Acetylcholine receptor | Post-synaptic (synapse) | Stimulation | Excitation | Spinosad |
| 5 | Organophosphates / Carbamates | Acetylcholinesterase enzyme | Synapse | Inhibition | Excitation (ACh accumulates) | Various ⚠️ |
### Non-Neurotoxic Insecticides (4 classes)
| # | Class | Target Site | Mode of Action | Effect on Insect | Representative Products |
|---|-------|-------------|----------------|-----------------|------------------------|
| 6 | Diamides | Neuromuscular calcium channels | Stimulation | Contraction → energy depletion → paralysis → death | Chlorantraniliprole, cyantraniliprole |
| 7a | Juvenile hormone analogs (IGR) | Hormonal regulation of molting | Mimicry | Cuticle deformation, extra juvenile stages, population crash | Pyriproxyfen |
| 7b | Chitin synthesis inhibitors (IGR) | Chitin synthesis enzyme | Inhibition | Death during molting; "jackknife effect" in termites | Various ⚠️ |
| 8 | Mitochondrial respiration inhibitors | Mitochondria (respiratory chain) | Inhibition | Energy production failure → death | Hydramethylnon, chlorfenapyr, sulfuryl fluoride, methyl bromide ⚠️, DSOBTH, boric acid |
| 9 | Cuticle dehydrating dusts | Epicuticular wax layer | Physical abrasion | Water loss → dehydration → death | Silica gel, diatomaceous earth |
---
## TABLE 2: Four Basic Modes of Action
| Mode of Action | What It Does | Example Target | Example Insecticide Class |
|----------------|-------------|----------------|--------------------------|
| **Stimulation** | Causes target to become more active | Sodium channels → fire more | Pyrethroids |
| **Blockage** | Shuts target off | Sodium channels → can't fire | Indoxacarb |
| **Modulation** | Subtly changes target shape/function | Sodium channel conformation | Pyrethroids (also modulators) |
| **Inhibition** | Prevents an enzyme from functioning | Acetylcholinesterase → can't degrade ACh | Organophosphates, carbamates |
*Note: Scharf emphasized that ALL insecticide effects can be categorized into just these four types.*
---
## TABLE 3: Target Sites on the Neuron — Spatial Relationships
| Location | Structure | Natural Function | Insecticides Targeting It |
|----------|-----------|-----------------|--------------------------|
| **Axon** (long body of nerve) | Sodium channels | "On switch" — opening initiates nerve impulse | Pyrethroids, pyrethrins, DDT (stimulate); Indoxacarb, metaflumizone (block) |
| **Post-synaptic membrane** | GABA-gated chloride channels | "Mellowing" — negative chloride dampens activity | Fipronil, isoxazolines (block → excitation) |
| **Post-synaptic membrane** | Glutamate-gated chloride channels | "Mellowing" — inhibitory | Avermectins/abamectin (stimulate → paralysis) |
| **Post-synaptic membrane** | Acetylcholine receptors (nAChR) | Carry signal across synapse (sodium channel) | Neonicotinoids, sulfoximines, spinosyns (stimulate) |
| **Synapse** | Acetylcholinesterase enzyme | Breaks down ACh after signal transmission | Organophosphates, carbamates (inhibit) |
| **Neuromuscular junction** | Calcium channels | Trigger muscle contraction | Diamides (stimulate → sustained contraction) |
---
## TABLE 4: Products and Active Ingredients Mentioned
| Active Ingredient / Product | Chemical Class | Target Site | Primary Use Mentioned | Notes |
|----------------------------|---------------|-------------|----------------------|-------|
| Pyrethrins | Natural pyrethroid | Sodium channels | General knockdown | Rapid knockdown; repellent |
| Pyrethroids (various) | Synthetic pyrethroids | Sodium channels | General pest control | "Like pepper spray" — highly repellent; widespread bedbug resistance |
| DDT | Organochlorine | Sodium channels | Historical reference | Same target site as pyrethroids |
| Indoxacarb | Oxadiazine | Sodium channels (blocker) | Urban pest control | "Really big urban insecticide" |
| Metaflumizone | Semicarbazone | Sodium channels (blocker) | Ectoparasites; possible urban | Newer product at time of presentation |
| Fipronil | Phenylpyrazole | Chloride channels (blocker) | Urban pest control | Off-patent; consumer products available; "one of our biggest" |
| Fluralaner | Isoxazoline | Chloride channels | Veterinary/pet (fleas) | Cross-resistance potential with fipronil |
| Sarolaner | Isoxazoline | Chloride channels | Veterinary/pet (fleas) | Cross-resistance potential with fipronil |
| Abamectin | Avermectin | Chloride channels (stimulator) | Gel baits | Opposite effect from fipronil despite similar target |
| Imidacloprid | Nicotinoid | Acetylcholine receptor | Various | Example of "nicotinoid" (looks more like nicotine) |
| Clothianidin | Neonicotinoid | Acetylcholine receptor | Various | Example of "neonicotinoid" (structurally evolved from nicotine) |
| Sulfoxaflor | Sulfoximine | Acetylcholine receptor | Newer product | New class at same target site as neonics |
| Spinosad | Spinosyn | Acetylcholine receptor | Landscape market | Same target site as neonics |
| Nicotine | Natural alkaloid | Acetylcholine receptor | Historical (tobacco) | The original — toxic to insects and mammals |
| Organophosphates (various) | Organophosphate | Acetylcholinesterase | Declining urban use | Not insect-specific; heavy restrictions |
| Carbamates (various) | Carbamate | Acetylcholinesterase | Declining urban use | Not insect-specific; heavy restrictions |
| Chlorantraniliprole | Diamide | Calcium channels (muscle) | Various | No signal word required by EPA; manufacturers added "Caution" |
| Cyantraniliprole | Diamide | Calcium channels (muscle) | Various | Newer diamide |
| Pyriproxyfen | Juvenile hormone analog | Hormonal (IGR) | Cockroach control | Wing twist indicator in cockroaches |
| Hydramethylnon | Amidinohydrazone | Mitochondria | Cockroach bait | Energy production inhibitor |
| Chlorfenapyr | Pyrrole | Mitochondria | Various (has food label) | Relatively safe; resistance potential noted |
| Sulfuryl fluoride | Inorganic fluoride | Mitochondria | Fumigation | |
| Methyl bromide | Halogenated hydrocarbon | Mitochondria | Fumigation | ⚠️ Largely phased out |
| DSOBTH | Borate | Mitochondria/respiration | Wood treatment | Disodium octaborate tetrahydrate |
| Boric acid | Borate | Mitochondria + gut lining | Various | Dual mode: chemical (respiration) + physical (abrasive/desiccant) |
| Silica gel | Inorganic dust | Epicuticular wax | Dust application | Physical mode — abrades waxy layer |
| Diatomaceous earth | Inorganic dust (biogenic) | Epicuticular wax | Dust application | Silicon from ground diatom exoskeletons |
---
## TABLE 5: Combination Products
| Component 1 | Component 2 | Mechanism | Notes |
|------------|------------|-----------|-------|
| Neonicotinoid (acetylcholine receptor) | Pyrethroid (sodium channels) | Potentiation — two target sites simultaneously; "1+1=3" synergy | "All start with tea"; dual resistance observed in roach populations; still require rotation |
---
## TABLE 6: Insect-Specificity Spectrum
| Insecticide Class | Mammalian Safety | Notes |
|-------------------|-----------------|-------|
| **Diamides** | Extremely high | No signal word required by EPA; 10,000+ x selectivity |
| **Avermectins** | High | Insect-specific target |
| **Isoxazolines** | High | Primarily vet/pet products |
| **IGRs (JH analogs, CSIs)** | High | Target insect-specific developmental processes |
| **Neonicotinoids** | Moderate-High | Insect-specific receptor but systemic/pollinator concerns |
| **Fipronil** | Moderate-High | GABA receptor differences provide selectivity |
| **Pyrethroids** | Moderate | Generally safe for mammals but repellent to insects |
| **Organophosphates / Carbamates** | **Low** | **Not insect-specific; work against mammals equally** |
*Spectrum based on Scharf's characterizations in the presentation. Not a quantitative ranking.*
---
## TABLE 7: Practical Field Indicators Mentioned
| What You See | What It Means | Relevant Product/Class |
|-------------|--------------|----------------------|
| Immediate knockdown/incoordination | Sodium channel excitation | Pyrethroids, pyrethrins |
| Paralysis (insect immobile but alive) | Sodium channel blockage OR chloride stimulation | Indoxacarb, abamectin |
| Wing twist in cockroach nymphs/adults | Juvenile hormone disruption | Pyriproxyfen (JH analog IGR) |
| "Jackknife" body curl in termites | Malformed cuticle from chitin synthesis disruption | Chitin synthesis inhibitors |
| Lethargy and desiccation | Epicuticular wax loss | Silica gel, diatomaceous earth |
| Sustained muscle contraction → stillness | Calcium channel stimulation → energy depletion | Diamides (chlorantraniliprole, cyantraniliprole) |
---
## TABLE 8: Key Physiological Barriers to Insecticide Penetration
| Barrier | Location | Challenge for Insecticide | Relevant Formulation Strategy |
|---------|----------|--------------------------|------------------------------|
| Cuticle | External body surface | Multi-layered; waterproof; waxy epicuticle | Contact formulations must penetrate all layers |
| Gut lining | Digestive tract interior | The "tube" inside is technically external to the body | Baits must cross gut wall to reach internal targets |
| Tracheal system | Throughout body | Physical tubes, not blood-carried oxygen | Fumigants exploit this unique insect anatomy |
---
## TABLE 9: Key Terminology and Definitions from Presentation
| Term | Definition (as explained by Scharf) |
|------|--------------------------------------|
| **LD50** | Lethal dose that kills 50% of test population; inverse relationship with toxicity (lower LD50 = more toxic) |
| **Mode of action** | The action of an insecticide at its target site (stimulation, blockage, modulation, or inhibition) |
| **Target site** | The specific protein or physiological location within the insect where an insecticide acts |
| **Signal word** | EPA-required label indicator of acute toxicity (Danger, Warning, Caution); diamides so safe none was required |
| **Potentiation** | Synergistic effect from hitting two target sites simultaneously; "one plus one equals three" |
| **Trophallaxis** | Food sharing among social insects (from mouth and anus); insecticide transfer mechanism |
| **Allogrooming** | Mutual grooming among social insects; insecticide transfer mechanism |
| **Secondary kill** | Death of an individual from consuming insecticide-contaminated feces or carcass of a treated individual |
| **Tertiary kill** | Death of a third individual from insecticide passed through two prior digestive tracts |
| **IRAC** | Insecticide Resistance Action Committee; industry body that classifies MOAs and publishes rotation guidance |
| **Wing twist** | Visible cuticle deformation in cockroaches exposed to juvenile hormone analog IGRs; field diagnostic indicator |
| **Jackknife effect** | Body curling in termites with malformed cuticle from chitin synthesis inhibitor exposure |
| **Epicuticle** | Outermost waxy/oily layer of insect cuticle; target of dehydrating dusts |
| **Synapse** | Gap between neurons where electrical signals convert to chemical (neurotransmitter) signals |
| **Acetylcholine** | Primary neurotransmitter that crosses synapses in the insect nervous system |
| **GABA receptor** | Chloride channel type at post-synaptic membrane; target of fipronil |
| **Glutamate receptor** | Chloride channel type; target of avermectins |
---
## Cross-Reference: Same Target Site, Different Effects
One of the presentation's key teaching points was that different insecticide classes can target the same site but have opposite effects:
| Target Site | Insecticide A | Effect A | Insecticide B | Effect B |
|------------|--------------|---------|--------------|---------|
| Sodium channels | Pyrethroids | Stimulation → excitation | Indoxacarb | Blockage → paralysis |
| Chloride channels | Fipronil | Blockage → excitation | Abamectin | Stimulation → paralysis |
*This contrast is valuable for teaching and for resistance management — switching between classes at the same site may still provide different selection pressures.*
---
*All data extracted exclusively from the October 18, 2017 GTBOP presentation by Dr. Michael Scharf as transcribed and corrected through the GTBOP archive pipeline. Items marked ⚠️ may have changed since the presentation date.*
docs/projects/insecticide-bulletin/index.md
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--- # Bulletin Writing Toolkit — Overview & Document Guide
tags: ## Insecticide Basics for the Pest Management Professional — Bulletin Update
- Writing Projects ### Based on Dr. Michael Scharf's GTBOP Presentation (October 18, 2017)
- Insecticides
- Scharf
- Suiter
---
# Insecticide Basics Bulletin — Writing Toolkit **Prepared by:** Rich Braman, UGA Cooperative Extension / Center for Urban Agriculture
**For:** Dr. Dan Suiter (UGA) & Dr. Michael Scharf (Purdue University)
**Source Webinar:** Dr. Michael Scharf — Principles of Insecticide Classification and Mode of Action (October 18, 2017)
**Collaborators:** Dr. Dan Suiter (UGA), Dr. Michael Scharf (Purdue)
**Target Publication:** UGA extension bulletin on insecticide classification and mode of action for pest control professionals
--- ---
## How This Toolkit Works This package contains three documents designed to work together as a writing toolkit for the bulletin revision, all derived exclusively from the corrected and verified prose transcript of Mike's October 2017 GTBOP presentation.
This set of writing resources reorganizes Dr. Scharf's GTBOP presentation into a publication-ready structure. All content derives exclusively from the corrected transcript — no external information has been introduced.
| Document | Purpose |
|----------|---------|
| [Bulletin Outline](outline.md) | Publication structure with content notes, transcript pointers, and writing notes |
| [Reference Compendium](compendium.md) | Consolidated tables of insecticide classes, active ingredients, MOA groups, and terminology |
| [Source Guide](source-guide.md) | Maps publication sections to exact transcript locations and video timestamps |
### Using These Documents
The **Outline** is your drafting roadmap — it tells you what goes where and flags areas needing current updates with ⚠️ markers. The **Compendium** is your quick-reference sheet for verifying classifications and relationships while writing. The **Source Guide** tells you exactly where to look in the video or transcript to verify any specific claim.
⚠️ markers indicate content that may need updating since the 2017 presentation. These are flags for the subject matter experts, not corrections — the writing resources preserve what the speaker actually said.
--- ---
*Source: GTBOP Structural Pest Control Series / Processed for UGA Center for Urban Agriculture* ### 1. Bulletin Draft Outline
Reorganizes Mike's conversational presentation flow into a publication-ready six-part structure. Each section has content notes, key details, transcript pointers, and writing notes flagging where things may need updating (neonicotinoid regulation, methyl bromide phase-out, etc.). The editorial notes at the end call out which Q&A exchanges are strong candidates for integration into the body text rather than staying as standalone Q&A.
### 2. Quick Reference Compendium
Nine consolidated tables extracting every classification, product, target site, field indicator, and terminology definition Mike mentioned. The master classification table (Table 1) is essentially a draft of the summary table that could appear in the finished bulletin. Table 6 on the insect-specificity spectrum and the "same target site, opposite effects" cross-reference are the kind of things that make a reference bulletin actually useful on the truck.
### 3. Source Guide
Maps every proposed bulletin section to the exact transcript heading and approximate video timestamp. Also flags which content came exclusively from the Q&A with Dan — eleven topics that would be missed if someone only worked from the prepared slides. The flow comparison table at the end shows how the webinar's live sequence was restructured for publication logic.
---
Everything traces back to the corrected prose transcript as the single source of truth, so nothing in these documents introduces outside information. Items marked with ⚠️ flag spots where 2017 content will need current updates.
---
*Prepared from GTBOP webinar archive materials for UGA Center for Urban Agriculture.*
docs/projects/insecticide-bulletin/outline.md
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# Bulletin Outline — Insecticide Basics # Insecticide Basics for the Pest Management Professional
## Bulletin Update Outline — Based on Dr. Michael Scharf's GTBOP Presentation (October 18, 2017)
> **Placeholder** — Paste your Stage 6 bulletin outline here. **Prepared by:** Rich Braman, UGA Cooperative Extension / Center for Urban Agriculture
**For:** Dr. Dan Suiter (UGA) & Dr. Michael Scharf (Purdue University)
**Purpose:** Working outline to facilitate the bulletin revision, reorganizing Dr. Scharf's presentation content into publication-ready sections
**Source document:** GTBOP_ProseTranscript_2017-10-18_InsecticideMOA.md (corrected and verified from 742-block SRT)
--- ---
*Source: Dr. Michael Scharf, GTBOP Structural — October 18, 2017* ## How to Use This Document
*Processed for UGA Center for Urban Agriculture / GTBOP Archives*
This outline restructures the webinar's conversational flow into a logical publication framework. Each section includes:
- **Content notes** summarizing what Dr. Scharf covered on this topic
- **Key details** listing specific facts, products, and examples mentioned
- **Transcript location** pointing to the relevant section of the prose transcript for exact wording
- **Writing notes** flagging areas that may need expansion, updating, or editorial decisions
The webinar naturally covered some topics in a sequence optimized for a live audience. This outline regroups that content into the structure of a reference bulletin, consolidating related material that was spread across different parts of the talk.
---
## PART I: WHY UNDERSTANDING INSECTICIDE MODE OF ACTION MATTERS
### Section 1.1 — Safety and Non-Target Toxicity
**Content notes:** Modern insecticides are dramatically more selective than older chemistries. Some classes (diamides) have mammalian toxicity so low that EPA did not initially require a signal word. The ratio of insecticide placed in the environment to what actually reaches a target site in a pest is on the order of billions to one.
**Key details from presentation:**
- Modern insecticides can be 10,000+ times more toxic to insects than to mammals
- Diamides had no signal word required by EPA; manufacturers voluntarily added "Caution"
- Organophosphates and carbamates are NOT insect-specific — they work equally well against mammals, hence heavy restrictions
**Transcript location:** "Why Understanding Mode of Action Matters" section; "Understanding LD50" section
**Writing notes:** This is a strong opening hook for the bulletin. The 10,000x selectivity figure and the diamide signal word story are compelling for a practitioner audience. May want to update with any newer selectivity data post-2017.
---
### Section 1.2 — Interpreting Trade Literature and Advertising
**Content notes:** Understanding how insecticides work gives practitioners the knowledge to critically evaluate manufacturer claims. Trade literature is not always technically accurate.
**Key details from presentation:**
- Scharf explicitly noted that advertising and trade literature "isn't always technically accurate"
- Knowledge of MOA helps practitioners evaluate product claims independently
**Transcript location:** "Why Understanding Mode of Action Matters" section
**Writing notes:** Brief section. Could be expanded with specific examples of misleading claims if Dan and Mike wish.
---
### Section 1.3 — Pollinator Protection
**Content notes:** Nicotinoids are systemic — they move through plants. Lawn applications can result in uptake by flowering plants in the landscape, exposing pollinators.
**Key details from presentation:**
- Nicotinoids move around in plants (systemic activity)
- Lawn applications → flowering landscape plants → pollinator exposure pathway
**Transcript location:** "Why Understanding Mode of Action Matters" section
**Writing notes:** This was a brief mention in the webinar but has become a much larger regulatory and public concern since 2017. Strong candidate for significant expansion in the updated bulletin with current EPA actions, label changes, and best practices.
---
### Section 1.4 — Resistance Management
**Content notes:** Product rotation is key to long-term success. Even combination products need rotation. Resistance is arguably the #1 cause of callbacks in cockroach accounts.
**Key details from presentation:**
- Resistance is "probably the number one cause of callbacks in cockroach accounts"
- Cockroaches observed surviving on bait as sole food source for a month
- Bedbug pyrethroid resistance is widespread; resistance to chlorfenapyr and nicotinoids emerging
- Rotation recommendation: switch active ingredients every 3 months, ideally monthly
- Combination products (neonicotinoid + pyrethroid) also need rotation — resistance to both AIs observed in roach populations
- Not all active ingredients are compatible in rotation sequences; research is ongoing
- IRAC (Insecticide Resistance Action Committee) provides mode of action classifications to guide rotation
**Transcript location:** "Resistance" subsection under Practical Factors; Q&A sections on combination products and IRAC
**Writing notes:** This section has substantial content from both the presentation body and the Q&A discussion. The Q&A exchange on combination product resistance is particularly valuable — Dan asked the tough question and Mike confirmed dual resistance. IRAC reference should include current web address and brief explanation of the classification numbering system.
---
### Section 1.5 — Product Sustainability and Customer Communication
**Content notes:** Each insecticide costs hundreds of millions (potentially billions) to bring to market. Wise use extends market life. Understanding MOA helps practitioners communicate competence to customers.
**Key details from presentation:**
- Development cost: hundreds of millions to billions per product
- Urban pest control market is a smaller slice of the pie than agriculture, which affects manufacturer investment in new urban AIs
- Knowledge of nine major classes enables better customer communication
- Q&A noted the industry is "generic heavy" — flow of new AIs has slowed
**Transcript location:** "Why Understanding Mode of Action Matters" section; Q&A on new active ingredients
**Writing notes:** The economics discussion from the Q&A adds good context. The point about urban market size vs. agriculture affecting R&D investment is practical industry knowledge worth including.
---
## PART II: INSECT PHYSIOLOGY — THE FOUNDATION
### Section 2.1 — Overview of Insecticide-Relevant Physiology
**Content notes:** Five key physiological systems are relevant to understanding how insecticides work. Scharf structured this as a compressed physiology primer — translating a semester course into key concepts.
**Key systems covered:**
1. **Nervous system** — controls all body functions; target of most insecticide classes
2. **Cuticle** — complex multi-layered barrier; target of IGRs and dehydrating dusts; also a penetration barrier
3. **Digestive system** — the gut interior is technically "outside" the body; a penetration barrier for ingested insecticides
4. **Tracheal system** — physical tubes delivering air directly to cells (unlike mammalian lungs/hemoglobin); entry route for fumigants
5. **Musculature** — controlled by nervous system; contains calcium channels targeted by diamides
**Transcript location:** "Insect Physiology Overview" section and its subsections
**Writing notes:** This section works well as a brief, illustrated primer in a bulletin. The tracheal system comparison (physical tubes vs. mammalian lungs/hemoglobin) and the gut-as-exterior concept are accessible explanations that help practitioners understand why different formulations work differently.
---
### Section 2.2 — How the Nervous System Works
**Content notes:** Detailed explanation of nerve impulse transmission — electrical signals along neurons, chemical transmission across synapses via neurotransmitters, receptor binding.
**Key details from presentation:**
- Nervous system = millions of nerve cells
- Central nervous system: brain, subesophageal ganglion, ventral nerve cord
- Peripheral nerves extend throughout body
- Electrical impulses travel along neurons
- Synapses = gaps between neurons
- Neurotransmitters (e.g., acetylcholine) carry signal across synapses
- Receptors on receiving neuron are specific to neurotransmitter type
- Finger-snap analogy for speed of neural transmission
**Transcript location:** "How the Nervous System Works" section
**Writing notes:** The finger-snap analogy is effective for a lay audience. The distinction between electrical (along neurons) and chemical (across synapses) transmission is foundational for understanding why different insecticide classes target different locations.
---
### Section 2.3 — Neurophysiology Demonstration
**Content notes:** Scharf's lab can measure insecticide effects on the cockroach nervous system in real time using electrodes on the ventral nerve cord.
**Key details from presentation:**
- American cockroach dissected to expose ventral nerve cord
- Electrode placed on nerve cord to measure electrical activity
- Baseline recording (5 minutes) compared to post-treatment
- Fipronil application → visible increase in firing rate and magnitude (neuroexcitation)
**Transcript location:** "Neurophysiology in the Lab" section
**Writing notes:** This is powerful visual content for a bulletin. If the electrophysiology traces (baseline vs. fipronil-treated) are available as figures, they would be excellent illustrations. Mike may have publication-quality versions of these from his research.
---
## PART III: INSECTICIDE CLASSIFICATION FUNDAMENTALS
### Section 3.1 — Chemical Structure and Classification
**Content notes:** Insecticide classification is based on chemical structure, analogous to how insect taxonomy is based on morphology. Different structures → different functions → different target sites.
**Transcript location:** "Insecticide Classification and Target Sites" section
---
### Section 3.2 — Target Site and Mode of Action — The Key and Lock
**Content notes:** The insecticide's chemical structure allows it to interact with a specific protein target in the insect. Modern computational chemistry can model these interactions (similar to drug discovery/design).
**Key details from presentation:**
- Target site = protein, usually with 3D structure
- Insecticide "docks" with target protein
- Key-and-lock analogy (simplified); actual molecular docking is far more complex
- Drug discovery and insecticide design have significant overlap
**Transcript location:** "The Key and Lock Analogy" section
---
### Section 3.3 — Four Basic Modes of Action
**Content notes:** All insecticide effects at target sites fall into just four categories. This simplifying framework is how Scharf teaches toxicology at Purdue.
**The four modes:**
1. **Stimulation** — causes target to become more active (e.g., nerve fires more rapidly)
2. **Blockage** — shuts target off (e.g., nerve kept from firing)
3. **Modulation** — changes the shape/function of target subtly (e.g., pyrethroids)
4. **Inhibition** — prevents an enzyme from doing its job (e.g., organophosphates inhibit acetylcholinesterase)
**Transcript location:** "Four Basic Modes of Action" section
**Writing notes:** This is a key pedagogical framework for the bulletin. The "only four ways" framing makes the whole topic approachable. A simple table or diagram showing these four categories with one example each would be very effective.
---
### Section 3.4 — Understanding LD50
**Content notes:** The LD50 concept — the dose that kills 50% of test subjects — is essential for understanding relative toxicity and safety.
**Key details from presentation:**
- LD50 is inverse to toxicity: smaller LD50 = higher toxicity
- Modern insecticides have high mammalian LD50s (safe) and low insect LD50s (effective)
- Some products are 10,000+ times more toxic to target insects than to mammals
- The actual amount of insecticide reaching a target site in a pest is a billionth or less of what's applied
**Transcript location:** "Understanding LD50" section
---
## PART IV: NEUROTOXIC INSECTICIDES — FIVE CLASSIFICATIONS
*Overview: Nine total insecticide classifications — five neurotoxic, four non-neurotoxic. This section covers the five that target the nervous system.*
### Section 4.1 — Target Site Roadmap
**Content notes:** Scharf provided a visual roadmap showing where each target site sits on the nerve/muscle junction. This is reference material for the detailed sections that follow.
**Target sites on neurons:**
- **Axon sodium channels** — the "on switch" for nerve firing (targeted by pyrethroids, indoxacarb, metaflumizone)
- **Chloride channels** — post-synaptic; mellowing/inhibitory function (targeted by fipronil, isoxazolines, avermectins)
- **Acetylcholine receptors** — post-synaptic; carry signal across synapse (targeted by neonicotinoids, spinosyns, sulfoximines)
- **Acetylcholinesterase enzyme** — breaks down acetylcholine in synapse (targeted by organophosphates, carbamates)
- **Neuromuscular calcium channels** — at nerve-muscle junction; control muscle contraction (targeted by diamides)
**Transcript location:** "Target Site Roadmap" section
**Writing notes:** This roadmap is the backbone of Part IV. A well-designed figure showing a schematic neuron/synapse/muscle junction with labeled target sites would be the single most valuable illustration in the bulletin. Scharf's presentation slides likely contain a version of this.
---
### Section 4.2 — Sodium Channel Insecticides
**Stimulators: Pyrethroids, Pyrethrins, DDT**
- Stimulate sodium channels → excitation → rapid knockdown
- The "on switch" is jammed open
- Pyrethroids are highly repellent to insects — "like pepper spray"
- Visible effect: immediate incoordination and knockdown
**Blockers: Indoxacarb (oxadiazine), Metaflumizone (semicarbazone)**
- Block sodium channels → inhibition → paralysis
- The "on switch" is stuck in the off position
- Indoxacarb is a major urban insecticide
- Metaflumizone has ectoparasite uses and possible urban applications
**Transcript location:** "Classification 1: Sodium Channel Insecticides" section; Q&A on repellent vs. non-repellent
**Writing notes:** The repellent/non-repellent distinction from the Q&A belongs here. Scharf's point that "the real distinction is pyrethroids and everything else" is a clean, practical takeaway. Pyrethroids are the repellent class; most other chemistries are not significantly detected by insects.
---
### Section 4.3 — Chloride Channel Insecticides
**Blockers: Fipronil (phenylpyrazole), Isoxazolines (fluralaner, sarolaner)**
- Chloride normally "mellows" neurons (negative charge dampens activity)
- Blocking chloride flow → loss of inhibition → excitation
- Fipronil is a major urban market product, now off-patent with consumer products available
- Isoxazolines: newer class, primarily veterinary/pet products (flea market); cross-resistance potential with fipronil
- Lab demonstration: fipronil application → rapid visible increase in nerve firing rate and magnitude
**Stimulators: Avermectins (abamectin)**
- Stimulate chloride channels → excess inhibition → paralysis
- Opposite effect from fipronil at the same target site type
- Abamectin is an effective gel bait active ingredient
**Transcript location:** "Classification 2: Chloride Channel Insecticides" section
**Writing notes:** The fipronil/abamectin contrast — same target site, opposite effects — is an excellent teaching point. Worth highlighting with a comparison callout or sidebar.
---
### Section 4.4 — Acetylcholine Receptor Insecticides
**Stimulators: Neonicotinoids, Sulfoximines (sulfoxaflor), Spinosyns (spinosad)**
- Stimulate the acetylcholine receptor → excitation
- Neonicotinoids: huge current market share
- Sulfoximines: newer class, same target site
- Spinosyns: relevant for landscape market
**Transcript location:** "Classification 3: Acetylcholine Receptor Insecticides" section
**Writing notes:** The Q&A on nicotinoids vs. neonicotinoids is relevant here. Scharf explained: nicotinoids look more like nicotine (e.g., imidacloprid); neonicotinoids have evolved structurally but still target the same receptor (e.g., clothianidin). Dan's anecdote about tobacco killing caterpillars ties back to nicotine as the original insecticide. Also connect back to the pollinator discussion — systemic movement through plants.
---
### Section 4.5 — Acetylcholinesterase Inhibitors
**Inhibitors: Organophosphates, Carbamates**
- Inhibit the enzyme that breaks down acetylcholine in the synapse
- Result: acetylcholine accumulates → continuous stimulation → excitation
- **Not insect-specific** — works equally well against mammals/humans
- Heavy regulatory restrictions for good reason
**Transcript location:** "Classification 4: Acetylcholinesterase Inhibitors" section
**Writing notes:** These are the "legacy" chemistry classes that most experienced practitioners know well. Worth noting their declining role in urban pest management and why (safety profile vs. newer options).
---
### Section 4.6 — Combination Products
**Neonicotinoid + Pyrethroid combinations**
- "All start with tea" (common naming pattern)
- Hit two target sites simultaneously: acetylcholine receptor + sodium channels
- Potentiation effect: synergy, "one plus one equals three"
- Still not immune to resistance — dual resistance observed in cockroach populations
- Must still be used in rotation
**Transcript location:** "Classification 5: Combination Products" section; Q&A on combination product resistance
**Writing notes:** The Q&A exchange adds important content here. Dan asked directly whether combo products at lower doses risk dual resistance, and Mike confirmed they do — evidence of resistance to both AIs in select roach populations. This is practical, industry-relevant information.
---
## PART V: NON-NEUROTOXIC INSECTICIDES — FOUR CLASSIFICATIONS
### Section 5.1 — Muscular Calcium Channel Insecticides (Diamides)
**Stimulators: Chlorantraniliprole, Cyantraniliprole**
- Stimulate neuromuscular calcium channels → muscle contraction → energy depletion → paralysis → death
- Timeline: contraction for hours, then paralyzed for days as energy depletes
- Extremely safe for mammals — EPA did not initially require signal word
- Manufacturers voluntarily added "Caution" signal word
- Possibly selective even among insect groups (noted in Q&A re: earthworm question)
**Transcript location:** "Muscular Calcium Channels (Diamides)" section; Q&A on chlorantraniliprole and earthworms
**Writing notes:** The safety profile of diamides is a significant selling point and an important counternarrative to public concerns about pesticides. The earthworm question from the Q&A is worth noting — Scharf suspected some effect but noted the molecule's selectivity even among invertebrates.
---
### Section 5.2 — Insect Growth Regulators
**Juvenile Hormone Analogs (e.g., pyriproxyfen)**
- Mimic juvenile hormone → cuticle deformation + extra juvenile stages → population crash (juveniles can't reproduce)
- Visible indicator: wing twist in cockroaches
- Practical field tip: if you see wing twist in a new account, IGRs are already affecting the population — consider rotating to a different chemistry
- Resistance concern with continuous use
**Chitin Synthesis Inhibitors**
- Inhibit the enzyme that forms cuticle during molting → death during molt
- Visible indicator in termites: "jackknife effect" (body curling from malformed cuticle)
- Effective against molting insects — acts at a very specific developmental window
**Background on insect development covered:**
- Three types of metamorphosis: ametabolous, hemimetabolous (roaches, termites, grasshoppers), holometabolous (flies, mosquitoes, caterpillars)
- Complex hormonal control of molting and development
- Cuticle tanning process in newly emerged adults (e.g., alate termites)
**Transcript location:** "Insect Growth Regulators" section
**Writing notes:** The wing-twist-as-field-indicator tip is highly practical for the target audience. The jackknife effect in termites is similarly useful. These are the kind of applied details that make a bulletin valuable to practitioners.
---
### Section 5.3 — Inhibitors of Energy Production
**Target: Mitochondria (cellular respiration)**
- Universal target — mitochondria exist in all organisms (plants, animals, insects, bacteria)
- Different products affect different parts of the respiratory chain
**Products mentioned:**
- **Hydramethylnon** — cockroach bait active ingredient
- **Chlorfenapyr** — has a food label; relatively safe; resistance potential noted
- **Sulfuryl fluoride** — fumigant
- **Methyl bromide** — fumigant (note: largely phased out since 2017)
- **Disodium octaborate tetrahydrate (DSOBTH)** — wood treatment; disrupts insect respiration
- **Boric acid** — disrupts respiration; also has physical mode of action (abrasive/desiccant effect on gut lining)
**Transcript location:** "Inhibitors of Energy Production" section
**Writing notes:** Boric acid's dual mode of action (chemical + physical) is an interesting detail worth highlighting. May need to update re: methyl bromide phase-out status and any newer products in this category since 2017.
---
### Section 5.4 — Cuticle Dehydrating Dusts
**Products: Silica gel, Diatomaceous earth (DE)**
- Physical mode of action — not a chemical toxicant
- Abrade the waxy epicuticular layer → water loss → dehydration → death
- Diatomaceous earth: ground exoskeletons of diatoms (silicon-based organisms)
- Active component: silicon
- Effect: lethargy, then death from desiccation
**Transcript location:** "Cuticle Dehydrating Dusts" section
**Writing notes:** Brief section. These products are simple in mechanism but important for IPM and for situations requiring non-chemical or minimal-chemical approaches.
---
## PART VI: PRACTICAL FACTORS AFFECTING INSECTICIDE PERFORMANCE
### Section 6.1 — Stability, Persistence, and Formulations
**Content notes:** Raw insecticides are oily, UV-sensitive, and would be unsafe to handle directly. Formulations solve all of these problems.
**Key details:**
- Most insecticides are oily (lipophilic) — helps cross cuticle and membranes but creates handling challenges
- UV light degrades raw active ingredients rapidly
- Insecticides can move with water despite not dissolving in it
**Formulation functions:**
- Enhance stability and extend longevity
- Enhance safety
- Ease handling and mixing
- Keep AI suspended/dissolved in water
**Formulation types mentioned:**
- Baits, granulars, dusts, aerosols, fumigants
- Liquid forms: emulsifiable concentrate (EC), wettable powder (WP), microencapsulated (ME), suspension concentrate (SC)
**Transcript location:** "Stability, Persistence, and Formulations" section
---
### Section 6.2 — Pest Behavior and Insecticide Delivery
**Content notes:** Natural pest behaviors can be exploited to enhance insecticide effectiveness. Three examples from the presentation.
**Example 1: Cockroach secondary and tertiary kill**
- Cockroach eats bait → dies → another roach feeds on carcass or feces → secondary kill
- Insecticide can pass through two digestive tracts and still cause tertiary kill in a third roach
**Example 2: Flea larval exposure**
- Treated pet → adult fleas defecate insecticide → flea larvae feed on adult feces for nutrition → secondary exposure
**Example 3: Social insect transfer (termites, ants)**
- Trophallaxis (food sharing from mouth and anus) and allogrooming spread insecticides through colony
- Slow-acting insecticides preferred → maximize colony penetration before detection
**Transcript location:** "Pest Behavior" section
**Writing notes:** These three examples are vivid and practical. The tertiary kill through two roach digestive tracts is a memorable detail. For the social insect section, note that Dave Oi's companion webinar on ants may have additional relevant content.
---
### Section 6.3 — Sanitation and IPM
**Content notes:** Poor sanitation undermines even the best insecticide programs.
**Key points:**
- Excess food competes with bait placements
- Clutter creates untreatable harborage
- Dirt and grease physically bind insecticides, reducing contact
- IPM mindset essential for maximizing insecticide effectiveness
**Transcript location:** "Sanitation" section
---
### Section 6.4 — Resistance (expanded from Section 1.4)
**Content notes:** Detailed resistance section drawing from both the main presentation and the extensive Q&A discussion.
*See Section 1.4 above for key details. Consider consolidating here or cross-referencing.*
**Additional Q&A content for this section:**
- Resistance is inevitable with overuse — possible to any product
- "Appropriate use for lengths of time and intensities of selection" determines outcome
- IRAC classification system helps guide rotation decisions
- IRAC website updated 1-2 times per year with complete landscape of available chemistries
- Research on optimal rotation sequences is ongoing (Scharf lab)
**Transcript location:** "Resistance" section; all Q&A segments on resistance and IRAC
---
### Section 6.5 — Oral vs. Dermal Toxicity
**Content notes:** From Q&A — insecticides are almost always more toxic via ingestion than by contact.
**Key details:**
- Insect cuticle: waterproof, multi-layered barrier
- Insect gut: thin cell layer, much less resistant to penetration
- Mammalian skin: incredibly resistant barrier to insecticides/toxins
- Practical implication: ingestion-based delivery (baits) can be highly effective at lower doses
**Transcript location:** Q&A section "On Oral vs. Dermal Toxicity"
**Writing notes:** This came up as an audience question but is foundational enough to warrant inclusion in the bulletin body rather than just Q&A.
---
### Section 6.6 — Essential Oils and 25B Products
**Content notes:** From Q&A — the green revolution in pest management.
**Key details:**
- Consumer demand is the primary driver
- 25B exempt actives (rosemary, spearmint, cedar) avoid registration costs
- Effective as repellents (Dan: "very good repellents — we've done a lot of work with them on ants")
- Not necessarily effective as toxicants
**Transcript location:** Q&A section "On Essential Oils and 25B Products"
**Writing notes:** This topic has grown considerably since 2017. Worth expanding with current market data and any efficacy research published since.
---
## SUPPORTING REFERENCES
### Publications Cited in Presentation
1. Scharf, M.E. & D.R. Suiter. 2011. "Insecticide Primer and Insecticide Mode of Action." *PCT Magazine*.
2. Scharf, M.E. & D.R. Suiter. ~2007. "Insecticide Basics for the Pest Management Professional." UGA Cooperative Extension publication. *(The bulletin being updated)*
### External Resources Mentioned
- IRAC (Insecticide Resistance Action Committee) — mode of action classification charts, updated 1-2x annually
---
## EDITORIAL NOTES FOR DAN AND MIKE
### Content that may need updating (2017 → present)
- Neonicotinoid regulatory landscape (significant EPA and state-level changes since 2017)
- Methyl bromide phase-out status
- New products in the diamide and isoxazoline classes
- Bedbug resistance — current scope of the problem
- Essential oils / 25B market growth
- Any new IRAC classifications added since 2017
- Current status of Scharf lab rotation research (papers published?)
- Fipronil patent/generic status update
### Structural suggestions
- The "nine classifications" framework (5 neurotoxic + 4 non-neurotoxic) is a clean organizing principle
- The "four basic modes of action" framework should appear early as a conceptual anchor
- Consider a one-page summary table at the end (see companion Reference Compendium)
- The neurophysiology figure (target site roadmap) deserves a full-page treatment
### Q&A content worth integrating
Several valuable exchanges from the Q&A are better suited to the bulletin body than a standalone Q&A section:
- Combination product resistance (Section 4.6)
- Nicotinoid vs. neonicotinoid terminology (Section 4.4)
- Oral vs. dermal toxicity (Section 6.5)
- Repellent vs. non-repellent (Section 4.2)
- IRAC as a practitioner resource (Section 6.4)
---
*Prepared from GTBOP webinar archive materials. All content derived exclusively from Dr. Scharf's October 18, 2017 presentation as transcribed and corrected through the GTBOP archive pipeline.*
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# Source Guide — Insecticide Basics # Bulletin Source Guide — Transcript Section Mapping
## Insecticide MOA Webinar → Bulletin Update
> **Placeholder** — Paste your Stage 6 source guide here. **Prepared by:** Rich Braman, UGA Cooperative Extension / Center for Urban Agriculture
**For:** Dr. Dan Suiter & Dr. Michael Scharf — Writing reference
**Source:** GTBOP_ProseTranscript_2017-10-18_InsecticideMOA.md
--- ---
*Source: Dr. Michael Scharf, GTBOP Structural — October 18, 2017* ## Purpose
*Processed for UGA Center for Urban Agriculture / GTBOP Archives*
This guide maps each proposed bulletin section (from the Bulletin Draft Outline) to the specific section of the prose transcript and the approximate video timestamps where that content appears. Use this to:
- Quickly locate Mike's exact wording on any topic
- Verify that bulletin content stays faithful to the source
- Find passages to quote, paraphrase, or expand upon
- Identify where Mike's Q&A responses add content beyond his prepared slides
---
## How to Use
The **Transcript Section** column tells you which heading to search for in the prose transcript file. The **Video Timestamp** column gives the approximate time range if you need to re-watch the original recording. The **Content Type** column indicates whether the material comes from the prepared presentation or from the Q&A discussion with Dan.
---
## Mapping Table
| Bulletin Section | Transcript Section | Video Timestamp | Content Type | Notes |
|-----------------|-------------------|----------------|-------------|-------|
| **PART I: Why Understanding MOA Matters** | | | | |
| 1.1 Safety & non-target toxicity | "Why Understanding Mode of Action Matters" + "Understanding LD50" | ~2:55–5:35 + ~19:50–22:45 | Presentation | Safety framing at start; LD50 details in classification section |
| 1.2 Interpreting trade literature | "Why Understanding Mode of Action Matters" | ~3:30–3:45 | Presentation | Brief mention — one sentence |
| 1.3 Pollinator protection | "Why Understanding Mode of Action Matters" | ~3:36–4:00 | Presentation | Brief but important; expand with current info |
| 1.4 Resistance management | "Resistance" + multiple Q&A sections | ~54:20–56:30 + ~57:55–59:50 | Both | Extensive Q&A content supplements presentation |
| 1.5 Product sustainability & communication | "Why Understanding Mode of Action Matters" + Q&A on new AIs | ~4:15–5:50 + ~59:55–1:01:10 | Both | Economics from Q&A adds industry context |
| | | | | |
| **PART II: Insect Physiology** | | | | |
| 2.1 Overview of relevant physiology | "Insect Physiology Overview" (all subsections) | ~8:25–13:58 | Presentation | Compressed physiology primer |
| 2.2 How the nervous system works | "How the Nervous System Works" | ~23:45–26:45 | Presentation | Electrical + chemical transmission; synapse explanation |
| 2.3 Neurophysiology demonstration | "Neurophysiology in the Lab" | ~26:50–28:40 | Presentation | Cockroach nerve cord + fipronil electrophysiology |
| | | | | |
| **PART III: Classification Fundamentals** | | | | |
| 3.1 Chemical structure & classification | "Insecticide Classification and Target Sites" | ~14:00–15:15 | Presentation | Structure → function → target site relationship |
| 3.2 Key and lock analogy | "The Key and Lock Analogy" | ~16:00–17:50 | Presentation | Key-lock + molecular docking + drug design parallel |
| 3.3 Four basic modes of action | "Four Basic Modes of Action" | ~17:50–19:35 | Presentation | Stimulation, blockage, modulation, inhibition |
| 3.4 Understanding LD50 | "Understanding LD50" | ~19:40–22:45 | Presentation | Inverse relationship; mammalian safety; billionths ratio |
| | | | | |
| **PART IV: Neurotoxic Insecticides** | | | | |
| 4.1 Target site roadmap | "Target Site Roadmap" | ~28:40–32:15 | Presentation | Visual overview of all target site locations on neuron |
| 4.2 Sodium channel insecticides | "Classification 1: Sodium Channel Insecticides" + Q&A repellency | ~32:20–34:10 + ~1:04:55–1:05:15 | Both | Pyrethroids/pyrethrins, indoxacarb, metaflumizone; "pepper spray" from Q&A |
| 4.3 Chloride channel insecticides | "Classification 2: Chloride Channel Insecticides" | ~34:10–36:20 | Presentation | Fipronil, isoxazolines, abamectin; opposite effects at same site |
| 4.4 Acetylcholine receptor insecticides | "Classification 3: Acetylcholine Receptor Insecticides" + Q&A nicotinoid terminology | ~36:20–37:30 + ~1:02:40–1:03:40 | Both | Neonics, sulfoximines, spinosyns; terminology clarification from Q&A |
| 4.5 Acetylcholinesterase inhibitors | "Classification 4: Acetylcholinesterase Inhibitors" | ~37:28–38:02 | Presentation | OPs and carbamates; not insect-specific; brief section |
| 4.6 Combination products | "Classification 5: Combination Products" + Q&A on dual resistance | ~38:03–39:10 + ~58:25–59:00 | Both | "Start with tea"; potentiation; confirmed dual resistance in Q&A |
| | | | | |
| **PART V: Non-Neurotoxic Insecticides** | | | | |
| 5.1 Diamides (calcium channels) | "Muscular Calcium Channels (Diamides)" + Q&A on earthworms | ~39:55–41:30 + ~1:01:05–1:01:40 | Both | Safety profile; contraction → depletion timeline; earthworm selectivity from Q&A |
| 5.2 Insect growth regulators | "Insect Growth Regulators" | ~41:40–45:20 | Presentation | JH analogs + CSIs; metamorphosis types; wing twist; jackknife effect |
| 5.3 Energy production inhibitors | "Inhibitors of Energy Production" | ~45:20–46:50 | Presentation | Mitochondria targeting; hydramethylnon, chlorfenapyr, fumigants, borates |
| 5.4 Cuticle dehydrating dusts | "Cuticle Dehydrating Dusts" | ~47:00–48:15 | Presentation | Silica gel, DE; physical mode of action; diatom origin |
| | | | | |
| **PART VI: Practical Factors** | | | | |
| 6.1 Stability & formulations | "Stability, Persistence, and Formulations" | ~48:45–51:00 | Presentation | Lipophilic nature; UV degradation; formulation types and functions |
| 6.2 Pest behavior | "Pest Behavior" | ~51:02–53:05 | Presentation | Secondary/tertiary kill; flea larvae; trophallaxis/allogrooming |
| 6.3 Sanitation & IPM | "Sanitation" | ~53:05–54:20 | Presentation | Food competition, clutter, grease; IPM mindset |
| 6.4 Resistance (expanded) | "Resistance" + Q&A segments | ~54:20–56:30 + multiple Q&A | Both | Rotation; cockroach bait resistance; IRAC; inevitability |
| 6.5 Oral vs. dermal toxicity | Q&A: "On Oral vs. Dermal Toxicity" | ~1:03:55–1:04:45 | Q&A only | Cuticle vs. gut barriers; mammalian skin resistance |
| 6.6 Essential oils & 25B | Q&A: "On Essential Oils and 25B Products" | ~1:05:30–1:06:40 | Q&A only | Consumer demand; repellent efficacy; registration cost advantage |
---
## Content That Comes Exclusively from Q&A
The following material was only discussed during the Q&A exchange with Dan and would be missed if working only from the prepared presentation portion of the transcript:
| Topic | Q&A Transcript Section | Why It Matters for the Bulletin |
|-------|----------------------|-------------------------------|
| Dual resistance to combo products | "On Combination Products and Resistance" | Confirms resistance to both AIs in field populations — critical practitioner info |
| Inevitability of resistance | Same section | "Possible always" — frames the urgency of rotation |
| New AI pipeline economics | "On New Active Ingredients" | Urban market size limits manufacturer investment — industry context |
| IRAC as a practitioner tool | "On IRAC Classification" | Actionable resource for product rotation decisions |
| Nicotinoid vs. neonicotinoid terminology | "On Nicotinoids vs. Neonicotinoids" | Clears up common confusion; imidacloprid vs. clothianidin example |
| Chlorantraniliprole earthworm selectivity | "On Chlorantraniliprole and Earthworms" | Unique selectivity even among invertebrates — safety story |
| Oral vs. dermal toxicity explanation | "On Oral vs. Dermal Toxicity" | Foundational concept not covered in prepared talk |
| Repellent = pyrethroids, non-repellent = everything else | "On Repellent vs. Non-Repellent Insecticides" | Clean practical distinction for practitioners |
| Essential oils / 25B market drivers | "On Essential Oils and 25B Products" | Consumer demand and green market trends |
| Nicotine as insecticide (tobacco anecdote) | Within nicotinoid terminology discussion | Memorable historical connection |
| Scharf's prior resistance webinar | Opening Q&A exchange | Suggests companion content exists for the resistance bulletin |
---
## Presentation Flow vs. Bulletin Structure
The webinar followed this sequence (left), which differs from the proposed bulletin structure (right):
| Webinar Order | → | Proposed Bulletin Order |
|---------------|---|------------------------|
| 1. Why MOA matters (motivation) | → | Part I: Why MOA Matters (motivation) |
| 2. Insect physiology overview | → | Part II: Insect Physiology (foundation) |
| 3. Insecticide classification basics | → | Part III: Classification Fundamentals |
| 4. LD50 concept | → | Moved into Part III (Section 3.4) |
| 5. Neurotoxic classes (5) | → | Part IV: Neurotoxic Insecticides |
| 6. Non-neurotoxic classes (4) | → | Part V: Non-Neurotoxic Insecticides |
| 7. Practical factors (stability, behavior, sanitation, resistance) | → | Part VI: Practical Factors |
| 8. Summary | → | Distributed as section conclusions |
| 9. Q&A with Dan | → | Integrated throughout relevant sections |
**Key reorganization choices:**
- LD50 was presented between physiology and classification; it fits better as a classification fundamental
- Combination products were discussed within neurotoxics but could also warrant their own sidebar
- Q&A content is distributed to the sections where it's most relevant rather than kept as a standalone section
- The resistance discussion appears in both Part I (motivation) and Part VI (practical detail) — cross-reference or consolidate as preferred
---
## Companion Documents
This source guide is part of a three-document set:
1. **Bulletin Draft Outline** (`GTBOP_BulletinOutline_InsecticideMOA_Scharf.md`) — Section-by-section content notes and writing guidance
2. **Quick Reference Compendium** (`GTBOP_ReferenceCompendium_InsecticideMOA_Scharf.md`) — Consolidated tables of all classifications, products, and relationships
3. **This Source Guide** (`GTBOP_SourceGuide_InsecticideMOA_Scharf.md`) — Transcript location mapping
All three draw exclusively from the same source: the corrected and verified prose transcript of Dr. Scharf's October 18, 2017 GTBOP presentation.
---
*Prepared from GTBOP webinar archive materials for UGA Center for Urban Agriculture.*
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# Matching Exercises — Scharf, Insecticide MOA # GTBOP Moodle Matching Exercises
## Principles of Insecticide Mode of Action — Dr. Michael Scharf
> **Placeholder** — Paste your Stage 4 pipeline output here. **Webinar Date:** October 18, 2017
**Series:** Structural Pest Control
**Activity Type:** Matching Exercises
**Exercises:** 3
**Total Pairs:** 26 (8 + 10 + 8)
--- ---
*Processed for UGA Center for Urban Agriculture / GTBOP Archives* ### CHAIN OF CUSTODY
- **Source documents:** Corrected SRT (GTBOP_Transcript_2017-10-18_InsecticideMOA.srt) + Archive Package (GTBOP_Archive_Summary_2017-10-18_InsecticideMOA.md)
- **All terms, definitions, and relationships derived exclusively from presentation content**
---
### Matching Exercise 1: Insecticide Classes and Their Target Sites
**Timestamp Reference:** 28:40 – 39:05 (primary coverage area)
**Type:** Product-Target Site Matching
**Instructions:** Match each insecticide class in Column A with the target site it affects in Column B. Note: Column B contains two extra items.
| # | Column A | | Column B |
|---|----------|-|----------|
| 1 | Pyrethroids | | a) Chloride channels |
| 2 | Fipronil (phenylpyrazole) | | b) Acetylcholine receptor |
| 3 | Nicotinoids | | c) Muscular calcium channels |
| 4 | Organophosphates and carbamates | | d) Axonal sodium channels |
| 5 | Diamides (chlorantraniliprole) | | e) Acetylcholinesterase enzyme |
| 6 | Indoxacarb (oxadiazine) | | f) Mitochondria (energy production) |
| 7 | Abamectin (avermectin) | | g) Chitin synthesis enzymes |
| 8 | Chitin synthesis inhibitors | | h) Glutamate-gated chloride channels |
| | | | i) Juvenile hormone receptors |
| | | | j) Axonal sodium channels (blockage) |
**Answer Key:**
1 → d, 2 → a, 3 → b, 4 → e, 5 → c, 6 → j, 7 → h, 8 → g
**Notes:**
- Items 1 and 6 both target sodium channels but through opposite mechanisms (stimulation vs. blockage), which is why they map to separate entries (d and j). This distinction is a key teaching point from the presentation.
- Distractors: (f) mitochondria and (i) juvenile hormone receptors are legitimate target sites discussed elsewhere in the presentation but do not match the classes listed in Column A.
**Source in transcript:** Blocks 301–343 (target site roadmap), 346–362 (sodium channels), 363–387 (chloride channels), 388–407 (acetylcholine), 429–444 (diamides), 466–482 (IGRs)
---
### Matching Exercise 2: Insecticide Mode of Action Effects
**Timestamp Reference:** 17:51 – 47:00 (spans full classification section)
**Type:** Product-Effect Matching
**Instructions:** Match each insecticide or insecticide class in Column A with the physiological effect it produces in insects, as described by Dr. Scharf, in Column B. Note: Column B contains two extra items.
| # | Column A | | Column B |
|---|----------|-|----------|
| 1 | Pyrethroids / pyrethrins | | a) Blocks chloride channels, causing nervous system excitation |
| 2 | Fipronil | | b) Stimulates muscular calcium channels, causing contraction followed by energy depletion and paralysis |
| 3 | Indoxacarb | | c) Stimulates sodium channels, causing rapid knockdown and excitation |
| 4 | Organophosphates | | d) Inhibits chitin synthesis enzyme, causing death during molting |
| 5 | Diamides | | e) Blocks sodium channels, causing paralysis ("on switch stuck in off position") |
| 6 | Juvenile hormone analogs (pyriproxyfen) | | f) Inhibits acetylcholinesterase, causing excitation from neurotransmitter buildup |
| 7 | Chitin synthesis inhibitors | | g) Mimics juvenile hormone, causing cuticle deformation and extra juvenile stages |
| 8 | Abamectin | | h) Stimulates chloride channels, causing inhibition and paralysis |
| 9 | Silica gel / diatomaceous earth | | i) Abrades waxy cuticle layer, causing water loss and dehydration |
| 10 | Nicotinoid-pyrethroid combinations | | j) Stimulates acetylcholine receptors and sodium channels simultaneously (potentiation) |
| | | | k) Disrupts mitochondrial respiration, depleting cellular energy |
| | | | l) Blocks acetylcholine receptors, preventing nerve signal transmission |
**Answer Key:**
1 → c, 2 → a, 3 → e, 4 → f, 5 → b, 6 → g, 7 → d, 8 → h, 9 → i, 10 → j
**Notes:**
- This exercise tests understanding of both the target site AND the specific mode of action (stimulation vs. blockage vs. inhibition) — the core teaching framework of the presentation.
- Distractors: (k) mitochondrial disruption is discussed for products like hydramethylnon but is not paired with any Column A item; (l) is a plausible-sounding but incorrect mechanism not described in the presentation.
**Source in transcript:** Blocks 184–205 (four modes of action), 346–362 (sodium channels), 363–387 (chloride channels), 388–407 (acetylcholine), 408–420 (combinations), 429–444 (diamides), 466–482 (IGRs), 499–511 (dusts)
---
### Matching Exercise 3: Practical Factors Affecting Insecticide Performance
**Timestamp Reference:** 48:15 – 56:30 (practical factors section)
**Type:** Timing-Practice Matching
**Instructions:** Match each practical factor or scenario in Column A with the correct explanation or outcome described by Dr. Scharf in Column B. Note: Column B contains two extra items.
| # | Column A | | Column B |
|---|----------|-|----------|
| 1 | Excess food in a cockroach account | | a) Can pass insecticide through two digestive tracts and still affect a third individual |
| 2 | Dirt and grease on treated surfaces | | b) Physically bind and tie up insecticides, reducing their effectiveness |
| 3 | Cockroach secondary/tertiary kill | | c) Enables slow-acting insecticides to spread through food sharing and grooming |
| 4 | Trophallaxis and allogrooming in social insects | | d) Competes directly with bait placements, reducing consumption by target pests |
| 5 | Flea larvae exposed through adult flea feces | | e) Causes the insecticide's active ingredient to degrade faster in the environment |
| 6 | UV light exposure on raw insecticides | | f) Larvae consume insecticide-laden feces of treated adults as a nutritional source |
| 7 | Formulations (inerts, stabilizers, attractants) | | g) Enhance stability, extend longevity, improve safety, and keep active ingredients dissolved in water |
| 8 | Product rotation every 3 months or monthly | | h) Helps manage resistance by alternating between different modes of action |
| | | | i) Increases the LD50 of the product, making it less toxic to target pests |
| | | | j) Converts neurotoxic insecticides into non-repellent formulations |
**Answer Key:**
1 → d, 2 → b, 3 → a, 4 → c, 5 → f, 6 → e, 7 → g, 8 → h
**Notes:**
- This exercise bridges the gap between toxicology and practice — the section of the presentation Scharf described as "where toxicology interfaces with practice."
- Distractors: (i) is plausible-sounding but reverses the relationship (formulations don't increase LD50 for targets); (j) is a fabricated mechanism not described in the presentation.
**Source in transcript:** Blocks 515–547 (stability and formulations), 548–567 (pest behavior), 568–585 (sanitation), 586–611 (resistance management)
---
## Moodle Activity Verification
- [x] All terms, definitions, and relationships derived from presentation content
- [x] Timestamp references verified against corrected SRT
- [x] No external knowledge required to answer correctly
- [x] Matching items unambiguous based on presentation content
- [x] 1–2 plausible distractors included per exercise to prevent elimination guessing
- [x] Answer keys unambiguously correct per speaker's content
- [x] Exercises cover early (target sites), middle (modes of action and effects), and late (practical factors) presentation content
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# Moodle Quiz — Scharf, Insecticide MOA # GTBOP Moodle Quiz
## Principles of Insecticide Mode of Action — Dr. Michael Scharf
> **Placeholder** — Paste your Stage 4 pipeline output here. **Webinar Date:** October 18, 2017
**Series:** Structural Pest Control
**Activity Type:** Multiple Choice Quiz
**Questions:** 15
**Difficulty Distribution:** 6 Recall (40%) / 6 Application (40%) / 3 Analysis (20%)
--- ---
*Processed for UGA Center for Urban Agriculture / GTBOP Archives* ### CHAIN OF CUSTODY
- **Source documents:** Corrected SRT (GTBOP_Transcript_2017-10-18_InsecticideMOA.srt) + Archive Package (GTBOP_Archive_Summary_2017-10-18_InsecticideMOA.md)
- **All questions and answers derived exclusively from presentation content**
- **No external knowledge required to answer correctly**
---
### Question 1
**Timestamp Reference:** 17:51 – 19:30
**Difficulty:** Recall
According to Dr. Scharf, how many basic modes of action do all insecticides fall into?
a) Two
b) Four
c) Six
d) Nine
**Correct Answer:** b
**Explanation:** Scharf states there are only four basic modes of action: stimulation, blockage, modulation, and inhibition. He emphasizes that all insecticide effects on target sites can be categorized into one of these four mechanisms.
**Source in transcript:** ~18:07 — "We can really break it down into four modes of action. There are only four kinds that occur."
---
### Question 2
**Timestamp Reference:** 32:24 – 34:07
**Difficulty:** Recall
Which insecticide class targets axonal sodium channels by stimulating them, causing rapid knockdown and excitation in insects?
a) Phenylpyrazoles
b) Diamides
c) Pyrethroids
d) Organophosphates
**Correct Answer:** c
**Explanation:** Scharf explains that pyrethroids (along with DDT and pyrethrins) stimulate sodium channels on the nerve axon, causing excitation and the rapid knockdown commonly observed when insects are treated with pyrethrins.
**Source in transcript:** ~32:56 — "We have pyrethroids and also DDT and pyrethrins... They stimulate sodium channels and cause excitation."
---
### Question 3
**Timestamp Reference:** 34:12 – 36:16
**Difficulty:** Application
A technician applies fipronil to a cockroach harborage area and observes insects exhibiting hyperexcitation rather than paralysis. Based on Dr. Scharf's explanation of fipronil's mode of action, why does fipronil cause excitation rather than sedation?
a) Fipronil stimulates sodium channels, causing nerves to fire rapidly
b) Fipronil blocks chloride channels, removing the calming effect of chloride on neurons
c) Fipronil inhibits acetylcholinesterase, causing neurotransmitter buildup
d) Fipronil stimulates muscular calcium channels, causing uncontrolled contraction
**Correct Answer:** b
**Explanation:** Scharf explains that chloride normally has a "mellowing" effect on neurons. Fipronil blocks the chloride channel, removing that calming influence, which leads to excitation. He demonstrated this with nerve recordings showing increased firing rate after fipronil application.
**Source in transcript:** ~34:48 — "Fipronil blocks the chloride channel so you're blocking this mellowing effect which leads to excitation."
---
### Question 4
**Timestamp Reference:** 33:22 – 34:10
**Difficulty:** Application
A pest management professional encounters a situation where rapid knockdown is undesirable and instead needs an insecticide that paralyzes insects by blocking nervous system function. Which sodium channel insecticide would best fit this need, based on the presentation?
a) Bifenthrin
b) Indoxacarb
c) Fipronil
d) Imidacloprid
**Correct Answer:** b
**Explanation:** Scharf explains that indoxacarb (an oxadiazine) blocks sodium channels rather than stimulating them, causing the "on switch" to be stuck in the off position, which paralyzes the insect. This contrasts with pyrethroids like bifenthrin, which stimulate sodium channels and cause excitation.
**Source in transcript:** ~33:34 — "Indoxacarb affects the sodium channel but it blocks it... the insect is actually paralyzed because its sodium channels don't work."
---
### Question 5
**Timestamp Reference:** 40:02 – 41:40
**Difficulty:** Recall
What is unique about the mammalian safety profile of diamide insecticides such as chlorantraniliprole?
a) They require a "Danger" signal word due to moderate toxicity
b) Their mammalian toxicity is so low that the EPA initially did not require a signal word
c) They are equally toxic to mammals and insects
d) They are safe only when applied as baits, not as sprays
**Correct Answer:** b
**Explanation:** Scharf states that diamides are so safe for mammals that the EPA initially required no signal word. Manufacturers voluntarily adopted a "caution" label. He still emphasized that safety guidelines should be followed.
**Source in transcript:** ~41:04 — "These products are actually so safe for mammals that no signal words were required by the EPA initially."
---
### Question 6
**Timestamp Reference:** 40:02 – 41:03
**Difficulty:** Recall
According to Dr. Scharf, what happens physiologically when a diamide insecticide like chlorantraniliprole affects an insect?
a) It blocks sodium channels, preventing nerve impulses
b) It inhibits chitin synthesis during molting
c) It stimulates muscular calcium channels, causing contraction followed by energy depletion and paralysis
d) It disrupts the insect's respiratory chain in the mitochondria
**Correct Answer:** c
**Explanation:** Scharf explains that diamides stimulate neuromuscular calcium channels, causing muscles to contract for hours until the insect's energy is burned up, after which it enters a paralyzed state for days until it dies.
**Source in transcript:** ~40:48 — "What these things do is they stimulate the neuromuscular calcium channel and that causes that muscle to contract for a few hours and then it burns up all its energy."
---
### Question 7
**Timestamp Reference:** 36:20 – 38:01
**Difficulty:** Recall
Which of the following target sites do nicotinoid insecticides affect?
a) Sodium channels on the nerve axon
b) Chloride channels on neurons
c) Acetylcholine receptors at the synapse
d) Muscular calcium channels
**Correct Answer:** c
**Explanation:** Scharf identifies nicotinoids as affecting the acetylcholine receptor by stimulating it and causing excitation in the insect. He also notes that sulfoximines and spinosyns share this same target site.
**Source in transcript:** ~36:54 — "We have our mainly the nicotinoids... They're affecting the acetylcholine receptor by stimulating it."
---
### Question 8
**Timestamp Reference:** 37:28 – 38:01
**Difficulty:** Analysis
Dr. Scharf notes that organophosphates and carbamates are subject to more regulatory restrictions than many newer insecticide classes. Based on his explanation, what is the underlying reason for these restrictions?
a) They are more expensive to manufacture than newer products
b) Their target site (acetylcholinesterase) is not insect-specific, so they are equally effective against mammals
c) They cause environmental persistence that exceeds all other insecticide classes
d) They are only effective against a narrow range of pest species
**Correct Answer:** b
**Explanation:** Scharf explicitly states that the acetylcholinesterase target site is "not a really insect specific target site" and that "these things work equally well against humans and mammals," which is the reason for restrictions on these product classes.
**Source in transcript:** ~37:53 — "This is not a really insect specific target site. You know these things work equally well against humans and mammals and so we have a lot of restrictions."
---
### Question 9
**Timestamp Reference:** 38:04 – 39:05
**Difficulty:** Application
A combination product pairs a nicotinoid with a pyrethroid. Based on Dr. Scharf's presentation, what advantage does this combination provide over a single active ingredient?
a) The two ingredients target the same site for a doubled dose effect
b) The combination eliminates the need for product rotation
c) Hitting two different target sites simultaneously produces a potentiation effect — synergy greater than either alone
d) The pyrethroid component makes the product non-repellent
**Correct Answer:** c
**Explanation:** Scharf explains that combination products produce potentiation by hitting two target sites at once — the nicotinoid targets the acetylcholine receptor while the pyrethroid targets sodium channels — creating a "one plus one equals three" synergistic effect.
**Source in transcript:** ~38:35 — "They cause this effect called potentiation, which is actually hitting two target sites at once. So you get this synergy, this one plus one equals three kind of effect."
---
### Question 10
**Timestamp Reference:** 51:02 – 53:01
**Difficulty:** Application
A pest control operator is treating a heavy German cockroach infestation with gel bait. Based on Dr. Scharf's discussion of pest behavior, why might the actual number of cockroaches killed exceed the number that directly consumed the bait?
a) Gel bait releases a fumigant vapor that kills nearby cockroaches
b) Cockroaches that eat bait excrete insecticide in their feces, which other cockroaches consume, producing secondary and even tertiary kill
c) The bait becomes more concentrated as it dries, increasing its toxicity over time
d) Cockroaches are attracted to the pheromones of dead individuals, bringing them into contact with remaining bait
**Correct Answer:** b
**Explanation:** Scharf describes secondary and tertiary kill in cockroaches: one cockroach eats bait, excretes insecticide, and other cockroaches consume the feces. He notes research showing the toxin can pass through two digestive tracts and still affect a third cockroach.
**Source in transcript:** ~51:24 — "If we have a cockroach that eats a bait and it either excretes, you know, some of the bait in its excrement... We can have secondary kill and even tertiary kill."
---
### Question 11
**Timestamp Reference:** 54:19 – 56:28
**Difficulty:** Recall
What rotation frequency does Dr. Scharf recommend for switching active ingredients in cockroach management to help manage resistance?
a) Every week
b) Every month or every three months
c) Every six months
d) Annually
**Correct Answer:** b
**Explanation:** Scharf recommends switching active ingredients every three months, or even every month if possible, as part of a resistance management rotation strategy for cockroach accounts.
**Source in transcript:** ~55:49 — "Every three months switch active ingredients, maybe even every month if you can do it."
---
### Question 12
**Timestamp Reference:** 53:04 – 54:11
**Difficulty:** Application
A technician is having difficulty achieving control with gel bait in a commercial kitchen. The kitchen has grease buildup on surfaces and abundant food debris. Based on Dr. Scharf's discussion, what is the most likely reason for reduced bait performance?
a) The bait has developed resistance to the cockroach population
b) Grease and dirt tie up insecticides on surfaces, and excess food competes directly with bait for cockroach feeding
c) The kitchen's humidity is degrading the active ingredient
d) The bait formulation is incompatible with commercial kitchen environments
**Correct Answer:** b
**Explanation:** Scharf specifically identifies three sanitation-related factors that reduce insecticide efficacy: excess food competing with bait, clutter creating untreatable harborage, and dirt and grease that physically bind insecticides. He frames sanitation as essential to making insecticides more effective.
**Source in transcript:** ~53:31 — "Excess food in an account will compete with bait" and ~54:02 — "dirt and grease tie up insecticides too."
---
### Question 13
**Timestamp Reference:** 41:42 – 44:46
**Difficulty:** Application
A technician inspects a cockroach account and notices several German cockroaches with twisted, malformed wings. Based on the presentation, what does this observation most likely indicate?
a) The cockroaches are infected with a fungal pathogen
b) The population has been exposed to insect growth regulators, specifically juvenile hormone analogs
c) The cockroaches have developed pyrethroid resistance
d) The cockroaches are immature nymphs that have not yet completed development
**Correct Answer:** b
**Explanation:** Scharf specifically identifies wing twist as a diagnostic sign that IGRs (particularly juvenile hormone analogs like pyriproxyfen) are active in a cockroach population. He advises that when wing twist is visible, it may be appropriate to rotate to a different product class.
**Source in transcript:** ~44:25 — "If you go into a new account and you see individuals with wing twist... you can put good money down on the fact that IGRs are in that population affecting it."
---
### Question 14
**Timestamp Reference:** 19:41 – 22:40
**Difficulty:** Analysis
Dr. Scharf states that the relationship between LD50 and product toxicity is inverse. A professional is comparing two insecticides: Product A has an LD50 of 5 mg/kg for cockroaches, and Product B has an LD50 of 500 mg/kg for cockroaches. Which product is more toxic to cockroaches, and why?
a) Product B, because a higher LD50 means more insecticide reaches the target site
b) Product A, because a smaller LD50 means a smaller dose is needed to kill 50% of the test population
c) Both are equally toxic; LD50 only measures speed of action
d) Product B, because a higher LD50 indicates greater potency
**Correct Answer:** b
**Explanation:** Scharf explains that LD50 is the lethal dose required to kill 50% of a test population, and the relationship to toxicity is inverse — the smaller the LD50, the higher the toxicity, because less product is needed to achieve the lethal effect.
**Source in transcript:** ~20:24 — "The smaller the LD50, the higher the toxicity of a product. That means... you only need a small dose to kill half of your test population."
---
### Question 15
**Timestamp Reference:** 46:56 – 48:09 and 04:01 – 04:00 (pollinator context)
**Difficulty:** Analysis
Dr. Scharf discusses cuticle dehydrating dusts like diatomaceous earth and silica gel. Considering his earlier discussion of insect physiology, why are these products effective against insects but pose minimal chemical toxicity risk to mammals?
a) They work through a physical mechanism — abrading the waxy cuticle layer and causing water loss — rather than through a biochemical target site interaction
b) They contain active ingredients that are specific to insect nervous systems
c) They are formulated with attractants that only insects will consume
d) They degrade too quickly in the environment to affect mammals
**Correct Answer:** a
**Explanation:** Scharf explains that silica gel and diatomaceous earth are essentially finely ground glass powder that abrades the protective waxy outer layer of the insect cuticle, leading to water loss and death. This is a physical mechanism rather than a chemical mode of action targeting a specific biochemical pathway, which is why these products do not pose the same chemical toxicity concerns for mammals.
**Source in transcript:** ~47:00 — "We have silica gel and diatomaceous earth which are just basically finely ground glass powder... they abrade the cuticle, they break it down, which leads to water loss."
---
## Moodle Activity Verification
- [x] All 15 questions traceable to specific presentation segments
- [x] Timestamp references verified against corrected SRT
- [x] No external knowledge required to answer correctly
- [x] Difficulty distribution: 6 Recall / 6 Application / 3 Analysis
- [x] Answer keys unambiguously correct based on presentation content
- [x] Distractors plausible but definitively wrong per speaker's content
- [x] Questions drawn from early (Q1, Q2, Q14), middle (Q3–Q9, Q13), and late (Q10–Q12, Q15) presentation content
- [x] No "all of the above" or "none of the above" options used
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# Archive Summary — Scharf, Insecticide MOA # GTBOP Webinar Archive Summary
## Principles of Insecticide Mode of Action
> **Placeholder** — Paste your Stage 2 pipeline output here. **Webinar Date:** October 18, 2017
**Speaker:** Dr. Michael Scharf, O.W. Rawlins Orkin Endowed Chair in Urban Entomology and Molecular Physiology, Department of Entomology, Purdue University
**Moderator:** Dr. Dan Suiter, Extension Entomologist, University of Georgia
**Duration:** 1:07:06
**Series:** Structural Pest Control
**CEU Categories:** GA — 2 HPC (Cat 35: Industrial, Institutional, Structural and Health Related)
---
## NARRATIVE SUMMARY
Dr. Michael Scharf of Purdue University presented a comprehensive overview of insecticide classification and mode of action designed to strengthen pest management professionals' understanding of how their chemical tools work. Scharf framed the practical importance of this knowledge around six themes: applicator and customer safety, accurate interpretation of trade literature, pollinator protection, resistance management, product sustainability, and the ability to design customized applications through situational pest management.
Scharf began with a condensed review of insect physiology, covering the five systems most relevant to insecticide activity: the nervous system, the cuticle, the digestive tract, the tracheal system, and the musculature. He explained that insecticides interact with specific protein target sites through a key-and-lock relationship, and that all insecticide effects can be reduced to just four modes of action — stimulation, blockage, modulation, and inhibition. He introduced the LD50 concept and emphasized that modern insecticides are dramatically more toxic to insects than to mammals, with some classes like the diamides carrying such low mammalian toxicity that the EPA initially required no signal word.
The presentation then systematically covered five neurotoxic insecticide classifications: sodium channel agents (pyrethroids, indoxacarb, metaflumizone), chloride channel agents (fipronil, isoxazolines, abamectin), acetylcholine receptor agents (nicotinoids, sulfoximines, spinosyns), acetylcholinesterase inhibitors (organophosphates, carbamates), and combination products pairing nicotinoids with pyrethroids for potentiation effects. Scharf followed with four non-neurotoxic classifications: muscular calcium channel agents (diamides such as chlorantraniliprole and cyantraniliprole), insect growth regulators (juvenile hormone analogs like pyriproxyfen and chitin synthesis inhibitors), inhibitors of energy production (hydramethylnon, chlorfenapyr, sulfuryl fluoride, boric acid), and cuticle dehydrating dusts (silica gel, diatomaceous earth).
Scharf concluded by discussing practical factors that affect insecticide performance, including formulation types, pest behavior that can amplify efficacy through secondary and tertiary kill, the role of sanitation in an IPM framework, and resistance management. He identified resistance as likely the number one cause of callbacks in cockroach accounts and recommended rotating active ingredients every three months or even monthly. A Q&A session moderated by Dr. Suiter addressed combination product resistance risks, the flow of new active ingredients to market, the IRAC classification system, the distinction between nicotinoids and neonicotinoids, oral versus dermal toxicity, repellent versus non-repellent insecticides, and the growing consumer demand for essential oil-based products.
---
## YOUTUBE TIMESTAMPS
0:00 Introduction and Speaker Credentials
1:45 Why Understanding Mode of Action Matters
6:03 Presentation Outline
7:13 Additional Resources — PCT Article and UGA Publication
8:26 Insect Physiology Overview — Nervous System, Cuticle, Gut, Trachea, Muscles
14:02 Insecticide Classification Basics — Chemical Structure
16:01 Target Site and Mode of Action — Key and Lock Analogy
17:51 Four Basic Modes of Action — Stimulation, Blockage, Modulation, Inhibition
19:41 The LD50 Concept and Mammalian Safety
22:46 Overview of Neurotoxic and Non-Neurotoxic Classifications
23:36 The Insect Nervous System — Neurons, Synapses, Neurotransmitters
26:45 Neurophysiology Demonstration — Fipronil and Nerve Excitation
28:40 Nervous System Target Sites — Roadmap of Ion Channels and Receptors
32:24 Sodium Channel Insecticides — Pyrethroids, Indoxacarb, Metaflumizone
34:12 Chloride Channel Insecticides — Fipronil, Isoxazolines, Abamectin
36:20 Acetylcholine Receptor Insecticides — Nicotinoids, Sulfoximines, Spinosyns
37:28 Acetylcholinesterase Inhibitors — Organophosphates and Carbamates
38:04 Combination Products — Nicotinoid-Pyrethroid Potentiation
39:07 Non-Neurotoxic Insecticides Overview
40:02 Muscular Calcium Channel Agents — Diamides
41:42 Insect Growth Regulators — JH Analogs and Chitin Synthesis Inhibitors
45:18 Inhibitors of Energy Production — Hydramethylnon, Chlorfenapyr, Fumigants
46:56 Cuticle Dehydrating Dusts — Silica Gel and Diatomaceous Earth
48:15 Factors Affecting Insecticide Efficacy
48:46 Stability, Persistence, and Formulations
51:02 Pest Behavior — Secondary and Tertiary Kill, Trophallaxis
53:04 Sanitation and IPM
54:19 Resistance Management — Rotation Strategies
56:30 Summary Points
57:44 Additional Resources
57:53 Q&A — Combination Product Resistance
59:53 Q&A — Flow of New Active Ingredients to Market
1:01:08 Q&A — Chlorantraniliprole and Non-Target Invertebrates
1:01:40 Q&A — IRAC Classification System
1:02:38 Q&A — Nicotinoids vs. Neonicotinoids
1:03:43 Q&A — Oral vs. Dermal Toxicity Routes
1:04:43 Q&A — Repellent vs. Non-Repellent Insecticides
1:05:32 Q&A — Essential Oils and 25B Exempt Products
---
## QUESTIONS & ANSWERS
**Q: What are the four basic modes of action that all insecticides fall into?**
A: According to Dr. Scharf, all insecticides disrupt target sites through one of just four mechanisms: stimulation (causing a target to fire more rapidly), blockage (shutting a target off), modulation (subtly changing the shape and function of a target, as pyrethroids do to sodium channels), and inhibition (preventing an enzyme from functioning, as organophosphates do to acetylcholinesterase). Understanding these four categories provides a framework for classifying any insecticide a professional might encounter.
**Q: Why are diamide insecticides like chlorantraniliprole considered especially safe for mammals?**
A: Diamides target muscular calcium channels that are highly specific to insects. They stimulate these channels, causing uncontrolled muscle contraction that burns up the insect's energy and leads to paralysis and death over several days. Their mammalian toxicity is so low that the EPA initially did not require a signal word, though manufacturers voluntarily adopted a "caution" label. Despite this safety profile, Scharf emphasized that applicators should still follow all safety guidelines when using them.
**Q: How does fipronil work at the neurological level?**
A: Fipronil is a phenylpyrazole that targets chloride channels in the insect nervous system. Under normal conditions, chloride channels allow negatively charged chloride ions into neurons, which has a calming or "mellowing" effect on nerve activity. Fipronil blocks these channels, removing that calming influence and causing excitation — the insect's nervous system essentially fires uncontrollably. Scharf demonstrated this visually using nerve recordings from dissected American cockroaches, showing a dramatic increase in firing rate and intensity after fipronil application.
**Q: What is the difference between repellent and non-repellent insecticides?**
A: Scharf explained that the distinction largely comes down to pyrethroids versus everything else. Pyrethroids are highly detectable to insects — he compared them to "pepper spray" — making them strongly repellent. Most other active ingredients, including fipronil and nicotinoids, are not nearly as detectable, which is why they are classified as non-repellent. This distinction became particularly prominent when non-repellent termiticides entered the market approximately 15 years before this presentation.
**Q: Why is resistance considered a major concern for cockroach management?**
A: Scharf identified resistance as likely the number one cause of callbacks in cockroach accounts. His research has documented cockroaches that can eat bait as their sole food source for a full month and survive. He noted that resistance is not limited to older chemistries — even combination products containing two active ingredients can face dual resistance when cockroach populations develop tolerance to both nicotinoids and pyrethroids simultaneously. He recommended rotating active ingredients every three months or even monthly to help manage resistance.
**Q: How do pest behaviors like trophallaxis and secondary kill affect insecticide efficacy?**
A: Scharf described three examples of behavior-mediated insecticide transfer. In cockroaches, secondary and tertiary kill occurs when one cockroach eats bait, excretes the insecticide, and other cockroaches consume the feces — research has shown the toxin can pass through two digestive tracts and still affect a third cockroach. Flea larvae can be exposed when adult fleas treated by veterinary products defecate insecticide-laden feces that larvae consume as nutrition. Social insects like termites and ants spread insecticides through trophallaxis (food sharing from both mouth and anus) and allogrooming, which is why slow-acting insecticides are preferred for these pests.
**Q: What role does sanitation play in insecticide effectiveness?**
A: Scharf emphasized that poor sanitation always makes insecticides less effective, regardless of how pest-specific modern products have become. Excess food in an account competes directly with bait placements, reducing consumption. Clutter creates untreatable harborage areas where pests can avoid contact with residual treatments. Dirt and grease on surfaces can physically bind and inactivate insecticides. He framed sanitation as a core component of the IPM mindset that directly enhances chemical efficacy.
**Q: What is the IRAC and how can it help pest management professionals?**
A: IRAC stands for the Insecticide Resistance Action Committee, a global organization with representatives from all major insecticide manufacturers. IRAC develops mode of action classifications that help professionals understand which products share the same target sites. Their classification chart, updated once or twice a year, shows the full landscape of available active ingredients organized by mode of action. Professionals can use this resource to plan effective product rotations by ensuring they alternate between different mode of action groups rather than simply switching trade names.
**Q: How do insect growth regulators work differently from neurotoxic insecticides?**
A: Unlike neurotoxins that target the nervous system for rapid effects, insect growth regulators disrupt the hormones and enzymes that control development and molting. Juvenile hormone analogs like pyriproxyfen mimic the insect's own juvenile hormone, leading to cuticle deformation and extra juvenile stages that cannot reproduce — causing the population to crash over time. Chitin synthesis inhibitors block the enzyme responsible for forming the exoskeleton during molting, leading to death during the molt or producing malformed cuticles that cause a characteristic "jackknife" effect in treated termites. Scharf noted that visible wing twist in cockroach populations is a reliable indicator that IGRs are already affecting that population.
**Q: Why are insecticides generally more toxic through ingestion than through contact exposure?**
A: Scharf explained that both the insect cuticle and mammalian skin serve as highly effective barriers to insecticide penetration. The insect cuticle is a complex, multi-layered, waterproof structure that contact insecticides must traverse to reach internal target sites. In contrast, the gut lining is a much thinner layer of cells, allowing ingested insecticides to penetrate far more readily. The same principle applies to mammals — human skin is an exceptionally resistant barrier compared to the gut, which is why oral exposure routes are almost always more toxic than dermal exposure for any given active ingredient.
**Q: What is the outlook for new active ingredients entering the urban pest management market?**
A: Scharf acknowledged that the flow of new active ingredients has slowed and the market has become heavily generic. While all major manufacturers maintain product pipelines, bringing a new active ingredient to market costs hundreds of millions to billions of dollars, and the economics must justify the investment. He noted that the urban pest management market represents a smaller slice of the overall pie compared to agriculture, which affects manufacturer incentives. Scharf encouraged the industry to advocate vocally to manufacturers about the need for new tools, particularly given growing resistance pressures.
---
## ADDITIONAL RESOURCES
*The following resources were referenced by the speaker during the presentation:*
- Scharf, M.E. and D.L. Suiter. "Insecticide Primer and Insecticide Mode of Action." *PCT Magazine*, 2011.
- Scharf, M.E. and D.L. Suiter. *Insecticide Basics for the Pest Management Professional.* University of Georgia publication (available free of charge; URL referenced in presentation slides).
- IRAC (Insecticide Resistance Action Committee) — Mode of action classification chart, updated annually.
---
## CHAIN OF CUSTODY
- **Source document:** Corrected SRT from Stage 1 (GTBOP_Transcript_2017-10-18_InsecticideMOA.srt)
- **Source verified:** 742 blocks, 2,968 lines, full read confirmed with coverage proof during Stage 1
- **Webinar date confirmed:** Via original program announcement email from Tami Adams Boyle
--- ---
docs/structural/2017-10-18-scharf-insecticide-moa/corrections.md
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# Transcript Corrections — Scharf, Insecticide MOA # SRT Transcript Correction Summary
## File: Principles of Insecticide Mode of Action — Mike Scharf
> **Placeholder** — Paste your Stage 1 pipeline output here. **Date Corrected:** February 10, 2026
**Webinar Date:** October 18, 2017
**Series:** Structural Pest Control
**Topic:** Entomology — Insecticide Classification and Mode of Action
**Speaker:** Dr. Michael Scharf, O.W. Rawlins Orkin Endowed Chair in Urban Entomology and Molecular Physiology, Department of Entomology, Purdue University, West Lafayette, IN
**Moderator:** Dr. Dan Suiter, Extension Entomologist, University of Georgia
--- ---
*Processed for UGA Center for Urban Agriculture / GTBOP Archives* ## SOURCE VERIFICATION
- **Original blocks:** 742
- **Corrected blocks:** 742 ✓ MATCH CONFIRMED
- **Time range:** 00:00:00,020 to 01:07:06,220
- **Runtime:** ~67 minutes
- **File reading:** COMPLETE ✓
- **Coverage proof:**
- Early [~1:45]: Speaker states overarching goal to improve general knowledge of how insecticides work; discusses nervous system targeting vs. insect growth regulators
- Middle [~40:00]: Discusses muscular calcium channels and diamide insecticides (chlorantraniliprole, cyantraniliprole); notes EPA initially required no signal word due to low mammalian toxicity
- Late [~55:00]: Identifies resistance as probably the #1 cause of callbacks in cockroach accounts; cockroaches observed surviving on bait as sole food source for a month; recommends rotating active ingredients every 3 months or monthly
---
## Corrections Applied
### Proper Nouns — Speaker Names
- "Dr. Sharf" → "Dr. Scharf" (Line 23)
- "Dan Suter" → "Dan Suiter" (Line 311)
- "Dave Oy" → "Dave Oi" (Line 2243) — Confirmed via webinar announcement: Dr. David Oi, USDA-ARS, Center for Medical, Agricultural and Veterinary Entomology, Gainesville, FL; presented "Fire Ants and Crazy Ants" in the same session
### Chemical/Product Names
- "chlorenterniliprol" → "chlorantraniliprole" (Line 559)
- "terniliprol" → "traniliprole" (Line 563 — continuation of "cyantraniliprole" split across blocks 140–141)
- "Metaflumazone" → "metaflumizone" (Line 1431)
- "Furilander and Sarlander" → "fluralaner and sarolaner" (Line 1499)
- "sulfoxyms or sulfoxifluor" → "sulfoximines or sulfoxaflor" (Line 1583)
- "spinosid" → "spinosad" (Line 1595)
- "chlorantraniliprol" → "chlorantraniliprole" (Line 1747)
- "cyan triniliprol" → "cyantraniliprole" (Line 1747)
- "pyroprosythin" → "pyriproxyfen" (Line 1883)
- "hydromethyl non" → "hydramethylnon" (Line 1951)
- "chlorphenipir" → "chlorfenapyr" (Line 1959)
- "sulfurofluoride" → "sulfuryl fluoride" (Line 1967)
- "disodium octoborate" → "disodium octaborate" (Line 1971)
- "chlorthenopyr" → "chlorfenapyr" (Line 2387)
- "chlorantrinoliprol" → "chlorantraniliprole" (Line 2691)
- "Amidocloprid" → "imidacloprid" (Line 2771)
### Technical Terms
- "semi-carbazone" → "semicarbazone" (Line 1435 — IRAC chemical subclass name)
- "spinosins" → "spinosyns" (Line 1347 — IRAC Group 5 class name)
- "aloe grooming" → "allogrooming" (Line 2247)
- "the nicotines target" → "the nicotinoids target" (Line 1663 — speaker consistently uses "nicotinoids" elsewhere; Whisper truncated the word)
- "Pubigants" → "Fumigants" (Line 1967)
- "acetylcholinesterase, which is a neurotransmitter" → "acetylcholine, which is a neurotransmitter" (Line 1287 — acetylcholinesterase is an enzyme, not a neurotransmitter; the speaker is clearly describing acetylcholine crossing the synapse to bind its receptor; Whisper appended "-esterase" to "acetylcholine")
### Grammar
- "Dr. Thank you very much Dan." → "Thank you very much, Dan." (Line 43 — "Dr." is a Whisper artifact from the end of the moderator's introduction bleeding into the speaker's first line; comma added after "Dan")
### Flagged for Verification
- None remaining. Line 1207 ("need this acetylcholinesterase enzyme") was reviewed against audio and confirmed as accurate speech. Speaker is casually listing target sites from a slide; phrasing is informal but intelligible and left as-is per the principle of maintaining natural speech patterns.
---
## Notes
### Speaker Not in Reference Roster
Dr. Michael Scharf (Purdue University) is not currently listed in the GTBOP Common Speakers reference. Recommend adding:
| Name | Affiliation |
|------|-------------|
| Dr. Michael Scharf | Purdue University, Urban Entomology |
### Additional Speaker Confirmed for Roster
Dr. David Oi is confirmed via webinar announcement as a GTBOP presenter but is not currently in the Common Speakers reference. Recommend adding:
| Name | Affiliation |
|------|-------------|
| Dr. David Oi | USDA-ARS, Center for Medical, Agricultural and Veterinary Entomology, Gainesville, FL |
### Nicotinoid vs. Neonicotinoid Terminology
The speaker intentionally uses "nicotinoids" (not "neonicotinoids") throughout most of the presentation. In the Q&A section (~01:02:46), he and Dr. Suiter discuss the distinction: nicotinoids structurally resemble nicotine, while neonicotinoids have evolved further structurally but still target the acetylcholine receptor. This is the speaker's deliberate classification framework and has not been altered.
### Webinar Date Confirmation
Date confirmed as October 18, 2017 via original program announcement email from Tami Adams Boyle. The event ran 7:00–10:00 AM EDT as part of the Structural Pest Control Webinar Series. Dr. Scharf's presentation "Principles of Insecticide Mode of Action" was paired with Dr. David Oi's "Fire Ants and Crazy Ants."
---
## SRT Format Compliance
✅ All timestamps preserved exactly as original
✅ All sequence numbers maintained (1–742)
✅ Blank lines between segments preserved
✅ Maximum 2 lines per subtitle segment maintained
✅ No segments merged or split
✅ Block count: 742 original = 742 corrected ✓
✅ Line count: 2,968 original = 2,968 corrected ✓
---
**Total Corrections:** 24 individual corrections across 24 lines
**Flagged for Verification:** 0 items (1 resolved via audio review)
**Processing:** Complete file (742 subtitle blocks, 2,968 lines)
docs/structural/2017-10-18-scharf-insecticide-moa/index.md
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- Insecticides - Insecticides
--- ---
# Dr. Michael Scharf — Principles of Insecticide Classification and Mode of Action # Insecticide Classification and Mode of Action
## GTBOP Structural Pest Control — October 18, 2017
**Webinar Date:** October 18, 2017 **Speaker:** Dr. Michael Scharf, O.W. Rawlins Orkin Endowed Chair in Urban Entomology and Molecular Physiology, Purdue University
**Speaker:** Dr. Michael Scharf, Purdue University, Department of Entomology **Moderator:** Dr. Dan Suiter, Extension Entomologist, University of Georgia
**Moderator:** Dr. Dan Suiter, Extension Entomologist, UGA **Duration:** ~67 minutes (1:07:06)
**Series:** Structural Pest Control **CEU Categories:** Georgia Cat 35 (Industrial/Structural); multi-state credits in 8 states and 3 Canadian provinces
**CEU Categories:** Category 35 (Industrial, Institutional, Structural and Health Related)
--- ---
## Deliverables ## Deliverables
| Deliverable | Stage | Description | | Stage | Deliverable | Status |
|-------------|-------|-------------| |-------|-------------|--------|
| [Archive Summary](archive-summary.md) | 2 | Narrative summary, YouTube timestamps, Q&A | | 1 | [Corrections Log](corrections.md) | Complete |
| [Prose Transcript](prose-transcript.md) | 5 | Full presentation in readable prose | | 2 | [Archive Summary](archive-summary.md) | Complete |
| [Transcript Corrections](corrections.md) | 1 | Correction log and verification | | 3 | [YouTube Version](platforms/youtube.md) | Complete |
| [YouTube Version](platforms/youtube.md) | 3 | Character-limited YouTube description | | 3 | [Website Version](platforms/website.md) | Complete |
| [Website Version](platforms/website.md) | 3 | Full web publication version | | 3 | [Extension Agent Version](platforms/ext-agent.md) | Complete |
| [Extension Agent Version](platforms/ext-agent.md) | 3 | CEU-focused asynchronous version | | 4 | [Quiz](activities/quiz.md) | Complete |
| [Quiz](activities/quiz.md) | 4 | Multiple choice assessment | | 4 | [Matching Exercises](activities/matching.md) | Complete |
| [Matching](activities/matching.md) | 4 | Term-to-definition exercises | | 5 | [Prose Transcript](prose-transcript.md) | Complete |
| [Corrected SRT](downloads.md) | 1 | Download corrected subtitle file | | — | [Corrected SRT](downloads.md) | Complete |
### Writing Resources ### Writing Resources
@@ -40,4 +40,13 @@ tags:
--- ---
*Processed for UGA Center for Urban Agriculture / GTBOP Archives* ## Session Overview
Dr. Michael Scharf of Purdue University presented a comprehensive overview of insecticide classification and mode of action designed to strengthen pest management professionals' understanding of how their chemical tools work. Scharf framed the practical importance of this knowledge around six themes: applicator and customer safety, accurate interpretation of trade literature, pollinator protection, resistance management, product sustainability, and the ability to design customized applications through situational pest management.
The presentation systematically covered five neurotoxic insecticide classifications — sodium channel agents, chloride channel agents, acetylcholine receptor agents, acetylcholinesterase inhibitors, and combination products — followed by four non-neurotoxic classifications including diamides, insect growth regulators, inhibitors of energy production, and cuticle dehydrating dusts. Scharf concluded with practical factors affecting insecticide performance, resistance management strategies, and a Q&A session moderated by Dr. Suiter.
---
*Source: Corrected SRT — GTBOP_Transcript_2017-10-18_InsecticideMOA.srt*
*Processed: 2026-03-17 | Pipeline v4.1*
docs/structural/2017-10-18-scharf-insecticide-moa/platforms/ext-agent.md
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# Extension Agent Version — Scharf, Insecticide MOA # GTBOP Webinar Archive — Extension Agent Resource
## Principles of Insecticide Mode of Action
> **Placeholder** — Paste your Stage 3 pipeline output here.
--- ---
*Processed for UGA Center for Urban Agriculture / GTBOP Archives* ### Webinar Information
| Field | Details |
|-------|---------|
| **Speaker** | Dr. Michael Scharf, Purdue University |
| **Moderator** | Dr. Dan Suiter, UGA Extension Entomologist |
| **Original Air Date** | October 18, 2017 |
| **Duration** | 1 hour, 7 minutes |
| **Series** | Getting the Best of Pests — Structural Pest Control |
---
### CEU Credit Information
**Georgia Applicator Category:**
- **Cat 35** — Industrial, Institutional, Structural and Health Related: **2 HPC**
**Credit Eligibility:** This archived presentation is suitable for asynchronous CEU delivery to licensed pest control operators holding Category 35 certification. Verify current CEU acceptance with the Georgia Department of Agriculture before scheduling.
**Sign-in sheet and CEU documentation:** Contact the UGA Center for Urban Agriculture or visit gabugs.uga.edu for current forms and procedures.
---
### Viewing Instructions for Asynchronous Use
1. Total viewing time is approximately 1 hour and 7 minutes, including the Q&A session.
2. Attendees must view the entire presentation to receive credit.
3. The presentation includes a 57-minute lecture followed by a 10-minute moderated Q&A.
4. A sign-in sheet must be completed and returned per standard GTBOP procedures.
---
### Content Summary
Dr. Michael Scharf of Purdue University covers insecticide classification and mode of action at a level appropriate for licensed pest control professionals. The presentation provides foundational knowledge that supports informed product selection, resistance management, and customer communication.
**Topics covered include:** a review of insect physiology as it relates to insecticide activity (nervous system, cuticle, digestive tract, tracheal system, musculature); the four basic modes of action (stimulation, blockage, modulation, inhibition); the LD50 concept and mammalian safety; five neurotoxic insecticide classifications (sodium channel agents, chloride channel agents, acetylcholine receptor agents, acetylcholinesterase inhibitors, combination products); four non-neurotoxic classifications (diamides, insect growth regulators, energy production inhibitors, cuticle dehydrating dusts); and practical factors affecting insecticide performance including formulations, pest behavior, sanitation, and resistance management through product rotation.
**The Q&A session addresses:** combination product resistance, new active ingredient development, IRAC classifications, nicotinoid vs. neonicotinoid terminology, oral vs. dermal toxicity routes, repellent vs. non-repellent insecticides, and essential oil-based products.
---
### Key Takeaways for Extension Programming
- All insecticides work through one of four basic mechanisms — a useful teaching framework for applicators at any experience level.
- Nine insecticide classifications (five neurotoxic, four non-neurotoxic) cover the full landscape of available tools.
- Diamides represent a notably safe chemistry class for mammals — EPA initially required no signal word.
- Resistance is identified as the probable #1 cause of callbacks in cockroach accounts; rotation every 3 months or monthly is recommended.
- The IRAC classification system is highlighted as a free, practical resource for planning product rotations by mode of action group.
- Sanitation and IPM practices are framed as direct enhancers of chemical efficacy, not just standalone strategies.
---
### Video Chapter Guide
For agents directing attendees to specific sections:
| Time | Topic |
|------|-------|
| 0:00 | Introduction and Speaker Credentials |
| 1:45 | Why Understanding Mode of Action Matters |
| 8:26 | Insect Physiology Overview |
| 14:02 | Insecticide Classification Basics |
| 17:51 | Four Basic Modes of Action |
| 19:41 | LD50 Concept and Mammalian Safety |
| 22:46 | Neurotoxic Insecticide Classifications Begin |
| 32:24 | Sodium Channel Insecticides |
| 34:12 | Chloride Channel Insecticides |
| 36:20 | Acetylcholine Receptor Insecticides |
| 38:04 | Combination Products |
| 39:07 | Non-Neurotoxic Insecticides Begin |
| 40:02 | Diamides |
| 41:42 | Insect Growth Regulators |
| 45:18 | Energy Production Inhibitors |
| 46:56 | Cuticle Dehydrating Dusts |
| 48:15 | Factors Affecting Insecticide Efficacy |
| 54:19 | Resistance Management |
| 57:53 | Q&A Session Begins |
---
### Additional Resources Referenced in Presentation
- Scharf & Suiter, "Insecticide Primer and Insecticide Mode of Action," *PCT Magazine*, 2011
- Scharf & Suiter, *Insecticide Basics for the Pest Management Professional*, UGA publication (free)
- IRAC Mode of Action Classification Chart — irac-online.org
---
*Getting the Best of Pests Webinar Series | University of Georgia Center for Urban Agriculture*
*For questions about this archive or CEU procedures, contact the Center for Urban Agriculture.*
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# Website Version — Scharf, Insecticide MOA # Principles of Insecticide Mode of Action
## GTBOP Structural Pest Control Webinar Series — Archive
> **Placeholder** — Paste your Stage 3 pipeline output here.
--- ---
**Webinar Date:** October 18, 2017
**Speaker:** Dr. Michael Scharf, O.W. Rawlins Orkin Endowed Chair in Urban Entomology and Molecular Physiology, Department of Entomology, Purdue University
**Moderator:** Dr. Dan Suiter, Extension Entomologist, University of Georgia
**Duration:** 1:07:06
**Series:** Getting the Best of Pests — Structural Pest Control Webinar Series
**CEU Credits:** GA — 2 HPC (Cat 35: Industrial, Institutional, Structural and Health Related)
---
## About This Presentation
Dr. Michael Scharf of Purdue University presented a comprehensive overview of insecticide classification and mode of action designed to strengthen pest management professionals' understanding of how their chemical tools work. Scharf framed the practical importance of this knowledge around six themes: applicator and customer safety, accurate interpretation of trade literature, pollinator protection, resistance management, product sustainability, and the ability to design customized applications through situational pest management.
Scharf began with a condensed review of insect physiology, covering the five systems most relevant to insecticide activity: the nervous system, the cuticle, the digestive tract, the tracheal system, and the musculature. He explained that insecticides interact with specific protein target sites through a key-and-lock relationship, and that all insecticide effects can be reduced to just four modes of action — stimulation, blockage, modulation, and inhibition. He introduced the LD50 concept and emphasized that modern insecticides are dramatically more toxic to insects than to mammals, with some classes like the diamides carrying such low mammalian toxicity that the EPA initially required no signal word.
The presentation then systematically covered five neurotoxic insecticide classifications: sodium channel agents (pyrethroids, indoxacarb, metaflumizone), chloride channel agents (fipronil, isoxazolines, abamectin), acetylcholine receptor agents (nicotinoids, sulfoximines, spinosyns), acetylcholinesterase inhibitors (organophosphates, carbamates), and combination products pairing nicotinoids with pyrethroids for potentiation effects. Scharf followed with four non-neurotoxic classifications: muscular calcium channel agents (diamides such as chlorantraniliprole and cyantraniliprole), insect growth regulators (juvenile hormone analogs like pyriproxyfen and chitin synthesis inhibitors), inhibitors of energy production (hydramethylnon, chlorfenapyr, sulfuryl fluoride, boric acid), and cuticle dehydrating dusts (silica gel, diatomaceous earth).
Scharf concluded by discussing practical factors that affect insecticide performance, including formulation types, pest behavior that can amplify efficacy through secondary and tertiary kill, the role of sanitation in an IPM framework, and resistance management. He identified resistance as likely the number one cause of callbacks in cockroach accounts and recommended rotating active ingredients every three months or even monthly. A Q&A session moderated by Dr. Suiter addressed combination product resistance risks, the flow of new active ingredients to market, the IRAC classification system, the distinction between nicotinoids and neonicotinoids, oral versus dermal toxicity, repellent versus non-repellent insecticides, and the growing consumer demand for essential oil-based products.
---
## Video Chapters
0:00 Introduction and Speaker Credentials
1:45 Why Understanding Mode of Action Matters
6:03 Presentation Outline
7:13 Additional Resources — PCT Article and UGA Publication
8:26 Insect Physiology Overview — Nervous System, Cuticle, Gut, Trachea, Muscles
14:02 Insecticide Classification Basics — Chemical Structure
16:01 Target Site and Mode of Action — Key and Lock Analogy
17:51 Four Basic Modes of Action — Stimulation, Blockage, Modulation, Inhibition
19:41 The LD50 Concept and Mammalian Safety
22:46 Overview of Neurotoxic and Non-Neurotoxic Classifications
23:36 The Insect Nervous System — Neurons, Synapses, Neurotransmitters
26:45 Neurophysiology Demonstration — Fipronil and Nerve Excitation
28:40 Nervous System Target Sites — Roadmap of Ion Channels and Receptors
32:24 Sodium Channel Insecticides — Pyrethroids, Indoxacarb, Metaflumizone
34:12 Chloride Channel Insecticides — Fipronil, Isoxazolines, Abamectin
36:20 Acetylcholine Receptor Insecticides — Nicotinoids, Sulfoximines, Spinosyns
37:28 Acetylcholinesterase Inhibitors — Organophosphates and Carbamates
38:04 Combination Products — Nicotinoid-Pyrethroid Potentiation
39:07 Non-Neurotoxic Insecticides Overview
40:02 Muscular Calcium Channel Agents — Diamides
41:42 Insect Growth Regulators — JH Analogs and Chitin Synthesis Inhibitors
45:18 Inhibitors of Energy Production — Hydramethylnon, Chlorfenapyr, Fumigants
46:56 Cuticle Dehydrating Dusts — Silica Gel and Diatomaceous Earth
48:15 Factors Affecting Insecticide Efficacy
48:46 Stability, Persistence, and Formulations
51:02 Pest Behavior — Secondary and Tertiary Kill, Trophallaxis
53:04 Sanitation and IPM
54:19 Resistance Management — Rotation Strategies
56:30 Summary Points
57:44 Additional Resources
57:53 Q&A — Combination Product Resistance
59:53 Q&A — Flow of New Active Ingredients to Market
1:01:08 Q&A — Chlorantraniliprole and Non-Target Invertebrates
1:01:40 Q&A — IRAC Classification System
1:02:38 Q&A — Nicotinoids vs. Neonicotinoids
1:03:43 Q&A — Oral vs. Dermal Toxicity Routes
1:04:43 Q&A — Repellent vs. Non-Repellent Insecticides
1:05:32 Q&A — Essential Oils and 25B Exempt Products
---
## Questions & Answers
**Q: What are the four basic modes of action that all insecticides fall into?**
A: According to Dr. Scharf, all insecticides disrupt target sites through one of just four mechanisms: stimulation (causing a target to fire more rapidly), blockage (shutting a target off), modulation (subtly changing the shape and function of a target, as pyrethroids do to sodium channels), and inhibition (preventing an enzyme from functioning, as organophosphates do to acetylcholinesterase). Understanding these four categories provides a framework for classifying any insecticide a professional might encounter.
**Q: Why are diamide insecticides like chlorantraniliprole considered especially safe for mammals?**
A: Diamides target muscular calcium channels that are highly specific to insects. They stimulate these channels, causing uncontrolled muscle contraction that burns up the insect's energy and leads to paralysis and death over several days. Their mammalian toxicity is so low that the EPA initially did not require a signal word, though manufacturers voluntarily adopted a "caution" label. Despite this safety profile, Scharf emphasized that applicators should still follow all safety guidelines when using them.
**Q: How does fipronil work at the neurological level?**
A: Fipronil is a phenylpyrazole that targets chloride channels in the insect nervous system. Under normal conditions, chloride channels allow negatively charged chloride ions into neurons, which has a calming or "mellowing" effect on nerve activity. Fipronil blocks these channels, removing that calming influence and causing excitation — the insect's nervous system essentially fires uncontrollably. Scharf demonstrated this visually using nerve recordings from dissected American cockroaches, showing a dramatic increase in firing rate and intensity after fipronil application.
**Q: What is the difference between repellent and non-repellent insecticides?**
A: Scharf explained that the distinction largely comes down to pyrethroids versus everything else. Pyrethroids are highly detectable to insects — he compared them to "pepper spray" — making them strongly repellent. Most other active ingredients, including fipronil and nicotinoids, are not nearly as detectable, which is why they are classified as non-repellent. This distinction became particularly prominent when non-repellent termiticides entered the market approximately 15 years before this presentation.
**Q: Why is resistance considered a major concern for cockroach management?**
A: Scharf identified resistance as likely the number one cause of callbacks in cockroach accounts. His research has documented cockroaches that can eat bait as their sole food source for a full month and survive. He noted that resistance is not limited to older chemistries — even combination products containing two active ingredients can face dual resistance when cockroach populations develop tolerance to both nicotinoids and pyrethroids simultaneously. He recommended rotating active ingredients every three months or even monthly to help manage resistance.
**Q: How do pest behaviors like trophallaxis and secondary kill affect insecticide efficacy?**
A: Scharf described three examples of behavior-mediated insecticide transfer. In cockroaches, secondary and tertiary kill occurs when one cockroach eats bait, excretes the insecticide, and other cockroaches consume the feces — research has shown the toxin can pass through two digestive tracts and still affect a third cockroach. Flea larvae can be exposed when adult fleas treated by veterinary products defecate insecticide-laden feces that larvae consume as nutrition. Social insects like termites and ants spread insecticides through trophallaxis (food sharing from both mouth and anus) and allogrooming, which is why slow-acting insecticides are preferred for these pests.
**Q: What role does sanitation play in insecticide effectiveness?**
A: Scharf emphasized that poor sanitation always makes insecticides less effective, regardless of how pest-specific modern products have become. Excess food in an account competes directly with bait placements, reducing consumption. Clutter creates untreatable harborage areas where pests can avoid contact with residual treatments. Dirt and grease on surfaces can physically bind and inactivate insecticides. He framed sanitation as a core component of the IPM mindset that directly enhances chemical efficacy.
**Q: What is the IRAC and how can it help pest management professionals?**
A: IRAC stands for the Insecticide Resistance Action Committee, a global organization with representatives from all major insecticide manufacturers. IRAC develops mode of action classifications that help professionals understand which products share the same target sites. Their classification chart, updated once or twice a year, shows the full landscape of available active ingredients organized by mode of action. Professionals can use this resource to plan effective product rotations by ensuring they alternate between different mode of action groups rather than simply switching trade names.
**Q: How do insect growth regulators work differently from neurotoxic insecticides?**
A: Unlike neurotoxins that target the nervous system for rapid effects, insect growth regulators disrupt the hormones and enzymes that control development and molting. Juvenile hormone analogs like pyriproxyfen mimic the insect's own juvenile hormone, leading to cuticle deformation and extra juvenile stages that cannot reproduce — causing the population to crash over time. Chitin synthesis inhibitors block the enzyme responsible for forming the exoskeleton during molting, leading to death during the molt or producing malformed cuticles that cause a characteristic "jackknife" effect in treated termites. Scharf noted that visible wing twist in cockroach populations is a reliable indicator that IGRs are already affecting that population.
**Q: Why are insecticides generally more toxic through ingestion than through contact exposure?**
A: Scharf explained that both the insect cuticle and mammalian skin serve as highly effective barriers to insecticide penetration. The insect cuticle is a complex, multi-layered, waterproof structure that contact insecticides must traverse to reach internal target sites. In contrast, the gut lining is a much thinner layer of cells, allowing ingested insecticides to penetrate far more readily. The same principle applies to mammals — human skin is an exceptionally resistant barrier compared to the gut, which is why oral exposure routes are almost always more toxic than dermal exposure for any given active ingredient.
**Q: What is the outlook for new active ingredients entering the urban pest management market?**
A: Scharf acknowledged that the flow of new active ingredients has slowed and the market has become heavily generic. While all major manufacturers maintain product pipelines, bringing a new active ingredient to market costs hundreds of millions to billions of dollars, and the economics must justify the investment. He noted that the urban pest management market represents a smaller slice of the overall pie compared to agriculture, which affects manufacturer incentives. Scharf encouraged the industry to advocate vocally to manufacturers about the need for new tools, particularly given growing resistance pressures.
---
## Additional Resources
*The following resources were referenced by the speaker during the presentation:*
- Scharf, M.E. and D.L. Suiter. "Insecticide Primer and Insecticide Mode of Action." *PCT Magazine*, 2011.
- Scharf, M.E. and D.L. Suiter. *Insecticide Basics for the Pest Management Professional.* University of Georgia publication (available free of charge; URL referenced in presentation slides).
- IRAC (Insecticide Resistance Action Committee) — Mode of action classification chart, updated annually. Visit [irac-online.org](https://irac-online.org).
---
*This archive is part of the Getting the Best of Pests Webinar Series, hosted by the University of Georgia Center for Urban Agriculture. For more information about the GTBOP program, visit gabugs.uga.edu.*
*Processed for UGA Center for Urban Agriculture / GTBOP Archives* *Processed for UGA Center for Urban Agriculture / GTBOP Archives*
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# YouTube Description — Scharf, Insecticide MOA Principles of Insecticide Mode of Action | Dr. Michael Scharf | GTBOP Structural Pest Control Webinar Series
> **Placeholder** — Paste your Stage 3 pipeline output here. Dr. Michael Scharf of Purdue University presents a comprehensive overview of insecticide classification and mode of action for pest management professionals. Scharf covers insect physiology fundamentals, the key-and-lock relationship between insecticides and target sites, and nine insecticide classifications — five neurotoxic and four non-neurotoxic. The presentation concludes with practical factors affecting performance including formulations, pest behavior, sanitation, and resistance management. Q&A moderated by Dr. Dan Suiter.
--- Presented: October 18, 2017
Series: Getting the Best of Pests — Structural Pest Control Webinar Series
Host: UGA Center for Urban Agriculture
CEU Credits: GA — 2 HPC (Cat 35)
*Processed for UGA Center for Urban Agriculture / GTBOP Archives* TIMESTAMPS
0:00 Introduction and Speaker Credentials
1:45 Why Understanding Mode of Action Matters
6:03 Presentation Outline
7:13 Additional Resources — PCT Article and UGA Publication
8:26 Insect Physiology Overview — Nervous System, Cuticle, Gut, Trachea, Muscles
14:02 Insecticide Classification Basics — Chemical Structure
16:01 Target Site and Mode of Action — Key and Lock Analogy
17:51 Four Basic Modes of Action — Stimulation, Blockage, Modulation, Inhibition
19:41 The LD50 Concept and Mammalian Safety
22:46 Overview of Neurotoxic and Non-Neurotoxic Classifications
23:36 The Insect Nervous System — Neurons, Synapses, Neurotransmitters
26:45 Neurophysiology Demonstration — Fipronil and Nerve Excitation
28:40 Nervous System Target Sites — Roadmap of Ion Channels and Receptors
32:24 Sodium Channel Insecticides — Pyrethroids, Indoxacarb, Metaflumizone
34:12 Chloride Channel Insecticides — Fipronil, Isoxazolines, Abamectin
36:20 Acetylcholine Receptor Insecticides — Nicotinoids, Sulfoximines, Spinosyns
37:28 Acetylcholinesterase Inhibitors — Organophosphates and Carbamates
38:04 Combination Products — Nicotinoid-Pyrethroid Potentiation
39:07 Non-Neurotoxic Insecticides Overview
40:02 Muscular Calcium Channel Agents — Diamides
41:42 Insect Growth Regulators — JH Analogs and Chitin Synthesis Inhibitors
45:18 Inhibitors of Energy Production — Hydramethylnon, Chlorfenapyr, Fumigants
46:56 Cuticle Dehydrating Dusts — Silica Gel and Diatomaceous Earth
48:15 Factors Affecting Insecticide Efficacy
48:46 Stability, Persistence, and Formulations
51:02 Pest Behavior — Secondary and Tertiary Kill, Trophallaxis
53:04 Sanitation and IPM
54:19 Resistance Management — Rotation Strategies
56:30 Summary Points
57:44 Additional Resources
57:53 Q&A — Combination Product Resistance
59:53 Q&A — Flow of New Active Ingredients to Market
1:01:08 Q&A — Chlorantraniliprole and Non-Target Invertebrates
1:01:40 Q&A — IRAC Classification System
1:02:38 Q&A — Nicotinoids vs. Neonicotinoids
1:03:43 Q&A — Oral vs. Dermal Toxicity Routes
1:04:43 Q&A — Repellent vs. Non-Repellent Insecticides
1:05:32 Q&A — Essential Oils and 25B Exempt Products
FREQUENTLY ASKED QUESTIONS
Q: What are the four basic insecticide modes of action?
A: All insecticides disrupt target sites through stimulation, blockage, modulation, or inhibition. Understanding these four mechanisms provides a framework for classifying any product a professional might encounter.
Q: Why are diamide insecticides considered especially safe for mammals?
A: Diamides target insect-specific muscular calcium channels. Their mammalian toxicity is so low that the EPA initially required no signal word, though manufacturers voluntarily adopted a "caution" label.
Q: Why is resistance a major concern in cockroach management?
A: Research has documented cockroaches surviving on bait as their sole food source for a month. Even combination products face dual resistance. Rotate active ingredients every three months or monthly.
Q: How does the IRAC help pest management professionals?
A: The Insecticide Resistance Action Committee classifies active ingredients by mode of action, helping professionals plan rotations between different target site groups rather than simply switching trade names.
Q: What is the difference between repellent and non-repellent insecticides?
A: The distinction largely comes down to pyrethroids versus everything else. Pyrethroids are highly detectable to insects — like "pepper spray" — while most other actives are not nearly as detectable.
RESOURCES
• Scharf & Suiter, "Insecticide Primer and Insecticide Mode of Action," PCT Magazine, 2011
• Scharf & Suiter, "Insecticide Basics for the Pest Management Professional," UGA publication
• IRAC Mode of Action Classification Chart: https://irac-online.org
#PestManagement #Insecticides #ModeOfAction #CEU #StructuralPestControl #IPM #UGA #GTBOP
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# Prose Transcript — Scharf, Insecticide MOA # Principles of Insecticide Classification and Mode of Action
## GTBOP Structural Pest Control Series — October 18, 2017
> **Placeholder** — Paste your Stage 5 pipeline output here. **Speaker:** Dr. Michael Scharf, O.W. Rawlins Orkin Endowed Chair in Urban Entomology and Molecular Physiology, Purdue University
**Moderator:** Dr. Dan Suiter, Extension Entomologist, University of Georgia
**Duration:** 1:07:06
--- ---
*Processed for UGA Center for Urban Agriculture / GTBOP Archives* ## Introduction
**Dan Suiter:** Welcome again, everyone. Dr. Michael Scharf is the O.W. Rawlins Orkin Endowed Chair in Urban Entomology and Molecular Physiology at Purdue University. He entered Purdue in 1986 as a freshman in agriculture and subsequently earned his BS, MS, and PhD degrees from Purdue University in 1991, 1993, and 1997. After graduation, Dr. Scharf spent time at the University of Nebraska and Cornell University as a postdoc in the University of Florida where he was a tenured professor for several years. In 2010, Mike returned to Purdue and his primary research interests at Purdue relate to understanding biochemical and physiological mechanisms insects that have practical implications for pest management. Welcome Dr. Scharf, the floor is yours.
**Mike Scharf:** Thank you very much, Dan. It's really nice to be here today and I definitely appreciate the invite to share some of this information with the urban pest management industry.
---
## Why Understanding Mode of Action Matters
So today I'll be talking about just some of the basics of insecticide classification and mode of action for pest management professionals. And I'll acknowledge right at the outset that this is probably not something that's on everybody's radar screen out there in the industry. And just one of my goals in this presentation is just to help, even if no matter what your experience level is with pesticides, just to help raise anyone's level of understanding for how these things work. So my goal in this presentation is just this one overarching goal, and that's to improve general knowledge of how insecticides work. So, if you're dealing with a product, you can ask yourself, does this product target the nervous system of the insect? And if so, in what way does it target it? Or does the product work in a completely different way like an insect growth regulator? These are things I'll get into in a little more depth as I go through this talk.
And so, knowing how these insecticide tools that we have available, how they actually work, this is essential knowledge for the industry. And so why is that? The first is just safety. So, some insecticide modes of action have lower non-target toxicity than others. So they affect insects more than they do mammals. Humans are mammals. And so there's the safety factor. Understanding how insecticides work can help with interpretation of advertising and trade literature which isn't always technically accurate, so it's good to have a little extra knowledge so you can interpret that trade literature. Pollinator health is really huge right now. It's becoming something that we all need to know about in the industry and how to protect pollinators. Especially with products like nicotinoids that actually move around in plants. And so if you're doing a lawn application, for example, the plants, flowering plants in the yard or the landscape can take up those nicotinoids and that can affect pollinators.
Resistance management is a really big factor. Knowing how to rotate products is really important and do other things that can help get around the resistance problem. Product sustainability — in the industry we're stewards of, we represent the manufacturers as well as the pest management industry. And you need to understand that every product, every insecticide product that makes it to the market, it costs hundreds of millions of dollars, if not more, billions of dollars to get to the market. And so, using products wisely so they have the longest market life is just good business sense for the whole industry.
Understanding how insecticides work can help design customized pesticide applications. And that goes along with situational pest management — designing customized applications with the right products for the right situation. Understanding how insecticides work and how they're formulated really comes into play with situational pest management. And then the last one here is just communicating with your customers and explaining to them how products work, but being able to do it in a way that communicates competence, that shows that you really understand what you're doing, you're going to be safe, you're going to protect pollinators. All these things are really important, I feel, and they all go together. And that's my motivation for putting together this particular talk, which I've given now several times over the last five years. And despite the technical nature of the information, I do get a lot of positive feedback on it. So hopefully everyone will feel the same today.
---
## Presentation Outline and Supporting Resources
So here's an outline of what I'll be presenting. I just covered some background and introductory information. If we want to know how insecticides work, we need to talk about some of the basics of insect physiology because that's how insecticides work. They disrupt the physiological function of the organism that they're targeting. And that's how they cause deleterious effects in those target organisms. I'll talk about some basics of insecticides and the modes of action and then break them up into two different groups: the neurotoxic insecticides and then the non-neurotoxic insecticides. And then I'll finish with some more of this practical knowledge like the situational pest management kind of information — kind of bringing things, concepts together and talking about factors that affect how well insecticides work.
So even if you don't follow along with everything in excruciating detail and it's all very new to you, the information that I'm presenting today, there are two additional sources of information. The first is an article published in 2011 called Insecticide Primer and Insecticide Mode of Action. This appeared in PCT Magazine. This was authored by myself and Dan Suiter. So there's some good supporting information to what I'll be presenting today. And then there's this publication that probably Dan and I, we co-authored, that we probably need to revise it soon — almost 10 years old now, Insecticide Basics for the Pest Management Professional. And this is available free of charge at this website shown at the bottom, sponsored by the University of Georgia. And I'll put these up at the end too in case you don't have time to write down this information here.
---
## Insect Physiology Overview
So, starting with insect physiology and just giving a really brief overview. If you were an entomology student like we have here in our department at Purdue University, you would take a whole semester course on insect physiology and biochemistry. I'm not going to cover that whole course today, but I've just compressed it down into a couple of slides here.
And there are just some critical physiological components of insects that is good to know about. These are the cuticle, the outer covering of the insect. The nervous system, which is basically what controls what's going on in the insects — the same thing happens in mammals and any animal has a nervous system that controls what's going on in the body. Muscles, of course, control movement and those muscles are controlled by the nervous system. The digestive system is where things happen with nutrition and food that's ingested in the insect, and there's this really important idea that the inside of the digestive tract is actually the outside of an organism. So it's kind of like we have this tube going down the middle of us that's actually outside of our bodies, and that's a barrier to digested insecticides. We talk about that too, and the respiratory system is really important as well. What we're talking about, for example, fumigant insecticides — that's how fumigants actually make it into the insect through the respiratory system.
### The Nervous System
So just talking about some of these features in more detail. First is the nervous system, and so in every insect they have a brain and there's a ganglion that controls their mouth parts and then this ventral nerve cord that runs along the ventral, the bottom side of their body. That's the central nervous system of the insect and then there are all these peripheral nerves that come out and go throughout the body. So all our neurotoxic insecticides that we have, they're targeting the nervous system throughout the body.
### The Cuticle
The insect cuticle is actually very complex and it's made up of a lot of different layers. So if we think about insect growth regulators — they're disrupting the formation of the cuticle and that can have really pronounced consequences on the insect, but we just disrupt the subtle nature of the cuticle. The cuticle is also important because it's a barrier to insecticides. So any contact insecticides that an insect picks up in the environment, they have to make it through all these layers of the cuticle in order to get to the inside where the nervous system is.
### The Digestive System
Over here is the gut. This is a really nice picture from my lab of a termite gut and you can see it's a pretty complex kind of thing. And again, here's this tube that goes down the middle of the gut which is actually the outside of the organism. So for example, insecticides that would be ingested, they have to penetrate through these barriers of the gut to make it into the body to affect their target sites. The gut is really complex.
### The Tracheal System
I'm jumping over here to the tracheal system. Within insects, they're a bit different than humans and other animals in that the tracheal system is this series of tubes, physical tubes that run through the whole body that bring air from the outside and deliver it to the inside of all the cells within an insect. That's different than animals and mammals like us — we have lungs, we breathe in the oxygen, we have gas exchange happening in our lungs, we have hemoglobin that carries all the oxygen around in our bodies. That's very different than what's actually happening in insects. Insects have this physical plumbing kind of system with all their trachea.
### Muscles and Calcium Channels
And then finally we have muscles, and so muscles are what control movement and responses to stimuli. Within the insect they have a really complex muscular system much like our own, and it's controlled by the nervous system of course. And we have some new insecticides that affect the insect calcium channels in their muscles, and this is a really important new mode of action that we have available that's actually very safe, it's very insect specific. And this would be insecticides like chlorantraniliprole or cyantraniliprole — really, those words just roll off your tongue, don't they? But those are insecticides that affect the insect muscles and they're very insect specific. It's good to know a little bit about musculature as well when we talk about this topic.
---
## Insecticide Classification and Target Sites
So, moving on from insect physiology, I next want to move over to insecticides and just some very basic concepts and then kind of moving towards modes of action, which gets a little more complex as we go on. But I promise not to get too technical, at least I'll try not to. It's a very technical topic so it's hard not to get too caught up in the technical details.
So just thinking about insecticide classification first. Insecticides have chemical structures that allow them to be classified. So we can think about, like if we think about all the different insect groups, they have different kinds of morphology, different forms that allow them to be classified in the different taxonomic groups of the insects like termites and roaches and flies and all the different groups. So here we just have some insecticides listed. There won't be a quiz over this, but you can see if you just look at their structures, they look very different. They're made up of different elements, different atoms make them up. And these different structures are what give them different functions and allow them to target different target sites, which I'll talk about next.
### The Key and Lock Analogy
But this idea of insecticide class, target site in the insect, and then the mode of action at that target site — those are all highly interconnected concepts. And it all comes back to the chemistry, unfortunately. Chemistry can be a really intimidating topic, but it all comes back to that.
So talking more about target site and mode of action — we can think about mode of action as almost like a key in a lock kind of scenario. So the insecticide has a very specific structure that allows it to interact with a very specific target site in the insect. Only that chemical is going to fit in that target site and then you imagine the lock would open and that's like the toxicity happening in the insect. You're disrupting the function of that physiological target site. And target sites are actual locations or physiological locations within the insects.
Of course, I talked about this lock and the key analogy, but in reality, what people who study insecticide mode of action and design new insecticides, they're thinking in terms of what you see down here at the bottom. The target site, it's a protein, usually within the insect. It's got three-dimensional structure like the lock. And the insecticides actually, chemical structures can dock up with that target and disrupt it. So it's actually way more complex than the key in the lock. But thanks to modern science we can predict these things very well. And it's actually very similar to drug discovery and drug design as well. So really the drug field and the insecticide field have a lot of overlap, believe it or not.
### Four Basic Modes of Action
But bringing it back to just these four very basic modes of action of the insecticides. Target sites are physiological locations. Modes of action are the actions of insecticides at those target sites. And we can really break it down into four modes of action. There are only four kinds that occur. So that would be stimulation or blockage, especially with nerves. So if you stimulate a nerve, you cause it to fire more rapidly. And if you block it, you basically shut it off — you keep it from firing. So we have pesticides that do both those things. We have other things that are called modulators, like pyrethroids. If you know anything about pyrethroids, they're modulators. So they're binding their target site and just kind of modulating its shape, changing the subtle ways that it functions. And then the last one here is inhibition. So we have a lot of insecticides that actually inhibit certain enzymes in the nervous system like acetylcholinesterase enzymes, which we may all know about are the target sites of organophosphates and carbamates, which I'll talk about too. But we have just these four very basic kinds of modes of action and it's very simple actually. When you just recognize there are only four ways that target sites can be disrupted.
### Understanding LD50
So there's another concept which is the concept of the LD50. LD50 is the lethal dose that would kill 50% of your test insect that you're looking at. So every insecticide has a different LD50 that's unique to that insecticide. Not all different insecticides have different dose ranges at which they're effective. That's just the very nature of the chemistry and the physiology that's going on.
So in general we can say that the relationship between product toxicity and LD50 is inverse. So the smaller the LD50, the higher the toxicity of a product. That means, so if an LD50 is small, that means that you only need a small dose to kill half of your test population. Insecticides that are more toxic or hazardous have lower LD50s.
And insecticides that we have today are actually much more toxic to insects and pests than they are to people and pets — some by over 10,000 times. So that's really amazing if you think about it, that thanks to modern science and advances and technology and human understanding, we're able to design insecticides today that — some are actually completely safe for mammals. I'll point out some of these as the talk goes on, but we have insecticide classes like the diamides which don't have a signal word, if you can imagine that. So their mammalian toxicity is so low that they are not required to have a signal word. Although, that doesn't mean that we shouldn't practice safety with them.
Another idea that's connected to this is that only very small amounts of insecticide that are placed in the environment of the pest actually reach their target site to cause toxicity. So the ratio is like billions to one, maybe even higher than that, of the actual amount of insecticide that goes out in the environment to what is contacted by the insect and travels through its body to reach the target site and have an effect. And a lot of that goes along with the insecticides just being so pest specific. So, I think we're moving in a really good direction as a whole in terms of being able to have safer products today. They have high mammalian LD50s and low insect LD50s.
---
## Neurotoxic Insecticides — Five Classifications
So moving on then to the different insecticide classifications by mode of action and different chemistry groups. We have insecticides that target the nervous system and there are five major classifications here that I'll talk about. And then we have insecticides that do not target the nervous system. So if you're just thinking about very broad classifications out there, we can break them down into things that target the nervous system and things that do not target the nervous system. And I'll talk about five classifications of neurotoxins and then four classifications of products that are not neurotoxins.
### How the Nervous System Works
So moving on — the insect nervous system is made up of millions of nerve cells. So it's pretty amazing when you think about it. When you think about nerve cells, individual nerve cells are what make up the whole nervous system. And so it's pretty amazing when you think about — hold your arm out and snap your finger. And think about the signal traveling through your whole nervous system, how fast that happens from your brain to the muscles in your finger. And then you heard the snap of your finger. That information traveled back from your ears to your brain. The nervous system moves at amazing speeds. Things happen incredibly fast. It's mind-boggling to think about.
Again, try not to get too technical here because this is not a neurobiology course, but we can say that information travels through the nervous system in the form of electrical impulses. So these impulses are moving at the speed of light, basically. So this is electrical energy moving down a nerve cell. And then, remember the nervous system is composed of millions of cells and there are gaps between these cells called synapses. And so the electrical information, when it reaches the end of a nerve cell, then it becomes chemical information in the form of a neurotransmitter that will cross that gap. And those neurotransmitters bind a receptor on the other side and those are very specific to the different kinds of neurotransmitters. And then instantly, at the speed of light, that becomes electrical information again moving down the next neuron. So we have impulses that move in the form of electricity through nerves and then those impulses cross gaps in the form of chemical messengers called neurotransmitters, and those neurotransmitters bind receptors that carry the information to the next neuron. And again, this is all happening at the speed of light. So pretty fascinating.
### Neurophysiology in the Lab
So in my lab, we study insecticide effects on the insect nervous system. How do we do that? We use a neurophysiology system, which is pretty fun and informative. You can do really good science with this kind of approach. And so here's an example — this is an American cockroach that's been dissected open by one of my students who has really good hands, hands of a surgeon as we joke and say. And you can see right here this is the ventral nerve cord of the American cockroach. And all these little squiggly lines here, those are the trachea I mentioned — those are the breathing tubes. You can't really see the nerve, but it's right down here in the middle. And we can stick an electrode onto that nerve cord and measure the electrical activity doing that. So this is an example of kind of like baseline activity. This is five minutes of recording, just the nerve firing away. And then if you apply an insecticide like fipronil — fipronil causes neuroexcitation. You can see here's an example of what happens to the nerve after that. It's firing at a much more rapid rate and with a higher magnitude of intensity. And so we can look at the nerves and see these effects very clearly with neurotoxins. So it's really informative and I think this kind of graphic really helps to bring it home and show some of the physiology that's going on.
### Target Site Roadmap
So moving along to insecticides that target sites in the nervous system — I'm going to talk about sodium channels, chloride channels, acetylcholine receptors, the acetylcholinesterase enzyme, and then we'll talk about combination products that target multiple locations at once. We have a lot more combination products available to us now and so it's good to understand how they work in collaboration.
So here are some of the target sites in the nervous system. I'm trying to show here where the different target sites are on neurons. We have chloride channels which occur after the synapse — the GABA receptor and the glutamate receptor are actually chloride channels. Here's the acetylcholine receptor — it's actually a sodium channel, lets sodium into neurons. Not to be confused with these other things called sodium channels — you realize that can be really confusing. But these sodium channels that are on the axon of the nerve, the long skinny part of it, these are the actual on switch for a nerve cell. So pyrethroids target these sodium channels. Here's a synapse, the acetylcholine receptor is here. Here's acetylcholine, which is a neurotransmitter that will cross that synapse and bind the acetylcholine receptor. And over here then you can imagine this would be a muscle that would be controlled by these nerves. And we have calcium channels that control muscle contraction — those are the targets of diamide insecticides. So all these different physiological target sites appear on different locations of the nerves. They're doing different things for the natural function of the nerves. So the insecticides, when they disrupt them, they'll have different effects that we can see.
And again, this is just a roadmap showing you the different physiological locations of the target sites and then the insecticide classes that affect them. Phenylpyrazoles like fipronil affect chloride channels, avermectins affect glutamate chloride channels, neonicotinoids and spinosyns affect the acetylcholine receptor, pyrethrins and pyrethroids and indoxacarb affect these axon sodium channels, diamides affect muscular calcium channels. And again, you can reference this information in some of the handouts that I'll show at the end.
---
### Classification 1: Sodium Channel Insecticides
So first off is the actual sodium channel insecticides. These sodium channels again, they're on the axon of the nerve — on this long skinny part of the nerve and they're really the on switch for the neuron. When they open, nerve impulses move in the form of electricity down the nerve.
So we have pyrethroids and also DDT and pyrethrins in this category. They stimulate sodium channels and cause excitation, so they'll cause that nerve to fire, which causes the insect to — I'm sure everybody has seen insects, for example, treated with pyrethrins. They get knocked down right away. So that's that incoordination of their nervous system caused by that hyper excitation from their sodium channels being stimulated.
We have oxadiazines — so this is indoxacarb, really big urban insecticides that we have. Indoxacarb affects the sodium channel but it blocks it. So it works in a completely different way, causes inhibition, and then the insect is actually paralyzed because its sodium channels don't work — the on switch is stuck in the off position, basically.
We also have a newer insecticide called metaflumizone, which is a semicarbazone. I know there are ectoparasite uses for this product and possibly some other urban product uses as well. It also blocks sodium channels. So at sodium channels we can stimulate them or block them depending on the different insecticide chemistries.
### Classification 2: Chloride Channel Insecticides
Moving along to chloride channels. Chloride channels are located along the neuron and they cause chloride to flow into neurons, which actually mellows them out. So chloride has a negative charge that kind of brings down the activity of the neuron under natural conditions.
But we have one of our biggest insecticides in the urban market — fipronil. Everybody knows that, I'm sure. It's actually off patent now. There's a lot of consumer products that have fipronil in them as well now. Fipronil blocks the chloride channel, so you're blocking this mellowing effect, which leads to excitation. And remember that nerve recording picture I showed you — we can apply fipronil and very quickly we can see the excitation happening in the nervous system.
We also have the isoxazolines — this new class of insecticides has a lot of anti-parasitic uses, especially on pet products. Names here are fluralaner and sarolaner. So this could be really big in the flea market. It's good to know because vets are prescribing these things. They're out there in probably really good quantities and they compete with fipronil, so we can see some cross-resistance issues between them. Something to keep an eye on. Those are still really new products. Again, those cause excitation.
We also have the avermectins like abamectin — a really good gel bait active ingredient that we have currently. Abamectin stimulates the chloride channels, which leads to inhibition — so that actually paralyzes the insect. It has the opposite effect of what fipronil would have, even though they're both affecting the same target site basically. They just do it in opposite ways.
### Classification 3: Acetylcholine Receptor Insecticides
Moving along to acetylcholine receptor insecticides. Remember, here we have one neuron with the electrical impulse traveling along it, we have a synapse here, and then we have another downstream neuron as we would say in the business. Acetylcholine is a neurotransmitter that crosses that synapse to bind its receptor on the next neuron.
And so we have mainly the nicotinoids — huge market share right now with these products. They're affecting the acetylcholine receptor by stimulating it and causing kind of excitation in the insect. And so we also have a new class called the sulfoximines, or sulfoxaflor — it's a new product you may be seeing. It acts at the same target site. And probably spinosyns, maybe for those working in the landscape market, have heard of spinosad — it basically affects the acetylcholine receptor in the same way.
### Classification 4: Acetylcholinesterase Inhibitors
We also have the acetylcholinesterase inhibitors, so they're acting to inhibit acetylcholinesterase — and that's the organophosphates and the carbamates, which we probably, anybody who's been in the industry a long time knows these products really well. They inhibit acetylcholinesterase and that causes excitation. This is not a really insect specific target site. These things work equally well against humans and mammals, and so we have a lot of restrictions on these kinds of products for a good reason.
### Classification 5: Combination Products
So next, moving along to the combination products. I think it's really important to talk about these. All of our combination products that we have, they all start with tea. I'm not going to name them here because I get confused really quickly, because I'm sure that's part of the logic in naming them all with tea. But they combine nicotinoids and pyrethroids. And they cause this effect called potentiation, which is actually hitting two target sites at once. So you get this synergy, this one plus one equals three kind of effect. So again, the nicotinoids target the acetylcholine receptor, then the pyrethroids that are in these combo products affect the sodium channels. So affecting two target sites at once gives this added kind of effect. These products generally work, I think, but just like anything, they're not immune to having resistance in the pest to them. Important to keep in mind.
---
## Non-Neurotoxic Insecticides — Four Classifications
So, that was things that targeted the nervous system. Now I want to quickly go through things that affect target sites outside the nervous system. And so these are the muscular calcium channels, insect growth regulators, inhibitors of energy production, and then the cuticle dehydrating dusts last.
### Muscular Calcium Channels (Diamides)
So the first one here is the muscular calcium channels. Again, this is where we have a nerve that's meeting up with a muscle — a muscle that's controlled by a nerve, they're all controlled by nerves. And we have these neuromuscular calcium channels that occur right at these locations. And when calcium comes out of them, that causes muscles to contract. So it's that simple — calcium equals muscle contraction.
And so these products we have here are the diamides. We have chlorantraniliprole and now cyantraniliprole and probably there are others on the way too. What these things do is they stimulate the neuromuscular calcium channel and that causes that muscle to contract for a few hours and then it burns up all its energy and then it's inhibited and the insect just kind of is laying there in a paralyzed state for a few days until all its energy is burned up and it eventually dies. And so these products are actually so safe for mammals that no signal words were required by the EPA initially. Now the manufacturers did a really smart thing in this case and said no, we're going to give them a caution signal word still, which I think is very wise. But these products are pretty safe. But that doesn't mean you should not follow safety guidelines when using them as well.
### Insect Growth Regulators
So talking next about insect growth regulators. Insects, as we all know, they have outer exoskeletons and they undergo metamorphosis. And we have different kinds of development that insects go through. You have the ametabolous development where the older insects look just like the younger ones except they're just bigger. We have incomplete metamorphosis, hemimetabolous insects like grasshoppers and roaches and termites, where really the only difference between adults and juveniles is that adults have wings and they're reproductively competent and the juveniles are not. And then we have complete metamorphosis like in mosquitoes and flies and caterpillars and those kinds of things where the immatures are larvae that don't really look anything like the adult.
And so my point in showing these is there's a lot of intricate changes that are going on in the insect cuticle as they move through development and that's all controlled by hormones and chitin synthesis enzymes that synthesize the chitin in the exoskeleton. Insect development is really intricate, and as an insect is going from egg to adult, there are all these different hormones that are changing their concentrations in the insect. And that's what's controlling — some are occurring together and some are occurring alone. And that's what controls these really subtle changes. And then eventually they molt. Lots of hormones here acting in concert that can be disrupted for insect control purposes. And that's where the insect growth regulators come into play.
We have the juvenile hormone analogs and the chitin synthesis inhibitors — those are the two big ones that we have in the urban market. Juvenile hormone analogs, they mimic juvenile hormone and this leads to cuticle deformation and actually extra juvenile stages, which — if you have juveniles that can't mate, that can cause the population to crash, so that's part of the strategy there. With IGRs like pyriproxyfen, for example, we see this wing twist happening in insects, like cockroaches especially, as they move through development. So if you go into a new account and you see individuals with wing twist, you can put good money down on the fact that IGRs are in that population affecting it. So you may not want to use them continuously, thinking of potential resistance issues. It might be okay to use a different product when you see wing twist in the population.
Chitin synthesis inhibitors — they inhibit the enzyme that causes the cuticle to form in the insect as it's going through the molting process, and chitin synthesis inhibitors can lead to death during molting. Some of the effects like you can see in termites treated with chitin synthesis inhibitors is they show this jackknife effect even well after they're done molting, and this is from their cuticle being malformed.
### Inhibitors of Energy Production
And inhibitors of energy production — a lot of products here, I don't want to get into them too much, but these things all target the mitochondria, which is like the energy in all cells of all organisms — plants, animals, insects, whatever, fish, bacteria — everybody's got mitochondria. And there's this thing called respiration happening here and different kinds of toxins are affecting different parts of the respiratory chain. I don't want to get into that in too much detail because there's a lot of different things going on here. But some of the products you may be familiar with are hydramethylnon — it's a cockroach bait. Chlorfenapyr, that's a good product that we have, it's got a food label, it's pretty safe. Fumigants like sulfuryl fluoride and others, methyl bromide — they inhibit mitochondria. And wood treatments like disodium octaborate tetrahydrate, DSOBTH, that actually can affect insect respiration, and boric acid is very similar, also affects insect respiration by disrupting this process. Although there's evidence also that boric acid can be abrasive, be like a desiccant and disrupt the actual gut lining.
### Cuticle Dehydrating Dusts
And lastly — congratulations, we've made it to the last mode of action here — we have the cuticle dehydrating dusts and it's pretty simple what they do. Here we have silica gel and diatomaceous earth which are just basically finely ground glass powder. On the outside of the insect surface there's this really fine waxy oily layer that helps protect the insect from water loss. So these things, they abrade the cuticle, they break it down, which leads to water loss in the insect and lethargy, for example. So you just can look at them and see they're not happy after they've been exposed to these things.
And we have diatomaceous earth which mainly contains silicon — that's the big active ingredient here, which actually comes from the ground exoskeletons of diatoms, which are organisms that have silicon in their outer exoskeleton. So it's a major source for these things. So that's how the dehydrating dusts work. I know that was really like a whirlwind tour of the different modes of action. But again, just trying to give you some basic information that you could follow up on later if you really wanted to. And again, I'll put up some references at the end that you can go to.
---
## Practical Factors Affecting Insecticide Performance
So the last part of the talk here — coming down the home stretch — there are several factors that affect how well insecticides work. And I just broke these down into stability and persistence, formulations, pest behavior, sanitation, and resistance. So this is where the toxicology of the insecticides comes into practice in these various areas.
### Stability, Persistence, and Formulations
So on the topic of stability and persistence — most insecticides are oily in nature, which helps them across the cuticle and membranes and reach their target sites within the insects. So if we think about we put oil and water, what happens? The two things partition in the phases. Usually the oil will float on top. And that's really the same thing that happens with a lot of our insecticides. They're very oily by their very nature. But unfortunately, in their pure raw form, insecticides not only would they be unsafe, but also they can degrade rapidly in UV light. So ultraviolet light can break them down and they can be lost in the environment. So even though they don't dissolve in water, they can move with water and end up moving to places where you didn't apply them. So that's why we have formulations.
And formulations are complex mixtures of the active ingredient, inert ingredients, and/or food attractants and stabilizers in the form of baits, for example. And these things, they enhance the stability and extend the longevity of the insecticide. They enhance safety, they make the product easier to handle or mix, and they keep the active ingredient dissolved in water effectively. And so some of our different formulations, which I'm sure everybody out there who is actually working in the industry on a day-to-day basis knows these things really intimately well — we have our bait insecticides, granulars, dusts, aerosols, fumigants, and then liquids. Of course, we have all these different forms that the insecticide will come in like the emulsifiable concentrate, wettable powder, microencapsulated, suspension concentrate, etc. So the formulations are physical factors, physical things that are added that are mixed with the insecticide active ingredient to help deliver it and make it safer and dissolve in water. We have to have formulations to make insecticides work.
### Pest Behavior
Another really interesting thing to think about is how pest behavior can impact how insecticides work. I just have three examples here, but I'm sure people who are out there working in the field and observing things can have other things to add.
With cockroaches we have secondary and tertiary kill. If we have a cockroach that eats a bait and it either excretes some of the bait in its excrement or it's dead and another roach feeds on it or another roach eats its feces, we can have secondary kill and even tertiary kill. It's even been shown that insecticides can pass through the digestive tracts of two roaches and if a third roach eats the feces from the second roach, it can still be affected in a tertiary way. That's pretty fascinating.
We have flea larvae that can be exposed to insecticides from their host, like a dog or a cat that's treated with a product that you would get from a vet, for example. And the adult fleas will defecate out the insecticide and the mature fleas in the nesting material will eat the feces of the adults — it's how they get some of their nutrition. And so they can be secondarily affected by insecticides through their behaviors, their natural behaviors that can be exploited.
And then another factor — social insects like termites and ants practice trophallaxis and allogrooming. So they're spreading food materials from both ends, from the mouth and the anus side. They're sharing materials. They're also grooming each other, and this can be a great way for insecticides to move from individual to individual. So typically we want slow-acting insecticides in these kinds of situations in order to affect the maximum number of individuals in a population.
### Sanitation
Briefly here, sanitation — we all know it's really important. Despite today's insecticides being mostly pest specific and even having very selective toxicity to insects, poor sanitation always makes them less effective. So this is where the IPM mindset really comes into play to help make insecticides more effective.
Excess food in an account will compete with bait — that's pretty logical. If we can eliminate that competing food, we can get more bait to be eaten by the pests we're trying to target. Clutter creates excess harborage that can't be treated. We've all been in that mega cockroach account that maybe looks like the top here where everything is moving, and you certainly can't treat all that surface. Legally we can't. And dirt and grease tie up insecticides too. So this is an extreme case here in the bottom, but the insecticide is going to be less effective in that environment. Absolutely no question. So this is where the IPM mindset comes into play with making insecticides more effective.
### Resistance
Another important factor here is resistance. So this is where toxicology interfaces with practice in a really big way. This is something I study — maybe I'm most well known for working on insecticide resistance. I would argue that resistance is probably the number one cause of callbacks in cockroach accounts. Some of the things we've seen in recent years are just amazing, even with baits. We've seen cockroaches that can eat bait as their only food source for a month and survive. Pretty mind-boggling.
Bedbugs — pyrethroid resistance is widespread, we know that. But there's also newer evidence of resistance to other active ingredients. Not picking on chlorfenapyr here, but the potential is there for resistance to not only this active ingredient, but to nicotinoids as well as others. It's just a really big problem. The pests are always adapting with resistance and we have to figure out how to stay ahead of it to have our products keep working.
One way to do that is product rotation — it seems to be key for long-term success. And even with mixture products, those mixture products that start with tea that combine two active ingredients, we even need to use those in rotation. This is a typical rotation scheme that we've been recommending for years for cockroaches. Every three months switch active ingredients, maybe even every month if you can do it. But we've also learned that it depends on the active ingredients you're using too. Not all active ingredients are going to be compatible, and unfortunately the science is really lacking here. We hope to publish some papers soon showing which products would work the best in combination in rotations. But that information is still evolving and it's something definitely I would encourage the industry to be paying attention to and asking for in the coming months and years.
---
## Summary
So that kind of brings me down the home stretch. My summary points here are insect physiology provides unique insecticide target sites, but also creates penetration barriers. I talked about five classifications of neurotoxic insecticides, so just try to keep that in mind that there are five, and you can follow up on what they are on your own time. And then with non-neurotoxic insecticides, there are four classifications here that we have. So if you know what these nine classes are, as a technician or a technical manager, you will be able to communicate this to your customers better and maybe communicate more competence and also maybe be more effective at pest management. I'm sure you will be more effective. And lastly, insecticide chemistry interacts with other factors like behavior and resistance and sanitation that impact both insecticide use and efficacy. So again, big take-home message here — increasing your knowledge in all these areas can make you a better pest manager. I'm completely sure of it.
So with that, I'll thank you for your attention and I'll put up this very last slide here. This is the two additional sources of information that you can go to for supporting information of what I presented here today. So thanks very much.
---
## Audience Discussion
**Dan Suiter:** All right, very good stuff, Mike. You commented on resistance there at the end. I think we may have to have you back for a webinar on resistance. Did you ever give a resistance webinar, Mike, in the past several years, or was it always a mode of action?
**Mike Scharf:** I did. I did give one on bedbugs and roaches. We've got more information now.
**Dan Suiter:** Okay. Well, I'll see you in Denver. I might have to hit you up on a something for next year. But we did have a few really good questions that came in, Mike. I'll kind of go through those. I don't know if we'll have time to get to all of them.
### On Combination Products and Resistance
**Dan Suiter:** I had one question here on combination products — since we're using combination products at lower doses, do we risk the potential of resistance to two chemistries at once?
**Mike Scharf:** I would say even though the manufacturers don't want to hear it, I would say yes. We've seen evidence of resistance to both active ingredients in select roach populations. Roaches that are resistant to both nicotinoids and pyrethroids — and that affects the product performance. So yes.
**Dan Suiter:** Is it a fair statement, Mike, that just the development of resistance is kind of inevitable with overuse of an active ingredient? Is that the inevitability of resistance?
**Mike Scharf:** Absolutely. I try not to pick on products because I think that resistance is possible to any product and we've seen it, and so it's just all a matter of appropriate use for lengths of time and intensities of selection. So it's possible always.
**Dan Suiter:** Yeah, I guess that's what those resistance management ideas you were talking about are so important.
### On New Active Ingredients
**Dan Suiter:** I had a question here — this is my question. Talk about the flow of new active ingredients into the pest control industry. It seems that over the years things have kind of slowed down and the industry is kind of generic heavy at this point. What's the horizon for new active ingredients that are coming into the industry? Do the big manufacturers — do they all have active ingredients that they're working on? Will we see new actives that are coming into the market?
**Mike Scharf:** Well, a lot of it depends on economics, of course, and I think all of our manufacturers have lots of things in the pipeline, it's just a matter of them being able to get it into the market and have it make money. The market's got to be right, and so they're very careful about how they move things and get them into the market. It's an expensive process, and we have to remember the urban slice of the pie is not as big as agriculture. This is just where we need a voice and need to keep after the manufacturers to let them know we need these things.
### On Chlorantraniliprole and Earthworms
**Dan Suiter:** I had a question here about chlorantraniliprole, Mike. Would it have an effect on nonvertebrates like earthworms?
**Mike Scharf:** That's a good question. I would suspect it probably does, but the way the labeling is, possibly not as much. It's a really unique molecule in terms of being super selective for even certain insect groups. It's possible there's some selectivity, I just haven't seen that info.
### On IRAC Classification
**Dan Suiter:** How about the IRAC? You didn't mention — this wasn't really a resistance talk — but can you mention IRAC and what that is for the audience?
**Mike Scharf:** Yeah, IRAC is I-R-A-C, the Insecticide Resistance Action Committee. And so all of our manufacturers have representatives who are part of IRAC globally, and they come up with different mode of action classifications that can help you decide how to rotate products. And so if you Google IRAC, I don't have their exact web address in front of me, but they have a really nice thing that they update once or twice a year with all the different chemistries available. So you can see the whole landscape of active ingredients available and you can get help there for choosing different modes of action to rotate through. That's one of their main functions.
### On Nicotinoids vs. Neonicotinoids
**Dan Suiter:** Another question here, Mike — you had talked about nicotinoid insecticides. One of the operators was familiar with the neonic. Is there a difference between the nicotinoids and the neonicotinoids?
**Mike Scharf:** I think it's just terminology. They're pretty much — so the nicotinoids look more like nicotine, which is what they were patterned after, and then the neonicotinoids, kind of they've evolved. They don't really look like nicotine anymore physically, but they still affect the acetylcholine receptor. Like clothianidin is a neonicotinoid, whereas —
**Dan Suiter:** Imidacloprid is a nicotinoid. I see. So nicotine is an insecticide.
**Mike Scharf:** Absolutely. We can talk about what happened the first time we chewed tobacco or smoked a cigarette way back as teenagers.
**Dan Suiter:** Yeah, I remember somebody at Purdue used to chew tobacco and put it inside of a jar and then put some caterpillars in there and it would kill them.
**Mike Scharf:** It's dangerous stuff.
### On Oral vs. Dermal Toxicity
**Dan Suiter:** Could you comment on the difference between the toxicity between — say you took the same active ingredient, it's typically more toxic via an oral route of entry, correct? As opposed to a contact toxicity?
**Mike Scharf:** Right. So yeah, all insecticides are going to be almost in all cases more active by ingestion than they are by dermal exposure.
**Dan Suiter:** And why is that?
**Mike Scharf:** Well, in terms of the insect, the cuticle, their outer cuticle, it's waterproof and it's got lots of layers. Whereas if you look at the gut — I showed that picture of the gut — it's just a thin layer of cells and stuff as opposed to the cuticle. And in mammals, our skin is an incredibly resistant barrier to insecticide and toxins, so things are always more active by ingestion.
### On Repellent vs. Non-Repellent Insecticides
**Dan Suiter:** And the final question here, Mike, and this is I think somewhat of a loaded question — the difference between repellent and non-repellent insecticides. I don't know that it's really that simple. Somebody here wants information on where they could go to find insecticides that are repellent and others that are non-repellent. Is it that simple?
**Mike Scharf:** I think probably in the trade magazines. I'm thinking back to when the non-repellent termiticides first hit the market 15 years ago. There was a lot of talk about that and I think the real distinction there is pyrethroids and everything else. Pyrethroids are like pepper spray to insects. All our other actives are not detected nearly as much.
### On Essential Oils and 25B Products
**Dan Suiter:** I have one final question here, Mike, before we let you go. So the essential oils seem to have really — the whole green revolution here over the past several years has really kind of taken off in terms of use of 25B exempt actives — rosemary and spearmint and cedar, that kind of thing. Can you comment on kind of — have any ideas on why that's happening in terms of — I guess you don't have the registration cost for one thing, but there seems to be a lot of products that have a lot of those essential oils in them now.
**Mike Scharf:** Right, well, consumers want them. The customers are — they have the ability to learn about these things more, and so there's the demand, I think, is probably what it comes down to. They can be effective.
**Dan Suiter:** Yeah, they're very good repellents. We've done a lot of work with them on ants. They're very repellent.
**Mike Scharf:** Right. They smell nice sometimes. You get aromatherapy in combination with —
**Dan Suiter:** Yeah, your house can smell like a peppermint candy.
---
## Closing
**Dan Suiter:** I think that's about it, Mike. We really appreciate this. I've seen this — this is something the industry just doesn't get enough of, and you really have put this together nicely. It's from A to Z here, it's really nice. So we appreciate your time and thanks everybody for paying attention. Again, don't log out — we're going to take a five-minute break now and get ready for ants. Appreciate it, Mike, and we'll see you in a couple weeks.
**Mike Scharf:** Yeah, thanks Dan. Thank you everybody.
---
*Transcript processed for UGA Center for Urban Agriculture / GTBOP Archives*
*Source: Corrected SRT (Stage 1) — GTBOP_Transcript_2017-10-18_InsecticideMOA.srt (742 blocks)*
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How This Toolkit Works Insecticide Basics for the Pest Management Professional — Bulletin Update
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Using These Documents Based on Dr. Michael Scharf's GTBOP Presentation (October 18, 2017)
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<h1 id="bulletin-writing-toolkit-overview-document-guide">Bulletin Writing Toolkit — Overview &amp; Document Guide<a class="headerlink" href="#bulletin-writing-toolkit-overview-document-guide" title="Permanent link">&para;</a></h1>
<h2 id="insecticide-basics-for-the-pest-management-professional-bulletin-update">Insecticide Basics for the Pest Management Professional — Bulletin Update<a class="headerlink" href="#insecticide-basics-for-the-pest-management-professional-bulletin-update" title="Permanent link">&para;</a></h2>
<h3 id="based-on-dr-michael-scharfs-gtbop-presentation-october-18-2017">Based on Dr. Michael Scharf's GTBOP Presentation (October 18, 2017)<a class="headerlink" href="#based-on-dr-michael-scharfs-gtbop-presentation-october-18-2017" title="Permanent link">&para;</a></h3>
<a href="../../tags/#tag:insecticides" class="md-tag">Insecticides</a> <p><strong>Prepared by:</strong> Rich Braman, UGA Cooperative Extension / Center for Urban Agriculture
<strong>For:</strong> Dr. Dan Suiter (UGA) &amp; Dr. Michael Scharf (Purdue University)</p>
<a href="../../tags/#tag:scharf" class="md-tag">Scharf</a>
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<h1 id="insecticide-basics-bulletin-writing-toolkit">Insecticide Basics Bulletin — Writing Toolkit<a class="headerlink" href="#insecticide-basics-bulletin-writing-toolkit" title="Permanent link">&para;</a></h1>
<p><strong>Source Webinar:</strong> Dr. Michael Scharf — Principles of Insecticide Classification and Mode of Action (October 18, 2017)
<strong>Collaborators:</strong> Dr. Dan Suiter (UGA), Dr. Michael Scharf (Purdue)
<strong>Target Publication:</strong> UGA extension bulletin on insecticide classification and mode of action for pest control professionals</p>
<hr /> <hr />
<h2 id="how-this-toolkit-works">How This Toolkit Works<a class="headerlink" href="#how-this-toolkit-works" title="Permanent link">&para;</a></h2> <p>This package contains three documents designed to work together as a writing toolkit for the bulletin revision, all derived exclusively from the corrected and verified prose transcript of Mike's October 2017 GTBOP presentation.</p>
<p>This set of writing resources reorganizes Dr. Scharf's GTBOP presentation into a publication-ready structure. All content derives exclusively from the corrected transcript — no external information has been introduced.</p>
<table>
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<th>Document</th>
<th>Purpose</th>
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<td><a href="outline/">Bulletin Outline</a></td>
<td>Publication structure with content notes, transcript pointers, and writing notes</td>
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<td><a href="compendium/">Reference Compendium</a></td>
<td>Consolidated tables of insecticide classes, active ingredients, MOA groups, and terminology</td>
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<td><a href="source-guide/">Source Guide</a></td>
<td>Maps publication sections to exact transcript locations and video timestamps</td>
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<h3 id="using-these-documents">Using These Documents<a class="headerlink" href="#using-these-documents" title="Permanent link">&para;</a></h3>
<p>The <strong>Outline</strong> is your drafting roadmap — it tells you what goes where and flags areas needing current updates with ⚠️ markers. The <strong>Compendium</strong> is your quick-reference sheet for verifying classifications and relationships while writing. The <strong>Source Guide</strong> tells you exactly where to look in the video or transcript to verify any specific claim.</p>
<p>⚠️ markers indicate content that may need updating since the 2017 presentation. These are flags for the subject matter experts, not corrections — the writing resources preserve what the speaker actually said.</p>
<hr /> <hr />
<p><em>Source: GTBOP Structural Pest Control Series / Processed for UGA Center for Urban Agriculture</em></p> <h3 id="1-bulletin-draft-outline">1. Bulletin Draft Outline<a class="headerlink" href="#1-bulletin-draft-outline" title="Permanent link">&para;</a></h3>
<p>Reorganizes Mike's conversational presentation flow into a publication-ready six-part structure. Each section has content notes, key details, transcript pointers, and writing notes flagging where things may need updating (neonicotinoid regulation, methyl bromide phase-out, etc.). The editorial notes at the end call out which Q&amp;A exchanges are strong candidates for integration into the body text rather than staying as standalone Q&amp;A.</p>
<h3 id="2-quick-reference-compendium">2. Quick Reference Compendium<a class="headerlink" href="#2-quick-reference-compendium" title="Permanent link">&para;</a></h3>
<p>Nine consolidated tables extracting every classification, product, target site, field indicator, and terminology definition Mike mentioned. The master classification table (Table 1) is essentially a draft of the summary table that could appear in the finished bulletin. Table 6 on the insect-specificity spectrum and the "same target site, opposite effects" cross-reference are the kind of things that make a reference bulletin actually useful on the truck.</p>
<h3 id="3-source-guide">3. Source Guide<a class="headerlink" href="#3-source-guide" title="Permanent link">&para;</a></h3>
<p>Maps every proposed bulletin section to the exact transcript heading and approximate video timestamp. Also flags which content came exclusively from the Q&amp;A with Dan — eleven topics that would be missed if someone only worked from the prepared slides. The flow comparison table at the end shows how the webinar's live sequence was restructured for publication logic.</p>
<hr />
<p>Everything traces back to the corrected prose transcript as the single source of truth, so nothing in these documents introduces outside information. Items marked with ⚠️ flag spots where 2017 content will need current updates.</p>
<hr />
<p><em>Prepared from GTBOP webinar archive materials for UGA Center for Urban Agriculture.</em></p>
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<li class="md-nav__item">
<a href="#insecticide-moa-webinar-bulletin-update" class="md-nav__link">
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Insecticide MOA Webinar → Bulletin Update
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Purpose
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How to Use
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Mapping Table
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Content That Comes Exclusively from Q&amp;A
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Presentation Flow vs. Bulletin Structure
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Companion Documents
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@@ -4181,13 +4380,455 @@
<h1 id="source-guide-insecticide-basics">Source Guide — Insecticide Basics<a class="headerlink" href="#source-guide-insecticide-basics" title="Permanent link">&para;</a></h1> <h1 id="bulletin-source-guide-transcript-section-mapping">Bulletin Source Guide — Transcript Section Mapping<a class="headerlink" href="#bulletin-source-guide-transcript-section-mapping" title="Permanent link">&para;</a></h1>
<blockquote> <h2 id="insecticide-moa-webinar-bulletin-update">Insecticide MOA Webinar → Bulletin Update<a class="headerlink" href="#insecticide-moa-webinar-bulletin-update" title="Permanent link">&para;</a></h2>
<p><strong>Placeholder</strong> — Paste your Stage 6 source guide here.</p> <p><strong>Prepared by:</strong> Rich Braman, UGA Cooperative Extension / Center for Urban Agriculture
</blockquote> <strong>For:</strong> Dr. Dan Suiter &amp; Dr. Michael Scharf — Writing reference
<strong>Source:</strong> GTBOP_ProseTranscript_2017-10-18_InsecticideMOA.md</p>
<hr /> <hr />
<p><em>Source: Dr. Michael Scharf, GTBOP Structural — October 18, 2017</em> <h2 id="purpose">Purpose<a class="headerlink" href="#purpose" title="Permanent link">&para;</a></h2>
<em>Processed for UGA Center for Urban Agriculture / GTBOP Archives</em></p> <p>This guide maps each proposed bulletin section (from the Bulletin Draft Outline) to the specific section of the prose transcript and the approximate video timestamps where that content appears. Use this to:</p>
<ul>
<li>Quickly locate Mike's exact wording on any topic</li>
<li>Verify that bulletin content stays faithful to the source</li>
<li>Find passages to quote, paraphrase, or expand upon</li>
<li>Identify where Mike's Q&amp;A responses add content beyond his prepared slides</li>
</ul>
<hr />
<h2 id="how-to-use">How to Use<a class="headerlink" href="#how-to-use" title="Permanent link">&para;</a></h2>
<p>The <strong>Transcript Section</strong> column tells you which heading to search for in the prose transcript file. The <strong>Video Timestamp</strong> column gives the approximate time range if you need to re-watch the original recording. The <strong>Content Type</strong> column indicates whether the material comes from the prepared presentation or from the Q&amp;A discussion with Dan.</p>
<hr />
<h2 id="mapping-table">Mapping Table<a class="headerlink" href="#mapping-table" title="Permanent link">&para;</a></h2>
<table>
<thead>
<tr>
<th>Bulletin Section</th>
<th>Transcript Section</th>
<th>Video Timestamp</th>
<th>Content Type</th>
<th>Notes</th>
</tr>
</thead>
<tbody>
<tr>
<td><strong>PART I: Why Understanding MOA Matters</strong></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr>
<td>1.1 Safety &amp; non-target toxicity</td>
<td>"Why Understanding Mode of Action Matters" + "Understanding LD50"</td>
<td>~2:55–5:35 + ~19:50–22:45</td>
<td>Presentation</td>
<td>Safety framing at start; LD50 details in classification section</td>
</tr>
<tr>
<td>1.2 Interpreting trade literature</td>
<td>"Why Understanding Mode of Action Matters"</td>
<td>~3:30–3:45</td>
<td>Presentation</td>
<td>Brief mention — one sentence</td>
</tr>
<tr>
<td>1.3 Pollinator protection</td>
<td>"Why Understanding Mode of Action Matters"</td>
<td>~3:36–4:00</td>
<td>Presentation</td>
<td>Brief but important; expand with current info</td>
</tr>
<tr>
<td>1.4 Resistance management</td>
<td>"Resistance" + multiple Q&amp;A sections</td>
<td>~54:20–56:30 + ~57:55–59:50</td>
<td>Both</td>
<td>Extensive Q&amp;A content supplements presentation</td>
</tr>
<tr>
<td>1.5 Product sustainability &amp; communication</td>
<td>"Why Understanding Mode of Action Matters" + Q&amp;A on new AIs</td>
<td>~4:15–5:50 + ~59:55–1:01:10</td>
<td>Both</td>
<td>Economics from Q&amp;A adds industry context</td>
</tr>
<tr>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr>
<td><strong>PART II: Insect Physiology</strong></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr>
<td>2.1 Overview of relevant physiology</td>
<td>"Insect Physiology Overview" (all subsections)</td>
<td>~8:25–13:58</td>
<td>Presentation</td>
<td>Compressed physiology primer</td>
</tr>
<tr>
<td>2.2 How the nervous system works</td>
<td>"How the Nervous System Works"</td>
<td>~23:45–26:45</td>
<td>Presentation</td>
<td>Electrical + chemical transmission; synapse explanation</td>
</tr>
<tr>
<td>2.3 Neurophysiology demonstration</td>
<td>"Neurophysiology in the Lab"</td>
<td>~26:50–28:40</td>
<td>Presentation</td>
<td>Cockroach nerve cord + fipronil electrophysiology</td>
</tr>
<tr>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr>
<td><strong>PART III: Classification Fundamentals</strong></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr>
<td>3.1 Chemical structure &amp; classification</td>
<td>"Insecticide Classification and Target Sites"</td>
<td>~14:00–15:15</td>
<td>Presentation</td>
<td>Structure → function → target site relationship</td>
</tr>
<tr>
<td>3.2 Key and lock analogy</td>
<td>"The Key and Lock Analogy"</td>
<td>~16:00–17:50</td>
<td>Presentation</td>
<td>Key-lock + molecular docking + drug design parallel</td>
</tr>
<tr>
<td>3.3 Four basic modes of action</td>
<td>"Four Basic Modes of Action"</td>
<td>~17:50–19:35</td>
<td>Presentation</td>
<td>Stimulation, blockage, modulation, inhibition</td>
</tr>
<tr>
<td>3.4 Understanding LD50</td>
<td>"Understanding LD50"</td>
<td>~19:40–22:45</td>
<td>Presentation</td>
<td>Inverse relationship; mammalian safety; billionths ratio</td>
</tr>
<tr>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr>
<td><strong>PART IV: Neurotoxic Insecticides</strong></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr>
<td>4.1 Target site roadmap</td>
<td>"Target Site Roadmap"</td>
<td>~28:40–32:15</td>
<td>Presentation</td>
<td>Visual overview of all target site locations on neuron</td>
</tr>
<tr>
<td>4.2 Sodium channel insecticides</td>
<td>"Classification 1: Sodium Channel Insecticides" + Q&amp;A repellency</td>
<td>~32:20–34:10 + ~1:04:55–1:05:15</td>
<td>Both</td>
<td>Pyrethroids/pyrethrins, indoxacarb, metaflumizone; "pepper spray" from Q&amp;A</td>
</tr>
<tr>
<td>4.3 Chloride channel insecticides</td>
<td>"Classification 2: Chloride Channel Insecticides"</td>
<td>~34:10–36:20</td>
<td>Presentation</td>
<td>Fipronil, isoxazolines, abamectin; opposite effects at same site</td>
</tr>
<tr>
<td>4.4 Acetylcholine receptor insecticides</td>
<td>"Classification 3: Acetylcholine Receptor Insecticides" + Q&amp;A nicotinoid terminology</td>
<td>~36:20–37:30 + ~1:02:40–1:03:40</td>
<td>Both</td>
<td>Neonics, sulfoximines, spinosyns; terminology clarification from Q&amp;A</td>
</tr>
<tr>
<td>4.5 Acetylcholinesterase inhibitors</td>
<td>"Classification 4: Acetylcholinesterase Inhibitors"</td>
<td>~37:28–38:02</td>
<td>Presentation</td>
<td>OPs and carbamates; not insect-specific; brief section</td>
</tr>
<tr>
<td>4.6 Combination products</td>
<td>"Classification 5: Combination Products" + Q&amp;A on dual resistance</td>
<td>~38:03–39:10 + ~58:25–59:00</td>
<td>Both</td>
<td>"Start with tea"; potentiation; confirmed dual resistance in Q&amp;A</td>
</tr>
<tr>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr>
<td><strong>PART V: Non-Neurotoxic Insecticides</strong></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr>
<td>5.1 Diamides (calcium channels)</td>
<td>"Muscular Calcium Channels (Diamides)" + Q&amp;A on earthworms</td>
<td>~39:55–41:30 + ~1:01:05–1:01:40</td>
<td>Both</td>
<td>Safety profile; contraction → depletion timeline; earthworm selectivity from Q&amp;A</td>
</tr>
<tr>
<td>5.2 Insect growth regulators</td>
<td>"Insect Growth Regulators"</td>
<td>~41:40–45:20</td>
<td>Presentation</td>
<td>JH analogs + CSIs; metamorphosis types; wing twist; jackknife effect</td>
</tr>
<tr>
<td>5.3 Energy production inhibitors</td>
<td>"Inhibitors of Energy Production"</td>
<td>~45:20–46:50</td>
<td>Presentation</td>
<td>Mitochondria targeting; hydramethylnon, chlorfenapyr, fumigants, borates</td>
</tr>
<tr>
<td>5.4 Cuticle dehydrating dusts</td>
<td>"Cuticle Dehydrating Dusts"</td>
<td>~47:00–48:15</td>
<td>Presentation</td>
<td>Silica gel, DE; physical mode of action; diatom origin</td>
</tr>
<tr>
<td></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr>
<td><strong>PART VI: Practical Factors</strong></td>
<td></td>
<td></td>
<td></td>
<td></td>
</tr>
<tr>
<td>6.1 Stability &amp; formulations</td>
<td>"Stability, Persistence, and Formulations"</td>
<td>~48:45–51:00</td>
<td>Presentation</td>
<td>Lipophilic nature; UV degradation; formulation types and functions</td>
</tr>
<tr>
<td>6.2 Pest behavior</td>
<td>"Pest Behavior"</td>
<td>~51:02–53:05</td>
<td>Presentation</td>
<td>Secondary/tertiary kill; flea larvae; trophallaxis/allogrooming</td>
</tr>
<tr>
<td>6.3 Sanitation &amp; IPM</td>
<td>"Sanitation"</td>
<td>~53:05–54:20</td>
<td>Presentation</td>
<td>Food competition, clutter, grease; IPM mindset</td>
</tr>
<tr>
<td>6.4 Resistance (expanded)</td>
<td>"Resistance" + Q&amp;A segments</td>
<td>~54:20–56:30 + multiple Q&amp;A</td>
<td>Both</td>
<td>Rotation; cockroach bait resistance; IRAC; inevitability</td>
</tr>
<tr>
<td>6.5 Oral vs. dermal toxicity</td>
<td>Q&amp;A: "On Oral vs. Dermal Toxicity"</td>
<td>~1:03:55–1:04:45</td>
<td>Q&amp;A only</td>
<td>Cuticle vs. gut barriers; mammalian skin resistance</td>
</tr>
<tr>
<td>6.6 Essential oils &amp; 25B</td>
<td>Q&amp;A: "On Essential Oils and 25B Products"</td>
<td>~1:05:30–1:06:40</td>
<td>Q&amp;A only</td>
<td>Consumer demand; repellent efficacy; registration cost advantage</td>
</tr>
</tbody>
</table>
<hr />
<h2 id="content-that-comes-exclusively-from-qa">Content That Comes Exclusively from Q&amp;A<a class="headerlink" href="#content-that-comes-exclusively-from-qa" title="Permanent link">&para;</a></h2>
<p>The following material was only discussed during the Q&amp;A exchange with Dan and would be missed if working only from the prepared presentation portion of the transcript:</p>
<table>
<thead>
<tr>
<th>Topic</th>
<th>Q&amp;A Transcript Section</th>
<th>Why It Matters for the Bulletin</th>
</tr>
</thead>
<tbody>
<tr>
<td>Dual resistance to combo products</td>
<td>"On Combination Products and Resistance"</td>
<td>Confirms resistance to both AIs in field populations — critical practitioner info</td>
</tr>
<tr>
<td>Inevitability of resistance</td>
<td>Same section</td>
<td>"Possible always" — frames the urgency of rotation</td>
</tr>
<tr>
<td>New AI pipeline economics</td>
<td>"On New Active Ingredients"</td>
<td>Urban market size limits manufacturer investment — industry context</td>
</tr>
<tr>
<td>IRAC as a practitioner tool</td>
<td>"On IRAC Classification"</td>
<td>Actionable resource for product rotation decisions</td>
</tr>
<tr>
<td>Nicotinoid vs. neonicotinoid terminology</td>
<td>"On Nicotinoids vs. Neonicotinoids"</td>
<td>Clears up common confusion; imidacloprid vs. clothianidin example</td>
</tr>
<tr>
<td>Chlorantraniliprole earthworm selectivity</td>
<td>"On Chlorantraniliprole and Earthworms"</td>
<td>Unique selectivity even among invertebrates — safety story</td>
</tr>
<tr>
<td>Oral vs. dermal toxicity explanation</td>
<td>"On Oral vs. Dermal Toxicity"</td>
<td>Foundational concept not covered in prepared talk</td>
</tr>
<tr>
<td>Repellent = pyrethroids, non-repellent = everything else</td>
<td>"On Repellent vs. Non-Repellent Insecticides"</td>
<td>Clean practical distinction for practitioners</td>
</tr>
<tr>
<td>Essential oils / 25B market drivers</td>
<td>"On Essential Oils and 25B Products"</td>
<td>Consumer demand and green market trends</td>
</tr>
<tr>
<td>Nicotine as insecticide (tobacco anecdote)</td>
<td>Within nicotinoid terminology discussion</td>
<td>Memorable historical connection</td>
</tr>
<tr>
<td>Scharf's prior resistance webinar</td>
<td>Opening Q&amp;A exchange</td>
<td>Suggests companion content exists for the resistance bulletin</td>
</tr>
</tbody>
</table>
<hr />
<h2 id="presentation-flow-vs-bulletin-structure">Presentation Flow vs. Bulletin Structure<a class="headerlink" href="#presentation-flow-vs-bulletin-structure" title="Permanent link">&para;</a></h2>
<p>The webinar followed this sequence (left), which differs from the proposed bulletin structure (right):</p>
<table>
<thead>
<tr>
<th>Webinar Order</th>
<th>→</th>
<th>Proposed Bulletin Order</th>
</tr>
</thead>
<tbody>
<tr>
<td>1. Why MOA matters (motivation)</td>
<td>→</td>
<td>Part I: Why MOA Matters (motivation)</td>
</tr>
<tr>
<td>2. Insect physiology overview</td>
<td>→</td>
<td>Part II: Insect Physiology (foundation)</td>
</tr>
<tr>
<td>3. Insecticide classification basics</td>
<td>→</td>
<td>Part III: Classification Fundamentals</td>
</tr>
<tr>
<td>4. LD50 concept</td>
<td>→</td>
<td>Moved into Part III (Section 3.4)</td>
</tr>
<tr>
<td>5. Neurotoxic classes (5)</td>
<td>→</td>
<td>Part IV: Neurotoxic Insecticides</td>
</tr>
<tr>
<td>6. Non-neurotoxic classes (4)</td>
<td>→</td>
<td>Part V: Non-Neurotoxic Insecticides</td>
</tr>
<tr>
<td>7. Practical factors (stability, behavior, sanitation, resistance)</td>
<td>→</td>
<td>Part VI: Practical Factors</td>
</tr>
<tr>
<td>8. Summary</td>
<td>→</td>
<td>Distributed as section conclusions</td>
</tr>
<tr>
<td>9. Q&amp;A with Dan</td>
<td>→</td>
<td>Integrated throughout relevant sections</td>
</tr>
</tbody>
</table>
<p><strong>Key reorganization choices:</strong>
- LD50 was presented between physiology and classification; it fits better as a classification fundamental
- Combination products were discussed within neurotoxics but could also warrant their own sidebar
- Q&amp;A content is distributed to the sections where it's most relevant rather than kept as a standalone section
- The resistance discussion appears in both Part I (motivation) and Part VI (practical detail) — cross-reference or consolidate as preferred</p>
<hr />
<h2 id="companion-documents">Companion Documents<a class="headerlink" href="#companion-documents" title="Permanent link">&para;</a></h2>
<p>This source guide is part of a three-document set:</p>
<ol>
<li><strong>Bulletin Draft Outline</strong> (<code>GTBOP_BulletinOutline_InsecticideMOA_Scharf.md</code>) — Section-by-section content notes and writing guidance</li>
<li><strong>Quick Reference Compendium</strong> (<code>GTBOP_ReferenceCompendium_InsecticideMOA_Scharf.md</code>) — Consolidated tables of all classifications, products, and relationships</li>
<li><strong>This Source Guide</strong> (<code>GTBOP_SourceGuide_InsecticideMOA_Scharf.md</code>) — Transcript location mapping</li>
</ol>
<p>All three draw exclusively from the same source: the corrected and verified prose transcript of Dr. Scharf's October 18, 2017 GTBOP presentation.</p>
<hr />
<p><em>Prepared from GTBOP webinar archive materials for UGA Center for Urban Agriculture.</em></p>
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Principles of Insecticide Mode of Action — Dr. Michael Scharf
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CHAIN OF CUSTODY
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Matching Exercise 1: Insecticide Classes and Their Target Sites
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Matching Exercise 2: Insecticide Mode of Action Effects
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Matching Exercise 3: Practical Factors Affecting Insecticide Performance
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Principles of Insecticide Mode of Action — Dr. Michael Scharf
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Matching Exercise 1: Insecticide Classes and Their Target Sites
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<h1 id="matching-exercises-scharf-insecticide-moa">Matching Exercises — Scharf, Insecticide MOA<a class="headerlink" href="#matching-exercises-scharf-insecticide-moa" title="Permanent link">&para;</a></h1> <h1 id="gtbop-moodle-matching-exercises">GTBOP Moodle Matching Exercises<a class="headerlink" href="#gtbop-moodle-matching-exercises" title="Permanent link">&para;</a></h1>
<blockquote> <h2 id="principles-of-insecticide-mode-of-action-dr-michael-scharf">Principles of Insecticide Mode of Action — Dr. Michael Scharf<a class="headerlink" href="#principles-of-insecticide-mode-of-action-dr-michael-scharf" title="Permanent link">&para;</a></h2>
<p><strong>Placeholder</strong> — Paste your Stage 4 pipeline output here.</p> <p><strong>Webinar Date:</strong> October 18, 2017
</blockquote> <strong>Series:</strong> Structural Pest Control
<strong>Activity Type:</strong> Matching Exercises
<strong>Exercises:</strong> 3
<strong>Total Pairs:</strong> 26 (8 + 10 + 8)</p>
<hr /> <hr />
<p><em>Processed for UGA Center for Urban Agriculture / GTBOP Archives</em></p> <h3 id="chain-of-custody">CHAIN OF CUSTODY<a class="headerlink" href="#chain-of-custody" title="Permanent link">&para;</a></h3>
<ul>
<li><strong>Source documents:</strong> Corrected SRT (GTBOP_Transcript_2017-10-18_InsecticideMOA.srt) + Archive Package (GTBOP_Archive_Summary_2017-10-18_InsecticideMOA.md)</li>
<li><strong>All terms, definitions, and relationships derived exclusively from presentation content</strong></li>
</ul>
<hr />
<h3 id="matching-exercise-1-insecticide-classes-and-their-target-sites">Matching Exercise 1: Insecticide Classes and Their Target Sites<a class="headerlink" href="#matching-exercise-1-insecticide-classes-and-their-target-sites" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 28:40 – 39:05 (primary coverage area)
<strong>Type:</strong> Product-Target Site Matching</p>
<p><strong>Instructions:</strong> Match each insecticide class in Column A with the target site it affects in Column B. Note: Column B contains two extra items.</p>
<table>
<thead>
<tr>
<th>#</th>
<th>Column A</th>
<th></th>
<th>Column B</th>
</tr>
</thead>
<tbody>
<tr>
<td>1</td>
<td>Pyrethroids</td>
<td></td>
<td>a) Chloride channels</td>
</tr>
<tr>
<td>2</td>
<td>Fipronil (phenylpyrazole)</td>
<td></td>
<td>b) Acetylcholine receptor</td>
</tr>
<tr>
<td>3</td>
<td>Nicotinoids</td>
<td></td>
<td>c) Muscular calcium channels</td>
</tr>
<tr>
<td>4</td>
<td>Organophosphates and carbamates</td>
<td></td>
<td>d) Axonal sodium channels</td>
</tr>
<tr>
<td>5</td>
<td>Diamides (chlorantraniliprole)</td>
<td></td>
<td>e) Acetylcholinesterase enzyme</td>
</tr>
<tr>
<td>6</td>
<td>Indoxacarb (oxadiazine)</td>
<td></td>
<td>f) Mitochondria (energy production)</td>
</tr>
<tr>
<td>7</td>
<td>Abamectin (avermectin)</td>
<td></td>
<td>g) Chitin synthesis enzymes</td>
</tr>
<tr>
<td>8</td>
<td>Chitin synthesis inhibitors</td>
<td></td>
<td>h) Glutamate-gated chloride channels</td>
</tr>
<tr>
<td></td>
<td></td>
<td></td>
<td>i) Juvenile hormone receptors</td>
</tr>
<tr>
<td></td>
<td></td>
<td></td>
<td>j) Axonal sodium channels (blockage)</td>
</tr>
</tbody>
</table>
<p><strong>Answer Key:</strong>
1 → d, 2 → a, 3 → b, 4 → e, 5 → c, 6 → j, 7 → h, 8 → g</p>
<p><strong>Notes:</strong>
- Items 1 and 6 both target sodium channels but through opposite mechanisms (stimulation vs. blockage), which is why they map to separate entries (d and j). This distinction is a key teaching point from the presentation.
- Distractors: (f) mitochondria and (i) juvenile hormone receptors are legitimate target sites discussed elsewhere in the presentation but do not match the classes listed in Column A.</p>
<p><strong>Source in transcript:</strong> Blocks 301–343 (target site roadmap), 346–362 (sodium channels), 363–387 (chloride channels), 388–407 (acetylcholine), 429–444 (diamides), 466–482 (IGRs)</p>
<hr />
<h3 id="matching-exercise-2-insecticide-mode-of-action-effects">Matching Exercise 2: Insecticide Mode of Action Effects<a class="headerlink" href="#matching-exercise-2-insecticide-mode-of-action-effects" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 17:51 – 47:00 (spans full classification section)
<strong>Type:</strong> Product-Effect Matching</p>
<p><strong>Instructions:</strong> Match each insecticide or insecticide class in Column A with the physiological effect it produces in insects, as described by Dr. Scharf, in Column B. Note: Column B contains two extra items.</p>
<table>
<thead>
<tr>
<th>#</th>
<th>Column A</th>
<th></th>
<th>Column B</th>
</tr>
</thead>
<tbody>
<tr>
<td>1</td>
<td>Pyrethroids / pyrethrins</td>
<td></td>
<td>a) Blocks chloride channels, causing nervous system excitation</td>
</tr>
<tr>
<td>2</td>
<td>Fipronil</td>
<td></td>
<td>b) Stimulates muscular calcium channels, causing contraction followed by energy depletion and paralysis</td>
</tr>
<tr>
<td>3</td>
<td>Indoxacarb</td>
<td></td>
<td>c) Stimulates sodium channels, causing rapid knockdown and excitation</td>
</tr>
<tr>
<td>4</td>
<td>Organophosphates</td>
<td></td>
<td>d) Inhibits chitin synthesis enzyme, causing death during molting</td>
</tr>
<tr>
<td>5</td>
<td>Diamides</td>
<td></td>
<td>e) Blocks sodium channels, causing paralysis ("on switch stuck in off position")</td>
</tr>
<tr>
<td>6</td>
<td>Juvenile hormone analogs (pyriproxyfen)</td>
<td></td>
<td>f) Inhibits acetylcholinesterase, causing excitation from neurotransmitter buildup</td>
</tr>
<tr>
<td>7</td>
<td>Chitin synthesis inhibitors</td>
<td></td>
<td>g) Mimics juvenile hormone, causing cuticle deformation and extra juvenile stages</td>
</tr>
<tr>
<td>8</td>
<td>Abamectin</td>
<td></td>
<td>h) Stimulates chloride channels, causing inhibition and paralysis</td>
</tr>
<tr>
<td>9</td>
<td>Silica gel / diatomaceous earth</td>
<td></td>
<td>i) Abrades waxy cuticle layer, causing water loss and dehydration</td>
</tr>
<tr>
<td>10</td>
<td>Nicotinoid-pyrethroid combinations</td>
<td></td>
<td>j) Stimulates acetylcholine receptors and sodium channels simultaneously (potentiation)</td>
</tr>
<tr>
<td></td>
<td></td>
<td></td>
<td>k) Disrupts mitochondrial respiration, depleting cellular energy</td>
</tr>
<tr>
<td></td>
<td></td>
<td></td>
<td>l) Blocks acetylcholine receptors, preventing nerve signal transmission</td>
</tr>
</tbody>
</table>
<p><strong>Answer Key:</strong>
1 → c, 2 → a, 3 → e, 4 → f, 5 → b, 6 → g, 7 → d, 8 → h, 9 → i, 10 → j</p>
<p><strong>Notes:</strong>
- This exercise tests understanding of both the target site AND the specific mode of action (stimulation vs. blockage vs. inhibition) — the core teaching framework of the presentation.
- Distractors: (k) mitochondrial disruption is discussed for products like hydramethylnon but is not paired with any Column A item; (l) is a plausible-sounding but incorrect mechanism not described in the presentation.</p>
<p><strong>Source in transcript:</strong> Blocks 184–205 (four modes of action), 346–362 (sodium channels), 363–387 (chloride channels), 388–407 (acetylcholine), 408–420 (combinations), 429–444 (diamides), 466–482 (IGRs), 499–511 (dusts)</p>
<hr />
<h3 id="matching-exercise-3-practical-factors-affecting-insecticide-performance">Matching Exercise 3: Practical Factors Affecting Insecticide Performance<a class="headerlink" href="#matching-exercise-3-practical-factors-affecting-insecticide-performance" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 48:15 – 56:30 (practical factors section)
<strong>Type:</strong> Timing-Practice Matching</p>
<p><strong>Instructions:</strong> Match each practical factor or scenario in Column A with the correct explanation or outcome described by Dr. Scharf in Column B. Note: Column B contains two extra items.</p>
<table>
<thead>
<tr>
<th>#</th>
<th>Column A</th>
<th></th>
<th>Column B</th>
</tr>
</thead>
<tbody>
<tr>
<td>1</td>
<td>Excess food in a cockroach account</td>
<td></td>
<td>a) Can pass insecticide through two digestive tracts and still affect a third individual</td>
</tr>
<tr>
<td>2</td>
<td>Dirt and grease on treated surfaces</td>
<td></td>
<td>b) Physically bind and tie up insecticides, reducing their effectiveness</td>
</tr>
<tr>
<td>3</td>
<td>Cockroach secondary/tertiary kill</td>
<td></td>
<td>c) Enables slow-acting insecticides to spread through food sharing and grooming</td>
</tr>
<tr>
<td>4</td>
<td>Trophallaxis and allogrooming in social insects</td>
<td></td>
<td>d) Competes directly with bait placements, reducing consumption by target pests</td>
</tr>
<tr>
<td>5</td>
<td>Flea larvae exposed through adult flea feces</td>
<td></td>
<td>e) Causes the insecticide's active ingredient to degrade faster in the environment</td>
</tr>
<tr>
<td>6</td>
<td>UV light exposure on raw insecticides</td>
<td></td>
<td>f) Larvae consume insecticide-laden feces of treated adults as a nutritional source</td>
</tr>
<tr>
<td>7</td>
<td>Formulations (inerts, stabilizers, attractants)</td>
<td></td>
<td>g) Enhance stability, extend longevity, improve safety, and keep active ingredients dissolved in water</td>
</tr>
<tr>
<td>8</td>
<td>Product rotation every 3 months or monthly</td>
<td></td>
<td>h) Helps manage resistance by alternating between different modes of action</td>
</tr>
<tr>
<td></td>
<td></td>
<td></td>
<td>i) Increases the LD50 of the product, making it less toxic to target pests</td>
</tr>
<tr>
<td></td>
<td></td>
<td></td>
<td>j) Converts neurotoxic insecticides into non-repellent formulations</td>
</tr>
</tbody>
</table>
<p><strong>Answer Key:</strong>
1 → d, 2 → b, 3 → a, 4 → c, 5 → f, 6 → e, 7 → g, 8 → h</p>
<p><strong>Notes:</strong>
- This exercise bridges the gap between toxicology and practice — the section of the presentation Scharf described as "where toxicology interfaces with practice."
- Distractors: (i) is plausible-sounding but reverses the relationship (formulations don't increase LD50 for targets); (j) is a fabricated mechanism not described in the presentation.</p>
<p><strong>Source in transcript:</strong> Blocks 515–547 (stability and formulations), 548–567 (pest behavior), 568–585 (sanitation), 586–611 (resistance management)</p>
<hr />
<h2 id="moodle-activity-verification">Moodle Activity Verification<a class="headerlink" href="#moodle-activity-verification" title="Permanent link">&para;</a></h2>
<ul>
<li>[x] All terms, definitions, and relationships derived from presentation content</li>
<li>[x] Timestamp references verified against corrected SRT</li>
<li>[x] No external knowledge required to answer correctly</li>
<li>[x] Matching items unambiguous based on presentation content</li>
<li>[x] 1–2 plausible distractors included per exercise to prevent elimination guessing</li>
<li>[x] Answer keys unambiguously correct per speaker's content</li>
<li>[x] Exercises cover early (target sites), middle (modes of action and effects), and late (practical factors) presentation content</li>
</ul>
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<h1 id="moodle-quiz-scharf-insecticide-moa">Moodle Quiz — Scharf, Insecticide MOA<a class="headerlink" href="#moodle-quiz-scharf-insecticide-moa" title="Permanent link">&para;</a></h1> <h1 id="gtbop-moodle-quiz">GTBOP Moodle Quiz<a class="headerlink" href="#gtbop-moodle-quiz" title="Permanent link">&para;</a></h1>
<blockquote> <h2 id="principles-of-insecticide-mode-of-action-dr-michael-scharf">Principles of Insecticide Mode of Action — Dr. Michael Scharf<a class="headerlink" href="#principles-of-insecticide-mode-of-action-dr-michael-scharf" title="Permanent link">&para;</a></h2>
<p><strong>Placeholder</strong> — Paste your Stage 4 pipeline output here.</p> <p><strong>Webinar Date:</strong> October 18, 2017
</blockquote> <strong>Series:</strong> Structural Pest Control
<strong>Activity Type:</strong> Multiple Choice Quiz
<strong>Questions:</strong> 15
<strong>Difficulty Distribution:</strong> 6 Recall (40%) / 6 Application (40%) / 3 Analysis (20%)</p>
<hr /> <hr />
<p><em>Processed for UGA Center for Urban Agriculture / GTBOP Archives</em></p> <h3 id="chain-of-custody">CHAIN OF CUSTODY<a class="headerlink" href="#chain-of-custody" title="Permanent link">&para;</a></h3>
<ul>
<li><strong>Source documents:</strong> Corrected SRT (GTBOP_Transcript_2017-10-18_InsecticideMOA.srt) + Archive Package (GTBOP_Archive_Summary_2017-10-18_InsecticideMOA.md)</li>
<li><strong>All questions and answers derived exclusively from presentation content</strong></li>
<li><strong>No external knowledge required to answer correctly</strong></li>
</ul>
<hr />
<h3 id="question-1">Question 1<a class="headerlink" href="#question-1" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 17:51 – 19:30
<strong>Difficulty:</strong> Recall</p>
<p>According to Dr. Scharf, how many basic modes of action do all insecticides fall into?</p>
<p>a) Two
b) Four
c) Six
d) Nine</p>
<p><strong>Correct Answer:</strong> b
<strong>Explanation:</strong> Scharf states there are only four basic modes of action: stimulation, blockage, modulation, and inhibition. He emphasizes that all insecticide effects on target sites can be categorized into one of these four mechanisms.
<strong>Source in transcript:</strong> ~18:07 — "We can really break it down into four modes of action. There are only four kinds that occur."</p>
<hr />
<h3 id="question-2">Question 2<a class="headerlink" href="#question-2" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 32:24 – 34:07
<strong>Difficulty:</strong> Recall</p>
<p>Which insecticide class targets axonal sodium channels by stimulating them, causing rapid knockdown and excitation in insects?</p>
<p>a) Phenylpyrazoles
b) Diamides
c) Pyrethroids
d) Organophosphates</p>
<p><strong>Correct Answer:</strong> c
<strong>Explanation:</strong> Scharf explains that pyrethroids (along with DDT and pyrethrins) stimulate sodium channels on the nerve axon, causing excitation and the rapid knockdown commonly observed when insects are treated with pyrethrins.
<strong>Source in transcript:</strong> ~32:56 — "We have pyrethroids and also DDT and pyrethrins... They stimulate sodium channels and cause excitation."</p>
<hr />
<h3 id="question-3">Question 3<a class="headerlink" href="#question-3" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 34:12 – 36:16
<strong>Difficulty:</strong> Application</p>
<p>A technician applies fipronil to a cockroach harborage area and observes insects exhibiting hyperexcitation rather than paralysis. Based on Dr. Scharf's explanation of fipronil's mode of action, why does fipronil cause excitation rather than sedation?</p>
<p>a) Fipronil stimulates sodium channels, causing nerves to fire rapidly
b) Fipronil blocks chloride channels, removing the calming effect of chloride on neurons
c) Fipronil inhibits acetylcholinesterase, causing neurotransmitter buildup
d) Fipronil stimulates muscular calcium channels, causing uncontrolled contraction</p>
<p><strong>Correct Answer:</strong> b
<strong>Explanation:</strong> Scharf explains that chloride normally has a "mellowing" effect on neurons. Fipronil blocks the chloride channel, removing that calming influence, which leads to excitation. He demonstrated this with nerve recordings showing increased firing rate after fipronil application.
<strong>Source in transcript:</strong> ~34:48 — "Fipronil blocks the chloride channel so you're blocking this mellowing effect which leads to excitation."</p>
<hr />
<h3 id="question-4">Question 4<a class="headerlink" href="#question-4" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 33:22 – 34:10
<strong>Difficulty:</strong> Application</p>
<p>A pest management professional encounters a situation where rapid knockdown is undesirable and instead needs an insecticide that paralyzes insects by blocking nervous system function. Which sodium channel insecticide would best fit this need, based on the presentation?</p>
<p>a) Bifenthrin
b) Indoxacarb
c) Fipronil
d) Imidacloprid</p>
<p><strong>Correct Answer:</strong> b
<strong>Explanation:</strong> Scharf explains that indoxacarb (an oxadiazine) blocks sodium channels rather than stimulating them, causing the "on switch" to be stuck in the off position, which paralyzes the insect. This contrasts with pyrethroids like bifenthrin, which stimulate sodium channels and cause excitation.
<strong>Source in transcript:</strong> ~33:34 — "Indoxacarb affects the sodium channel but it blocks it... the insect is actually paralyzed because its sodium channels don't work."</p>
<hr />
<h3 id="question-5">Question 5<a class="headerlink" href="#question-5" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 40:02 – 41:40
<strong>Difficulty:</strong> Recall</p>
<p>What is unique about the mammalian safety profile of diamide insecticides such as chlorantraniliprole?</p>
<p>a) They require a "Danger" signal word due to moderate toxicity
b) Their mammalian toxicity is so low that the EPA initially did not require a signal word
c) They are equally toxic to mammals and insects
d) They are safe only when applied as baits, not as sprays</p>
<p><strong>Correct Answer:</strong> b
<strong>Explanation:</strong> Scharf states that diamides are so safe for mammals that the EPA initially required no signal word. Manufacturers voluntarily adopted a "caution" label. He still emphasized that safety guidelines should be followed.
<strong>Source in transcript:</strong> ~41:04 — "These products are actually so safe for mammals that no signal words were required by the EPA initially."</p>
<hr />
<h3 id="question-6">Question 6<a class="headerlink" href="#question-6" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 40:02 – 41:03
<strong>Difficulty:</strong> Recall</p>
<p>According to Dr. Scharf, what happens physiologically when a diamide insecticide like chlorantraniliprole affects an insect?</p>
<p>a) It blocks sodium channels, preventing nerve impulses
b) It inhibits chitin synthesis during molting
c) It stimulates muscular calcium channels, causing contraction followed by energy depletion and paralysis
d) It disrupts the insect's respiratory chain in the mitochondria</p>
<p><strong>Correct Answer:</strong> c
<strong>Explanation:</strong> Scharf explains that diamides stimulate neuromuscular calcium channels, causing muscles to contract for hours until the insect's energy is burned up, after which it enters a paralyzed state for days until it dies.
<strong>Source in transcript:</strong> ~40:48 — "What these things do is they stimulate the neuromuscular calcium channel and that causes that muscle to contract for a few hours and then it burns up all its energy."</p>
<hr />
<h3 id="question-7">Question 7<a class="headerlink" href="#question-7" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 36:20 – 38:01
<strong>Difficulty:</strong> Recall</p>
<p>Which of the following target sites do nicotinoid insecticides affect?</p>
<p>a) Sodium channels on the nerve axon
b) Chloride channels on neurons
c) Acetylcholine receptors at the synapse
d) Muscular calcium channels</p>
<p><strong>Correct Answer:</strong> c
<strong>Explanation:</strong> Scharf identifies nicotinoids as affecting the acetylcholine receptor by stimulating it and causing excitation in the insect. He also notes that sulfoximines and spinosyns share this same target site.
<strong>Source in transcript:</strong> ~36:54 — "We have our mainly the nicotinoids... They're affecting the acetylcholine receptor by stimulating it."</p>
<hr />
<h3 id="question-8">Question 8<a class="headerlink" href="#question-8" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 37:28 – 38:01
<strong>Difficulty:</strong> Analysis</p>
<p>Dr. Scharf notes that organophosphates and carbamates are subject to more regulatory restrictions than many newer insecticide classes. Based on his explanation, what is the underlying reason for these restrictions?</p>
<p>a) They are more expensive to manufacture than newer products
b) Their target site (acetylcholinesterase) is not insect-specific, so they are equally effective against mammals
c) They cause environmental persistence that exceeds all other insecticide classes
d) They are only effective against a narrow range of pest species</p>
<p><strong>Correct Answer:</strong> b
<strong>Explanation:</strong> Scharf explicitly states that the acetylcholinesterase target site is "not a really insect specific target site" and that "these things work equally well against humans and mammals," which is the reason for restrictions on these product classes.
<strong>Source in transcript:</strong> ~37:53 — "This is not a really insect specific target site. You know these things work equally well against humans and mammals and so we have a lot of restrictions."</p>
<hr />
<h3 id="question-9">Question 9<a class="headerlink" href="#question-9" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 38:04 – 39:05
<strong>Difficulty:</strong> Application</p>
<p>A combination product pairs a nicotinoid with a pyrethroid. Based on Dr. Scharf's presentation, what advantage does this combination provide over a single active ingredient?</p>
<p>a) The two ingredients target the same site for a doubled dose effect
b) The combination eliminates the need for product rotation
c) Hitting two different target sites simultaneously produces a potentiation effect — synergy greater than either alone
d) The pyrethroid component makes the product non-repellent</p>
<p><strong>Correct Answer:</strong> c
<strong>Explanation:</strong> Scharf explains that combination products produce potentiation by hitting two target sites at once — the nicotinoid targets the acetylcholine receptor while the pyrethroid targets sodium channels — creating a "one plus one equals three" synergistic effect.
<strong>Source in transcript:</strong> ~38:35 — "They cause this effect called potentiation, which is actually hitting two target sites at once. So you get this synergy, this one plus one equals three kind of effect."</p>
<hr />
<h3 id="question-10">Question 10<a class="headerlink" href="#question-10" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 51:02 – 53:01
<strong>Difficulty:</strong> Application</p>
<p>A pest control operator is treating a heavy German cockroach infestation with gel bait. Based on Dr. Scharf's discussion of pest behavior, why might the actual number of cockroaches killed exceed the number that directly consumed the bait?</p>
<p>a) Gel bait releases a fumigant vapor that kills nearby cockroaches
b) Cockroaches that eat bait excrete insecticide in their feces, which other cockroaches consume, producing secondary and even tertiary kill
c) The bait becomes more concentrated as it dries, increasing its toxicity over time
d) Cockroaches are attracted to the pheromones of dead individuals, bringing them into contact with remaining bait</p>
<p><strong>Correct Answer:</strong> b
<strong>Explanation:</strong> Scharf describes secondary and tertiary kill in cockroaches: one cockroach eats bait, excretes insecticide, and other cockroaches consume the feces. He notes research showing the toxin can pass through two digestive tracts and still affect a third cockroach.
<strong>Source in transcript:</strong> ~51:24 — "If we have a cockroach that eats a bait and it either excretes, you know, some of the bait in its excrement... We can have secondary kill and even tertiary kill."</p>
<hr />
<h3 id="question-11">Question 11<a class="headerlink" href="#question-11" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 54:19 – 56:28
<strong>Difficulty:</strong> Recall</p>
<p>What rotation frequency does Dr. Scharf recommend for switching active ingredients in cockroach management to help manage resistance?</p>
<p>a) Every week
b) Every month or every three months
c) Every six months
d) Annually</p>
<p><strong>Correct Answer:</strong> b
<strong>Explanation:</strong> Scharf recommends switching active ingredients every three months, or even every month if possible, as part of a resistance management rotation strategy for cockroach accounts.
<strong>Source in transcript:</strong> ~55:49 — "Every three months switch active ingredients, maybe even every month if you can do it."</p>
<hr />
<h3 id="question-12">Question 12<a class="headerlink" href="#question-12" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 53:04 – 54:11
<strong>Difficulty:</strong> Application</p>
<p>A technician is having difficulty achieving control with gel bait in a commercial kitchen. The kitchen has grease buildup on surfaces and abundant food debris. Based on Dr. Scharf's discussion, what is the most likely reason for reduced bait performance?</p>
<p>a) The bait has developed resistance to the cockroach population
b) Grease and dirt tie up insecticides on surfaces, and excess food competes directly with bait for cockroach feeding
c) The kitchen's humidity is degrading the active ingredient
d) The bait formulation is incompatible with commercial kitchen environments</p>
<p><strong>Correct Answer:</strong> b
<strong>Explanation:</strong> Scharf specifically identifies three sanitation-related factors that reduce insecticide efficacy: excess food competing with bait, clutter creating untreatable harborage, and dirt and grease that physically bind insecticides. He frames sanitation as essential to making insecticides more effective.
<strong>Source in transcript:</strong> ~53:31 — "Excess food in an account will compete with bait" and ~54:02 — "dirt and grease tie up insecticides too."</p>
<hr />
<h3 id="question-13">Question 13<a class="headerlink" href="#question-13" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 41:42 – 44:46
<strong>Difficulty:</strong> Application</p>
<p>A technician inspects a cockroach account and notices several German cockroaches with twisted, malformed wings. Based on the presentation, what does this observation most likely indicate?</p>
<p>a) The cockroaches are infected with a fungal pathogen
b) The population has been exposed to insect growth regulators, specifically juvenile hormone analogs
c) The cockroaches have developed pyrethroid resistance
d) The cockroaches are immature nymphs that have not yet completed development</p>
<p><strong>Correct Answer:</strong> b
<strong>Explanation:</strong> Scharf specifically identifies wing twist as a diagnostic sign that IGRs (particularly juvenile hormone analogs like pyriproxyfen) are active in a cockroach population. He advises that when wing twist is visible, it may be appropriate to rotate to a different product class.
<strong>Source in transcript:</strong> ~44:25 — "If you go into a new account and you see individuals with wing twist... you can put good money down on the fact that IGRs are in that population affecting it."</p>
<hr />
<h3 id="question-14">Question 14<a class="headerlink" href="#question-14" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 19:41 – 22:40
<strong>Difficulty:</strong> Analysis</p>
<p>Dr. Scharf states that the relationship between LD50 and product toxicity is inverse. A professional is comparing two insecticides: Product A has an LD50 of 5 mg/kg for cockroaches, and Product B has an LD50 of 500 mg/kg for cockroaches. Which product is more toxic to cockroaches, and why?</p>
<p>a) Product B, because a higher LD50 means more insecticide reaches the target site
b) Product A, because a smaller LD50 means a smaller dose is needed to kill 50% of the test population
c) Both are equally toxic; LD50 only measures speed of action
d) Product B, because a higher LD50 indicates greater potency</p>
<p><strong>Correct Answer:</strong> b
<strong>Explanation:</strong> Scharf explains that LD50 is the lethal dose required to kill 50% of a test population, and the relationship to toxicity is inverse — the smaller the LD50, the higher the toxicity, because less product is needed to achieve the lethal effect.
<strong>Source in transcript:</strong> ~20:24 — "The smaller the LD50, the higher the toxicity of a product. That means... you only need a small dose to kill half of your test population."</p>
<hr />
<h3 id="question-15">Question 15<a class="headerlink" href="#question-15" title="Permanent link">&para;</a></h3>
<p><strong>Timestamp Reference:</strong> 46:56 – 48:09 and 04:01 – 04:00 (pollinator context)
<strong>Difficulty:</strong> Analysis</p>
<p>Dr. Scharf discusses cuticle dehydrating dusts like diatomaceous earth and silica gel. Considering his earlier discussion of insect physiology, why are these products effective against insects but pose minimal chemical toxicity risk to mammals?</p>
<p>a) They work through a physical mechanism — abrading the waxy cuticle layer and causing water loss — rather than through a biochemical target site interaction
b) They contain active ingredients that are specific to insect nervous systems
c) They are formulated with attractants that only insects will consume
d) They degrade too quickly in the environment to affect mammals</p>
<p><strong>Correct Answer:</strong> a
<strong>Explanation:</strong> Scharf explains that silica gel and diatomaceous earth are essentially finely ground glass powder that abrades the protective waxy outer layer of the insect cuticle, leading to water loss and death. This is a physical mechanism rather than a chemical mode of action targeting a specific biochemical pathway, which is why these products do not pose the same chemical toxicity concerns for mammals.
<strong>Source in transcript:</strong> ~47:00 — "We have silica gel and diatomaceous earth which are just basically finely ground glass powder... they abrade the cuticle, they break it down, which leads to water loss."</p>
<hr />
<h2 id="moodle-activity-verification">Moodle Activity Verification<a class="headerlink" href="#moodle-activity-verification" title="Permanent link">&para;</a></h2>
<ul>
<li>[x] All 15 questions traceable to specific presentation segments</li>
<li>[x] Timestamp references verified against corrected SRT</li>
<li>[x] No external knowledge required to answer correctly</li>
<li>[x] Difficulty distribution: 6 Recall / 6 Application / 3 Analysis</li>
<li>[x] Answer keys unambiguously correct based on presentation content</li>
<li>[x] Distractors plausible but definitively wrong per speaker's content</li>
<li>[x] Questions drawn from early (Q1, Q2, Q14), middle (Q3–Q9, Q13), and late (Q10–Q12, Q15) presentation content</li>
<li>[x] No "all of the above" or "none of the above" options used</li>
</ul>
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<h1 id="archive-summary-scharf-insecticide-moa">Archive Summary — Scharf, Insecticide MOA<a class="headerlink" href="#archive-summary-scharf-insecticide-moa" title="Permanent link">&para;</a></h1> <h1 id="gtbop-webinar-archive-summary">GTBOP Webinar Archive Summary<a class="headerlink" href="#gtbop-webinar-archive-summary" title="Permanent link">&para;</a></h1>
<blockquote> <h2 id="principles-of-insecticide-mode-of-action">Principles of Insecticide Mode of Action<a class="headerlink" href="#principles-of-insecticide-mode-of-action" title="Permanent link">&para;</a></h2>
<p><strong>Placeholder</strong> — Paste your Stage 2 pipeline output here.</p> <p><strong>Webinar Date:</strong> October 18, 2017
</blockquote> <strong>Speaker:</strong> Dr. Michael Scharf, O.W. Rawlins Orkin Endowed Chair in Urban Entomology and Molecular Physiology, Department of Entomology, Purdue University
<strong>Moderator:</strong> Dr. Dan Suiter, Extension Entomologist, University of Georgia
<strong>Duration:</strong> 1:07:06
<strong>Series:</strong> Structural Pest Control
<strong>CEU Categories:</strong> GA — 2 HPC (Cat 35: Industrial, Institutional, Structural and Health Related)</p>
<hr />
<h2 id="narrative-summary">NARRATIVE SUMMARY<a class="headerlink" href="#narrative-summary" title="Permanent link">&para;</a></h2>
<p>Dr. Michael Scharf of Purdue University presented a comprehensive overview of insecticide classification and mode of action designed to strengthen pest management professionals' understanding of how their chemical tools work. Scharf framed the practical importance of this knowledge around six themes: applicator and customer safety, accurate interpretation of trade literature, pollinator protection, resistance management, product sustainability, and the ability to design customized applications through situational pest management.</p>
<p>Scharf began with a condensed review of insect physiology, covering the five systems most relevant to insecticide activity: the nervous system, the cuticle, the digestive tract, the tracheal system, and the musculature. He explained that insecticides interact with specific protein target sites through a key-and-lock relationship, and that all insecticide effects can be reduced to just four modes of action — stimulation, blockage, modulation, and inhibition. He introduced the LD50 concept and emphasized that modern insecticides are dramatically more toxic to insects than to mammals, with some classes like the diamides carrying such low mammalian toxicity that the EPA initially required no signal word.</p>
<p>The presentation then systematically covered five neurotoxic insecticide classifications: sodium channel agents (pyrethroids, indoxacarb, metaflumizone), chloride channel agents (fipronil, isoxazolines, abamectin), acetylcholine receptor agents (nicotinoids, sulfoximines, spinosyns), acetylcholinesterase inhibitors (organophosphates, carbamates), and combination products pairing nicotinoids with pyrethroids for potentiation effects. Scharf followed with four non-neurotoxic classifications: muscular calcium channel agents (diamides such as chlorantraniliprole and cyantraniliprole), insect growth regulators (juvenile hormone analogs like pyriproxyfen and chitin synthesis inhibitors), inhibitors of energy production (hydramethylnon, chlorfenapyr, sulfuryl fluoride, boric acid), and cuticle dehydrating dusts (silica gel, diatomaceous earth).</p>
<p>Scharf concluded by discussing practical factors that affect insecticide performance, including formulation types, pest behavior that can amplify efficacy through secondary and tertiary kill, the role of sanitation in an IPM framework, and resistance management. He identified resistance as likely the number one cause of callbacks in cockroach accounts and recommended rotating active ingredients every three months or even monthly. A Q&amp;A session moderated by Dr. Suiter addressed combination product resistance risks, the flow of new active ingredients to market, the IRAC classification system, the distinction between nicotinoids and neonicotinoids, oral versus dermal toxicity, repellent versus non-repellent insecticides, and the growing consumer demand for essential oil-based products.</p>
<hr />
<h2 id="youtube-timestamps">YOUTUBE TIMESTAMPS<a class="headerlink" href="#youtube-timestamps" title="Permanent link">&para;</a></h2>
<p>0:00 Introduction and Speaker Credentials
1:45 Why Understanding Mode of Action Matters
6:03 Presentation Outline
7:13 Additional Resources — PCT Article and UGA Publication
8:26 Insect Physiology Overview — Nervous System, Cuticle, Gut, Trachea, Muscles
14:02 Insecticide Classification Basics — Chemical Structure
16:01 Target Site and Mode of Action — Key and Lock Analogy
17:51 Four Basic Modes of Action — Stimulation, Blockage, Modulation, Inhibition
19:41 The LD50 Concept and Mammalian Safety
22:46 Overview of Neurotoxic and Non-Neurotoxic Classifications
23:36 The Insect Nervous System — Neurons, Synapses, Neurotransmitters
26:45 Neurophysiology Demonstration — Fipronil and Nerve Excitation
28:40 Nervous System Target Sites — Roadmap of Ion Channels and Receptors
32:24 Sodium Channel Insecticides — Pyrethroids, Indoxacarb, Metaflumizone
34:12 Chloride Channel Insecticides — Fipronil, Isoxazolines, Abamectin
36:20 Acetylcholine Receptor Insecticides — Nicotinoids, Sulfoximines, Spinosyns
37:28 Acetylcholinesterase Inhibitors — Organophosphates and Carbamates
38:04 Combination Products — Nicotinoid-Pyrethroid Potentiation
39:07 Non-Neurotoxic Insecticides Overview
40:02 Muscular Calcium Channel Agents — Diamides
41:42 Insect Growth Regulators — JH Analogs and Chitin Synthesis Inhibitors
45:18 Inhibitors of Energy Production — Hydramethylnon, Chlorfenapyr, Fumigants
46:56 Cuticle Dehydrating Dusts — Silica Gel and Diatomaceous Earth
48:15 Factors Affecting Insecticide Efficacy
48:46 Stability, Persistence, and Formulations
51:02 Pest Behavior — Secondary and Tertiary Kill, Trophallaxis
53:04 Sanitation and IPM
54:19 Resistance Management — Rotation Strategies
56:30 Summary Points
57:44 Additional Resources
57:53 Q&amp;A — Combination Product Resistance
59:53 Q&amp;A — Flow of New Active Ingredients to Market
1:01:08 Q&amp;A — Chlorantraniliprole and Non-Target Invertebrates
1:01:40 Q&amp;A — IRAC Classification System
1:02:38 Q&amp;A — Nicotinoids vs. Neonicotinoids
1:03:43 Q&amp;A — Oral vs. Dermal Toxicity Routes
1:04:43 Q&amp;A — Repellent vs. Non-Repellent Insecticides
1:05:32 Q&amp;A — Essential Oils and 25B Exempt Products</p>
<hr />
<h2 id="questions-answers">QUESTIONS &amp; ANSWERS<a class="headerlink" href="#questions-answers" title="Permanent link">&para;</a></h2>
<p><strong>Q: What are the four basic modes of action that all insecticides fall into?</strong>
A: According to Dr. Scharf, all insecticides disrupt target sites through one of just four mechanisms: stimulation (causing a target to fire more rapidly), blockage (shutting a target off), modulation (subtly changing the shape and function of a target, as pyrethroids do to sodium channels), and inhibition (preventing an enzyme from functioning, as organophosphates do to acetylcholinesterase). Understanding these four categories provides a framework for classifying any insecticide a professional might encounter.</p>
<p><strong>Q: Why are diamide insecticides like chlorantraniliprole considered especially safe for mammals?</strong>
A: Diamides target muscular calcium channels that are highly specific to insects. They stimulate these channels, causing uncontrolled muscle contraction that burns up the insect's energy and leads to paralysis and death over several days. Their mammalian toxicity is so low that the EPA initially did not require a signal word, though manufacturers voluntarily adopted a "caution" label. Despite this safety profile, Scharf emphasized that applicators should still follow all safety guidelines when using them.</p>
<p><strong>Q: How does fipronil work at the neurological level?</strong>
A: Fipronil is a phenylpyrazole that targets chloride channels in the insect nervous system. Under normal conditions, chloride channels allow negatively charged chloride ions into neurons, which has a calming or "mellowing" effect on nerve activity. Fipronil blocks these channels, removing that calming influence and causing excitation — the insect's nervous system essentially fires uncontrollably. Scharf demonstrated this visually using nerve recordings from dissected American cockroaches, showing a dramatic increase in firing rate and intensity after fipronil application.</p>
<p><strong>Q: What is the difference between repellent and non-repellent insecticides?</strong>
A: Scharf explained that the distinction largely comes down to pyrethroids versus everything else. Pyrethroids are highly detectable to insects — he compared them to "pepper spray" — making them strongly repellent. Most other active ingredients, including fipronil and nicotinoids, are not nearly as detectable, which is why they are classified as non-repellent. This distinction became particularly prominent when non-repellent termiticides entered the market approximately 15 years before this presentation.</p>
<p><strong>Q: Why is resistance considered a major concern for cockroach management?</strong>
A: Scharf identified resistance as likely the number one cause of callbacks in cockroach accounts. His research has documented cockroaches that can eat bait as their sole food source for a full month and survive. He noted that resistance is not limited to older chemistries — even combination products containing two active ingredients can face dual resistance when cockroach populations develop tolerance to both nicotinoids and pyrethroids simultaneously. He recommended rotating active ingredients every three months or even monthly to help manage resistance.</p>
<p><strong>Q: How do pest behaviors like trophallaxis and secondary kill affect insecticide efficacy?</strong>
A: Scharf described three examples of behavior-mediated insecticide transfer. In cockroaches, secondary and tertiary kill occurs when one cockroach eats bait, excretes the insecticide, and other cockroaches consume the feces — research has shown the toxin can pass through two digestive tracts and still affect a third cockroach. Flea larvae can be exposed when adult fleas treated by veterinary products defecate insecticide-laden feces that larvae consume as nutrition. Social insects like termites and ants spread insecticides through trophallaxis (food sharing from both mouth and anus) and allogrooming, which is why slow-acting insecticides are preferred for these pests.</p>
<p><strong>Q: What role does sanitation play in insecticide effectiveness?</strong>
A: Scharf emphasized that poor sanitation always makes insecticides less effective, regardless of how pest-specific modern products have become. Excess food in an account competes directly with bait placements, reducing consumption. Clutter creates untreatable harborage areas where pests can avoid contact with residual treatments. Dirt and grease on surfaces can physically bind and inactivate insecticides. He framed sanitation as a core component of the IPM mindset that directly enhances chemical efficacy.</p>
<p><strong>Q: What is the IRAC and how can it help pest management professionals?</strong>
A: IRAC stands for the Insecticide Resistance Action Committee, a global organization with representatives from all major insecticide manufacturers. IRAC develops mode of action classifications that help professionals understand which products share the same target sites. Their classification chart, updated once or twice a year, shows the full landscape of available active ingredients organized by mode of action. Professionals can use this resource to plan effective product rotations by ensuring they alternate between different mode of action groups rather than simply switching trade names.</p>
<p><strong>Q: How do insect growth regulators work differently from neurotoxic insecticides?</strong>
A: Unlike neurotoxins that target the nervous system for rapid effects, insect growth regulators disrupt the hormones and enzymes that control development and molting. Juvenile hormone analogs like pyriproxyfen mimic the insect's own juvenile hormone, leading to cuticle deformation and extra juvenile stages that cannot reproduce — causing the population to crash over time. Chitin synthesis inhibitors block the enzyme responsible for forming the exoskeleton during molting, leading to death during the molt or producing malformed cuticles that cause a characteristic "jackknife" effect in treated termites. Scharf noted that visible wing twist in cockroach populations is a reliable indicator that IGRs are already affecting that population.</p>
<p><strong>Q: Why are insecticides generally more toxic through ingestion than through contact exposure?</strong>
A: Scharf explained that both the insect cuticle and mammalian skin serve as highly effective barriers to insecticide penetration. The insect cuticle is a complex, multi-layered, waterproof structure that contact insecticides must traverse to reach internal target sites. In contrast, the gut lining is a much thinner layer of cells, allowing ingested insecticides to penetrate far more readily. The same principle applies to mammals — human skin is an exceptionally resistant barrier compared to the gut, which is why oral exposure routes are almost always more toxic than dermal exposure for any given active ingredient.</p>
<p><strong>Q: What is the outlook for new active ingredients entering the urban pest management market?</strong>
A: Scharf acknowledged that the flow of new active ingredients has slowed and the market has become heavily generic. While all major manufacturers maintain product pipelines, bringing a new active ingredient to market costs hundreds of millions to billions of dollars, and the economics must justify the investment. He noted that the urban pest management market represents a smaller slice of the overall pie compared to agriculture, which affects manufacturer incentives. Scharf encouraged the industry to advocate vocally to manufacturers about the need for new tools, particularly given growing resistance pressures.</p>
<hr />
<h2 id="additional-resources">ADDITIONAL RESOURCES<a class="headerlink" href="#additional-resources" title="Permanent link">&para;</a></h2>
<p><em>The following resources were referenced by the speaker during the presentation:</em></p>
<ul>
<li>Scharf, M.E. and D.L. Suiter. "Insecticide Primer and Insecticide Mode of Action." <em>PCT Magazine</em>, 2011.</li>
<li>Scharf, M.E. and D.L. Suiter. <em>Insecticide Basics for the Pest Management Professional.</em> University of Georgia publication (available free of charge; URL referenced in presentation slides).</li>
<li>IRAC (Insecticide Resistance Action Committee) — Mode of action classification chart, updated annually.</li>
</ul>
<hr />
<h2 id="chain-of-custody">CHAIN OF CUSTODY<a class="headerlink" href="#chain-of-custody" title="Permanent link">&para;</a></h2>
<ul>
<li><strong>Source document:</strong> Corrected SRT from Stage 1 (GTBOP_Transcript_2017-10-18_InsecticideMOA.srt)</li>
<li><strong>Source verified:</strong> 742 blocks, 2,968 lines, full read confirmed with coverage proof during Stage 1</li>
<li><strong>Webinar date confirmed:</strong> Via original program announcement email from Tami Adams Boyle</li>
</ul>
<hr /> <hr />
<p><em>Processed for UGA Center for Urban Agriculture / GTBOP Archives</em></p> <p><em>Processed for UGA Center for Urban Agriculture / GTBOP Archives</em></p>
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<h1 id="transcript-corrections-scharf-insecticide-moa">Transcript Corrections — Scharf, Insecticide MOA<a class="headerlink" href="#transcript-corrections-scharf-insecticide-moa" title="Permanent link">&para;</a></h1> <h1 id="srt-transcript-correction-summary">SRT Transcript Correction Summary<a class="headerlink" href="#srt-transcript-correction-summary" title="Permanent link">&para;</a></h1>
<blockquote> <h2 id="file-principles-of-insecticide-mode-of-action-mike-scharf">File: Principles of Insecticide Mode of Action — Mike Scharf<a class="headerlink" href="#file-principles-of-insecticide-mode-of-action-mike-scharf" title="Permanent link">&para;</a></h2>
<p><strong>Placeholder</strong> — Paste your Stage 1 pipeline output here.</p> <p><strong>Date Corrected:</strong> February 10, 2026
</blockquote> <strong>Webinar Date:</strong> October 18, 2017
<strong>Series:</strong> Structural Pest Control
<strong>Topic:</strong> Entomology — Insecticide Classification and Mode of Action
<strong>Speaker:</strong> Dr. Michael Scharf, O.W. Rawlins Orkin Endowed Chair in Urban Entomology and Molecular Physiology, Department of Entomology, Purdue University, West Lafayette, IN
<strong>Moderator:</strong> Dr. Dan Suiter, Extension Entomologist, University of Georgia</p>
<hr /> <hr />
<p><em>Processed for UGA Center for Urban Agriculture / GTBOP Archives</em></p> <h2 id="source-verification">SOURCE VERIFICATION<a class="headerlink" href="#source-verification" title="Permanent link">&para;</a></h2>
<ul>
<li><strong>Original blocks:</strong> 742</li>
<li><strong>Corrected blocks:</strong> 742 ✓ MATCH CONFIRMED</li>
<li><strong>Time range:</strong> 00:00:00,020 to 01:07:06,220</li>
<li><strong>Runtime:</strong> ~67 minutes</li>
<li><strong>File reading:</strong> COMPLETE ✓</li>
<li><strong>Coverage proof:</strong></li>
<li>Early [~1:45]: Speaker states overarching goal to improve general knowledge of how insecticides work; discusses nervous system targeting vs. insect growth regulators</li>
<li>Middle [~40:00]: Discusses muscular calcium channels and diamide insecticides (chlorantraniliprole, cyantraniliprole); notes EPA initially required no signal word due to low mammalian toxicity</li>
<li>Late [~55:00]: Identifies resistance as probably the #1 cause of callbacks in cockroach accounts; cockroaches observed surviving on bait as sole food source for a month; recommends rotating active ingredients every 3 months or monthly</li>
</ul>
<hr />
<h2 id="corrections-applied">Corrections Applied<a class="headerlink" href="#corrections-applied" title="Permanent link">&para;</a></h2>
<h3 id="proper-nouns-speaker-names">Proper Nouns — Speaker Names<a class="headerlink" href="#proper-nouns-speaker-names" title="Permanent link">&para;</a></h3>
<ul>
<li>"Dr. Sharf" → "Dr. Scharf" (Line 23)</li>
<li>"Dan Suter" → "Dan Suiter" (Line 311)</li>
<li>"Dave Oy" → "Dave Oi" (Line 2243) — Confirmed via webinar announcement: Dr. David Oi, USDA-ARS, Center for Medical, Agricultural and Veterinary Entomology, Gainesville, FL; presented "Fire Ants and Crazy Ants" in the same session</li>
</ul>
<h3 id="chemicalproduct-names">Chemical/Product Names<a class="headerlink" href="#chemicalproduct-names" title="Permanent link">&para;</a></h3>
<ul>
<li>"chlorenterniliprol" → "chlorantraniliprole" (Line 559)</li>
<li>"terniliprol" → "traniliprole" (Line 563 — continuation of "cyantraniliprole" split across blocks 140–141)</li>
<li>"Metaflumazone" → "metaflumizone" (Line 1431)</li>
<li>"Furilander and Sarlander" → "fluralaner and sarolaner" (Line 1499)</li>
<li>"sulfoxyms or sulfoxifluor" → "sulfoximines or sulfoxaflor" (Line 1583)</li>
<li>"spinosid" → "spinosad" (Line 1595)</li>
<li>"chlorantraniliprol" → "chlorantraniliprole" (Line 1747)</li>
<li>"cyan triniliprol" → "cyantraniliprole" (Line 1747)</li>
<li>"pyroprosythin" → "pyriproxyfen" (Line 1883)</li>
<li>"hydromethyl non" → "hydramethylnon" (Line 1951)</li>
<li>"chlorphenipir" → "chlorfenapyr" (Line 1959)</li>
<li>"sulfurofluoride" → "sulfuryl fluoride" (Line 1967)</li>
<li>"disodium octoborate" → "disodium octaborate" (Line 1971)</li>
<li>"chlorthenopyr" → "chlorfenapyr" (Line 2387)</li>
<li>"chlorantrinoliprol" → "chlorantraniliprole" (Line 2691)</li>
<li>"Amidocloprid" → "imidacloprid" (Line 2771)</li>
</ul>
<h3 id="technical-terms">Technical Terms<a class="headerlink" href="#technical-terms" title="Permanent link">&para;</a></h3>
<ul>
<li>"semi-carbazone" → "semicarbazone" (Line 1435 — IRAC chemical subclass name)</li>
<li>"spinosins" → "spinosyns" (Line 1347 — IRAC Group 5 class name)</li>
<li>"aloe grooming" → "allogrooming" (Line 2247)</li>
<li>"the nicotines target" → "the nicotinoids target" (Line 1663 — speaker consistently uses "nicotinoids" elsewhere; Whisper truncated the word)</li>
<li>"Pubigants" → "Fumigants" (Line 1967)</li>
<li>"acetylcholinesterase, which is a neurotransmitter" → "acetylcholine, which is a neurotransmitter" (Line 1287 — acetylcholinesterase is an enzyme, not a neurotransmitter; the speaker is clearly describing acetylcholine crossing the synapse to bind its receptor; Whisper appended "-esterase" to "acetylcholine")</li>
</ul>
<h3 id="grammar">Grammar<a class="headerlink" href="#grammar" title="Permanent link">&para;</a></h3>
<ul>
<li>"Dr. Thank you very much Dan." → "Thank you very much, Dan." (Line 43 — "Dr." is a Whisper artifact from the end of the moderator's introduction bleeding into the speaker's first line; comma added after "Dan")</li>
</ul>
<h3 id="flagged-for-verification">Flagged for Verification<a class="headerlink" href="#flagged-for-verification" title="Permanent link">&para;</a></h3>
<ul>
<li>None remaining. Line 1207 ("need this acetylcholinesterase enzyme") was reviewed against audio and confirmed as accurate speech. Speaker is casually listing target sites from a slide; phrasing is informal but intelligible and left as-is per the principle of maintaining natural speech patterns.</li>
</ul>
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<h2 id="notes">Notes<a class="headerlink" href="#notes" title="Permanent link">&para;</a></h2>
<h3 id="speaker-not-in-reference-roster">Speaker Not in Reference Roster<a class="headerlink" href="#speaker-not-in-reference-roster" title="Permanent link">&para;</a></h3>
<p>Dr. Michael Scharf (Purdue University) is not currently listed in the GTBOP Common Speakers reference. Recommend adding:</p>
<table>
<thead>
<tr>
<th>Name</th>
<th>Affiliation</th>
</tr>
</thead>
<tbody>
<tr>
<td>Dr. Michael Scharf</td>
<td>Purdue University, Urban Entomology</td>
</tr>
</tbody>
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<h3 id="additional-speaker-confirmed-for-roster">Additional Speaker Confirmed for Roster<a class="headerlink" href="#additional-speaker-confirmed-for-roster" title="Permanent link">&para;</a></h3>
<p>Dr. David Oi is confirmed via webinar announcement as a GTBOP presenter but is not currently in the Common Speakers reference. Recommend adding:</p>
<table>
<thead>
<tr>
<th>Name</th>
<th>Affiliation</th>
</tr>
</thead>
<tbody>
<tr>
<td>Dr. David Oi</td>
<td>USDA-ARS, Center for Medical, Agricultural and Veterinary Entomology, Gainesville, FL</td>
</tr>
</tbody>
</table>
<h3 id="nicotinoid-vs-neonicotinoid-terminology">Nicotinoid vs. Neonicotinoid Terminology<a class="headerlink" href="#nicotinoid-vs-neonicotinoid-terminology" title="Permanent link">&para;</a></h3>
<p>The speaker intentionally uses "nicotinoids" (not "neonicotinoids") throughout most of the presentation. In the Q&amp;A section (~01:02:46), he and Dr. Suiter discuss the distinction: nicotinoids structurally resemble nicotine, while neonicotinoids have evolved further structurally but still target the acetylcholine receptor. This is the speaker's deliberate classification framework and has not been altered.</p>
<h3 id="webinar-date-confirmation">Webinar Date Confirmation<a class="headerlink" href="#webinar-date-confirmation" title="Permanent link">&para;</a></h3>
<p>Date confirmed as October 18, 2017 via original program announcement email from Tami Adams Boyle. The event ran 7:00–10:00 AM EDT as part of the Structural Pest Control Webinar Series. Dr. Scharf's presentation "Principles of Insecticide Mode of Action" was paired with Dr. David Oi's "Fire Ants and Crazy Ants."</p>
<hr />
<h2 id="srt-format-compliance">SRT Format Compliance<a class="headerlink" href="#srt-format-compliance" title="Permanent link">&para;</a></h2>
<p>✅ All timestamps preserved exactly as original
✅ All sequence numbers maintained (1–742)
✅ Blank lines between segments preserved
✅ Maximum 2 lines per subtitle segment maintained
✅ No segments merged or split
✅ Block count: 742 original = 742 corrected ✓
✅ Line count: 2,968 original = 2,968 corrected ✓</p>
<hr />
<p><strong>Total Corrections:</strong> 24 individual corrections across 24 lines
<strong>Flagged for Verification:</strong> 0 items (1 resolved via audio review)
<strong>Processing:</strong> Complete file (742 subtitle blocks, 2,968 lines)</p>
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GTBOP Structural Pest Control — October 18, 2017
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<h1 id="dr-michael-scharf-principles-of-insecticide-classification-and-mode-of-action">Dr. Michael Scharf — Principles of Insecticide Classification and Mode of Action<a class="headerlink" href="#dr-michael-scharf-principles-of-insecticide-classification-and-mode-of-action" title="Permanent link">&para;</a></h1> <h1 id="insecticide-classification-and-mode-of-action">Insecticide Classification and Mode of Action<a class="headerlink" href="#insecticide-classification-and-mode-of-action" title="Permanent link">&para;</a></h1>
<p><strong>Webinar Date:</strong> October 18, 2017 <h2 id="gtbop-structural-pest-control-october-18-2017">GTBOP Structural Pest Control — October 18, 2017<a class="headerlink" href="#gtbop-structural-pest-control-october-18-2017" title="Permanent link">&para;</a></h2>
<strong>Speaker:</strong> Dr. Michael Scharf, Purdue University, Department of Entomology <p><strong>Speaker:</strong> Dr. Michael Scharf, O.W. Rawlins Orkin Endowed Chair in Urban Entomology and Molecular Physiology, Purdue University
<strong>Moderator:</strong> Dr. Dan Suiter, Extension Entomologist, UGA <strong>Moderator:</strong> Dr. Dan Suiter, Extension Entomologist, University of Georgia
<strong>Series:</strong> Structural Pest Control <strong>Duration:</strong> ~67 minutes (1:07:06)
<strong>CEU Categories:</strong> Category 35 (Industrial, Institutional, Structural and Health Related)</p> <strong>CEU Categories:</strong> Georgia Cat 35 (Industrial/Structural); multi-state credits in 8 states and 3 Canadian provinces</p>
<hr /> <hr />
<h2 id="deliverables">Deliverables<a class="headerlink" href="#deliverables" title="Permanent link">&para;</a></h2> <h2 id="deliverables">Deliverables<a class="headerlink" href="#deliverables" title="Permanent link">&para;</a></h2>
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<td><a href="archive-summary/">Archive Summary</a></td> <td>1</td>
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<td>5</td>
<td>Full presentation in readable prose</td>
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<td><a href="platforms/youtube/">YouTube Version</a></td> <td><a href="platforms/youtube/">YouTube Version</a></td>
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<td><a href="platforms/website/">Website Version</a></td> <td><a href="platforms/website/">Website Version</a></td>
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<td><a href="platforms/ext-agent/">Extension Agent Version</a></td> <td><a href="platforms/ext-agent/">Extension Agent Version</a></td>
<td>3</td> <td>Complete</td>
<td>CEU-focused asynchronous version</td>
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<td>Multiple choice assessment</td>
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<td>Complete</td>
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<td>5</td>
<td><a href="prose-transcript/">Prose Transcript</a></td>
<td>Complete</td>
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<td>—</td>
<td><a href="downloads/">Corrected SRT</a></td> <td><a href="downloads/">Corrected SRT</a></td>
<td>1</td> <td>Complete</td>
<td>Download corrected subtitle file</td>
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<p><em>Processed for UGA Center for Urban Agriculture / GTBOP Archives</em></p> <h2 id="session-overview">Session Overview<a class="headerlink" href="#session-overview" title="Permanent link">&para;</a></h2>
<p>Dr. Michael Scharf of Purdue University presented a comprehensive overview of insecticide classification and mode of action designed to strengthen pest management professionals' understanding of how their chemical tools work. Scharf framed the practical importance of this knowledge around six themes: applicator and customer safety, accurate interpretation of trade literature, pollinator protection, resistance management, product sustainability, and the ability to design customized applications through situational pest management.</p>
<p>The presentation systematically covered five neurotoxic insecticide classifications — sodium channel agents, chloride channel agents, acetylcholine receptor agents, acetylcholinesterase inhibitors, and combination products — followed by four non-neurotoxic classifications including diamides, insect growth regulators, inhibitors of energy production, and cuticle dehydrating dusts. Scharf concluded with practical factors affecting insecticide performance, resistance management strategies, and a Q&amp;A session moderated by Dr. Suiter.</p>
<hr />
<p><em>Source: Corrected SRT — GTBOP_Transcript_2017-10-18_InsecticideMOA.srt</em>
<em>Processed: 2026-03-17 | Pipeline v4.1</em></p>
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<h1 id="extension-agent-version-scharf-insecticide-moa">Extension Agent Version — Scharf, Insecticide MOA<a class="headerlink" href="#extension-agent-version-scharf-insecticide-moa" title="Permanent link">&para;</a></h1> <h1 id="gtbop-webinar-archive-extension-agent-resource">GTBOP Webinar Archive — Extension Agent Resource<a class="headerlink" href="#gtbop-webinar-archive-extension-agent-resource" title="Permanent link">&para;</a></h1>
<blockquote> <h2 id="principles-of-insecticide-mode-of-action">Principles of Insecticide Mode of Action<a class="headerlink" href="#principles-of-insecticide-mode-of-action" title="Permanent link">&para;</a></h2>
<p><strong>Placeholder</strong> — Paste your Stage 3 pipeline output here.</p>
</blockquote>
<hr /> <hr />
<p><em>Processed for UGA Center for Urban Agriculture / GTBOP Archives</em></p> <h3 id="webinar-information">Webinar Information<a class="headerlink" href="#webinar-information" title="Permanent link">&para;</a></h3>
<table>
<thead>
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<th>Field</th>
<th>Details</th>
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<td><strong>Speaker</strong></td>
<td>Dr. Michael Scharf, Purdue University</td>
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<tr>
<td><strong>Moderator</strong></td>
<td>Dr. Dan Suiter, UGA Extension Entomologist</td>
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<td><strong>Original Air Date</strong></td>
<td>October 18, 2017</td>
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<td><strong>Duration</strong></td>
<td>1 hour, 7 minutes</td>
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<td><strong>Series</strong></td>
<td>Getting the Best of Pests — Structural Pest Control</td>
</tr>
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<h3 id="ceu-credit-information">CEU Credit Information<a class="headerlink" href="#ceu-credit-information" title="Permanent link">&para;</a></h3>
<p><strong>Georgia Applicator Category:</strong>
- <strong>Cat 35</strong> — Industrial, Institutional, Structural and Health Related: <strong>2 HPC</strong></p>
<p><strong>Credit Eligibility:</strong> This archived presentation is suitable for asynchronous CEU delivery to licensed pest control operators holding Category 35 certification. Verify current CEU acceptance with the Georgia Department of Agriculture before scheduling.</p>
<p><strong>Sign-in sheet and CEU documentation:</strong> Contact the UGA Center for Urban Agriculture or visit gabugs.uga.edu for current forms and procedures.</p>
<hr />
<h3 id="viewing-instructions-for-asynchronous-use">Viewing Instructions for Asynchronous Use<a class="headerlink" href="#viewing-instructions-for-asynchronous-use" title="Permanent link">&para;</a></h3>
<ol>
<li>Total viewing time is approximately 1 hour and 7 minutes, including the Q&amp;A session.</li>
<li>Attendees must view the entire presentation to receive credit.</li>
<li>The presentation includes a 57-minute lecture followed by a 10-minute moderated Q&amp;A.</li>
<li>A sign-in sheet must be completed and returned per standard GTBOP procedures.</li>
</ol>
<hr />
<h3 id="content-summary">Content Summary<a class="headerlink" href="#content-summary" title="Permanent link">&para;</a></h3>
<p>Dr. Michael Scharf of Purdue University covers insecticide classification and mode of action at a level appropriate for licensed pest control professionals. The presentation provides foundational knowledge that supports informed product selection, resistance management, and customer communication.</p>
<p><strong>Topics covered include:</strong> a review of insect physiology as it relates to insecticide activity (nervous system, cuticle, digestive tract, tracheal system, musculature); the four basic modes of action (stimulation, blockage, modulation, inhibition); the LD50 concept and mammalian safety; five neurotoxic insecticide classifications (sodium channel agents, chloride channel agents, acetylcholine receptor agents, acetylcholinesterase inhibitors, combination products); four non-neurotoxic classifications (diamides, insect growth regulators, energy production inhibitors, cuticle dehydrating dusts); and practical factors affecting insecticide performance including formulations, pest behavior, sanitation, and resistance management through product rotation.</p>
<p><strong>The Q&amp;A session addresses:</strong> combination product resistance, new active ingredient development, IRAC classifications, nicotinoid vs. neonicotinoid terminology, oral vs. dermal toxicity routes, repellent vs. non-repellent insecticides, and essential oil-based products.</p>
<hr />
<h3 id="key-takeaways-for-extension-programming">Key Takeaways for Extension Programming<a class="headerlink" href="#key-takeaways-for-extension-programming" title="Permanent link">&para;</a></h3>
<ul>
<li>All insecticides work through one of four basic mechanisms — a useful teaching framework for applicators at any experience level.</li>
<li>Nine insecticide classifications (five neurotoxic, four non-neurotoxic) cover the full landscape of available tools.</li>
<li>Diamides represent a notably safe chemistry class for mammals — EPA initially required no signal word.</li>
<li>Resistance is identified as the probable #1 cause of callbacks in cockroach accounts; rotation every 3 months or monthly is recommended.</li>
<li>The IRAC classification system is highlighted as a free, practical resource for planning product rotations by mode of action group.</li>
<li>Sanitation and IPM practices are framed as direct enhancers of chemical efficacy, not just standalone strategies.</li>
</ul>
<hr />
<h3 id="video-chapter-guide">Video Chapter Guide<a class="headerlink" href="#video-chapter-guide" title="Permanent link">&para;</a></h3>
<p>For agents directing attendees to specific sections:</p>
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<td>0:00</td>
<td>Introduction and Speaker Credentials</td>
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<td>1:45</td>
<td>Why Understanding Mode of Action Matters</td>
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<td>8:26</td>
<td>Insect Physiology Overview</td>
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<td>14:02</td>
<td>Insecticide Classification Basics</td>
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<td>17:51</td>
<td>Four Basic Modes of Action</td>
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<td>19:41</td>
<td>LD50 Concept and Mammalian Safety</td>
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<td>Neurotoxic Insecticide Classifications Begin</td>
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<td>Sodium Channel Insecticides</td>
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<td>Chloride Channel Insecticides</td>
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<td>Acetylcholine Receptor Insecticides</td>
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<td>Combination Products</td>
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<td>Non-Neurotoxic Insecticides Begin</td>
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<td>Diamides</td>
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<td>Energy Production Inhibitors</td>
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<td>Factors Affecting Insecticide Efficacy</td>
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<td>Resistance Management</td>
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<td>57:53</td>
<td>Q&amp;A Session Begins</td>
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<hr />
<h3 id="additional-resources-referenced-in-presentation">Additional Resources Referenced in Presentation<a class="headerlink" href="#additional-resources-referenced-in-presentation" title="Permanent link">&para;</a></h3>
<ul>
<li>Scharf &amp; Suiter, "Insecticide Primer and Insecticide Mode of Action," <em>PCT Magazine</em>, 2011</li>
<li>Scharf &amp; Suiter, <em>Insecticide Basics for the Pest Management Professional</em>, UGA publication (free)</li>
<li>IRAC Mode of Action Classification Chart — irac-online.org</li>
</ul>
<hr />
<p><em>Getting the Best of Pests Webinar Series | University of Georgia Center for Urban Agriculture</em>
<em>For questions about this archive or CEU procedures, contact the Center for Urban Agriculture.</em></p>
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<h1 id="website-version-scharf-insecticide-moa">Website Version — Scharf, Insecticide MOA<a class="headerlink" href="#website-version-scharf-insecticide-moa" title="Permanent link">&para;</a></h1> <h1 id="principles-of-insecticide-mode-of-action">Principles of Insecticide Mode of Action<a class="headerlink" href="#principles-of-insecticide-mode-of-action" title="Permanent link">&para;</a></h1>
<blockquote> <h2 id="gtbop-structural-pest-control-webinar-series-archive">GTBOP Structural Pest Control Webinar Series — Archive<a class="headerlink" href="#gtbop-structural-pest-control-webinar-series-archive" title="Permanent link">&para;</a></h2>
<p><strong>Placeholder</strong> — Paste your Stage 3 pipeline output here.</p>
</blockquote>
<hr /> <hr />
<p><strong>Webinar Date:</strong> October 18, 2017
<strong>Speaker:</strong> Dr. Michael Scharf, O.W. Rawlins Orkin Endowed Chair in Urban Entomology and Molecular Physiology, Department of Entomology, Purdue University
<strong>Moderator:</strong> Dr. Dan Suiter, Extension Entomologist, University of Georgia
<strong>Duration:</strong> 1:07:06
<strong>Series:</strong> Getting the Best of Pests — Structural Pest Control Webinar Series
<strong>CEU Credits:</strong> GA — 2 HPC (Cat 35: Industrial, Institutional, Structural and Health Related)</p>
<hr />
<h2 id="about-this-presentation">About This Presentation<a class="headerlink" href="#about-this-presentation" title="Permanent link">&para;</a></h2>
<p>Dr. Michael Scharf of Purdue University presented a comprehensive overview of insecticide classification and mode of action designed to strengthen pest management professionals' understanding of how their chemical tools work. Scharf framed the practical importance of this knowledge around six themes: applicator and customer safety, accurate interpretation of trade literature, pollinator protection, resistance management, product sustainability, and the ability to design customized applications through situational pest management.</p>
<p>Scharf began with a condensed review of insect physiology, covering the five systems most relevant to insecticide activity: the nervous system, the cuticle, the digestive tract, the tracheal system, and the musculature. He explained that insecticides interact with specific protein target sites through a key-and-lock relationship, and that all insecticide effects can be reduced to just four modes of action — stimulation, blockage, modulation, and inhibition. He introduced the LD50 concept and emphasized that modern insecticides are dramatically more toxic to insects than to mammals, with some classes like the diamides carrying such low mammalian toxicity that the EPA initially required no signal word.</p>
<p>The presentation then systematically covered five neurotoxic insecticide classifications: sodium channel agents (pyrethroids, indoxacarb, metaflumizone), chloride channel agents (fipronil, isoxazolines, abamectin), acetylcholine receptor agents (nicotinoids, sulfoximines, spinosyns), acetylcholinesterase inhibitors (organophosphates, carbamates), and combination products pairing nicotinoids with pyrethroids for potentiation effects. Scharf followed with four non-neurotoxic classifications: muscular calcium channel agents (diamides such as chlorantraniliprole and cyantraniliprole), insect growth regulators (juvenile hormone analogs like pyriproxyfen and chitin synthesis inhibitors), inhibitors of energy production (hydramethylnon, chlorfenapyr, sulfuryl fluoride, boric acid), and cuticle dehydrating dusts (silica gel, diatomaceous earth).</p>
<p>Scharf concluded by discussing practical factors that affect insecticide performance, including formulation types, pest behavior that can amplify efficacy through secondary and tertiary kill, the role of sanitation in an IPM framework, and resistance management. He identified resistance as likely the number one cause of callbacks in cockroach accounts and recommended rotating active ingredients every three months or even monthly. A Q&amp;A session moderated by Dr. Suiter addressed combination product resistance risks, the flow of new active ingredients to market, the IRAC classification system, the distinction between nicotinoids and neonicotinoids, oral versus dermal toxicity, repellent versus non-repellent insecticides, and the growing consumer demand for essential oil-based products.</p>
<hr />
<h2 id="video-chapters">Video Chapters<a class="headerlink" href="#video-chapters" title="Permanent link">&para;</a></h2>
<p>0:00 Introduction and Speaker Credentials
1:45 Why Understanding Mode of Action Matters
6:03 Presentation Outline
7:13 Additional Resources — PCT Article and UGA Publication
8:26 Insect Physiology Overview — Nervous System, Cuticle, Gut, Trachea, Muscles
14:02 Insecticide Classification Basics — Chemical Structure
16:01 Target Site and Mode of Action — Key and Lock Analogy
17:51 Four Basic Modes of Action — Stimulation, Blockage, Modulation, Inhibition
19:41 The LD50 Concept and Mammalian Safety
22:46 Overview of Neurotoxic and Non-Neurotoxic Classifications
23:36 The Insect Nervous System — Neurons, Synapses, Neurotransmitters
26:45 Neurophysiology Demonstration — Fipronil and Nerve Excitation
28:40 Nervous System Target Sites — Roadmap of Ion Channels and Receptors
32:24 Sodium Channel Insecticides — Pyrethroids, Indoxacarb, Metaflumizone
34:12 Chloride Channel Insecticides — Fipronil, Isoxazolines, Abamectin
36:20 Acetylcholine Receptor Insecticides — Nicotinoids, Sulfoximines, Spinosyns
37:28 Acetylcholinesterase Inhibitors — Organophosphates and Carbamates
38:04 Combination Products — Nicotinoid-Pyrethroid Potentiation
39:07 Non-Neurotoxic Insecticides Overview
40:02 Muscular Calcium Channel Agents — Diamides
41:42 Insect Growth Regulators — JH Analogs and Chitin Synthesis Inhibitors
45:18 Inhibitors of Energy Production — Hydramethylnon, Chlorfenapyr, Fumigants
46:56 Cuticle Dehydrating Dusts — Silica Gel and Diatomaceous Earth
48:15 Factors Affecting Insecticide Efficacy
48:46 Stability, Persistence, and Formulations
51:02 Pest Behavior — Secondary and Tertiary Kill, Trophallaxis
53:04 Sanitation and IPM
54:19 Resistance Management — Rotation Strategies
56:30 Summary Points
57:44 Additional Resources
57:53 Q&amp;A — Combination Product Resistance
59:53 Q&amp;A — Flow of New Active Ingredients to Market
1:01:08 Q&amp;A — Chlorantraniliprole and Non-Target Invertebrates
1:01:40 Q&amp;A — IRAC Classification System
1:02:38 Q&amp;A — Nicotinoids vs. Neonicotinoids
1:03:43 Q&amp;A — Oral vs. Dermal Toxicity Routes
1:04:43 Q&amp;A — Repellent vs. Non-Repellent Insecticides
1:05:32 Q&amp;A — Essential Oils and 25B Exempt Products</p>
<hr />
<h2 id="questions-answers">Questions &amp; Answers<a class="headerlink" href="#questions-answers" title="Permanent link">&para;</a></h2>
<p><strong>Q: What are the four basic modes of action that all insecticides fall into?</strong>
A: According to Dr. Scharf, all insecticides disrupt target sites through one of just four mechanisms: stimulation (causing a target to fire more rapidly), blockage (shutting a target off), modulation (subtly changing the shape and function of a target, as pyrethroids do to sodium channels), and inhibition (preventing an enzyme from functioning, as organophosphates do to acetylcholinesterase). Understanding these four categories provides a framework for classifying any insecticide a professional might encounter.</p>
<p><strong>Q: Why are diamide insecticides like chlorantraniliprole considered especially safe for mammals?</strong>
A: Diamides target muscular calcium channels that are highly specific to insects. They stimulate these channels, causing uncontrolled muscle contraction that burns up the insect's energy and leads to paralysis and death over several days. Their mammalian toxicity is so low that the EPA initially did not require a signal word, though manufacturers voluntarily adopted a "caution" label. Despite this safety profile, Scharf emphasized that applicators should still follow all safety guidelines when using them.</p>
<p><strong>Q: How does fipronil work at the neurological level?</strong>
A: Fipronil is a phenylpyrazole that targets chloride channels in the insect nervous system. Under normal conditions, chloride channels allow negatively charged chloride ions into neurons, which has a calming or "mellowing" effect on nerve activity. Fipronil blocks these channels, removing that calming influence and causing excitation — the insect's nervous system essentially fires uncontrollably. Scharf demonstrated this visually using nerve recordings from dissected American cockroaches, showing a dramatic increase in firing rate and intensity after fipronil application.</p>
<p><strong>Q: What is the difference between repellent and non-repellent insecticides?</strong>
A: Scharf explained that the distinction largely comes down to pyrethroids versus everything else. Pyrethroids are highly detectable to insects — he compared them to "pepper spray" — making them strongly repellent. Most other active ingredients, including fipronil and nicotinoids, are not nearly as detectable, which is why they are classified as non-repellent. This distinction became particularly prominent when non-repellent termiticides entered the market approximately 15 years before this presentation.</p>
<p><strong>Q: Why is resistance considered a major concern for cockroach management?</strong>
A: Scharf identified resistance as likely the number one cause of callbacks in cockroach accounts. His research has documented cockroaches that can eat bait as their sole food source for a full month and survive. He noted that resistance is not limited to older chemistries — even combination products containing two active ingredients can face dual resistance when cockroach populations develop tolerance to both nicotinoids and pyrethroids simultaneously. He recommended rotating active ingredients every three months or even monthly to help manage resistance.</p>
<p><strong>Q: How do pest behaviors like trophallaxis and secondary kill affect insecticide efficacy?</strong>
A: Scharf described three examples of behavior-mediated insecticide transfer. In cockroaches, secondary and tertiary kill occurs when one cockroach eats bait, excretes the insecticide, and other cockroaches consume the feces — research has shown the toxin can pass through two digestive tracts and still affect a third cockroach. Flea larvae can be exposed when adult fleas treated by veterinary products defecate insecticide-laden feces that larvae consume as nutrition. Social insects like termites and ants spread insecticides through trophallaxis (food sharing from both mouth and anus) and allogrooming, which is why slow-acting insecticides are preferred for these pests.</p>
<p><strong>Q: What role does sanitation play in insecticide effectiveness?</strong>
A: Scharf emphasized that poor sanitation always makes insecticides less effective, regardless of how pest-specific modern products have become. Excess food in an account competes directly with bait placements, reducing consumption. Clutter creates untreatable harborage areas where pests can avoid contact with residual treatments. Dirt and grease on surfaces can physically bind and inactivate insecticides. He framed sanitation as a core component of the IPM mindset that directly enhances chemical efficacy.</p>
<p><strong>Q: What is the IRAC and how can it help pest management professionals?</strong>
A: IRAC stands for the Insecticide Resistance Action Committee, a global organization with representatives from all major insecticide manufacturers. IRAC develops mode of action classifications that help professionals understand which products share the same target sites. Their classification chart, updated once or twice a year, shows the full landscape of available active ingredients organized by mode of action. Professionals can use this resource to plan effective product rotations by ensuring they alternate between different mode of action groups rather than simply switching trade names.</p>
<p><strong>Q: How do insect growth regulators work differently from neurotoxic insecticides?</strong>
A: Unlike neurotoxins that target the nervous system for rapid effects, insect growth regulators disrupt the hormones and enzymes that control development and molting. Juvenile hormone analogs like pyriproxyfen mimic the insect's own juvenile hormone, leading to cuticle deformation and extra juvenile stages that cannot reproduce — causing the population to crash over time. Chitin synthesis inhibitors block the enzyme responsible for forming the exoskeleton during molting, leading to death during the molt or producing malformed cuticles that cause a characteristic "jackknife" effect in treated termites. Scharf noted that visible wing twist in cockroach populations is a reliable indicator that IGRs are already affecting that population.</p>
<p><strong>Q: Why are insecticides generally more toxic through ingestion than through contact exposure?</strong>
A: Scharf explained that both the insect cuticle and mammalian skin serve as highly effective barriers to insecticide penetration. The insect cuticle is a complex, multi-layered, waterproof structure that contact insecticides must traverse to reach internal target sites. In contrast, the gut lining is a much thinner layer of cells, allowing ingested insecticides to penetrate far more readily. The same principle applies to mammals — human skin is an exceptionally resistant barrier compared to the gut, which is why oral exposure routes are almost always more toxic than dermal exposure for any given active ingredient.</p>
<p><strong>Q: What is the outlook for new active ingredients entering the urban pest management market?</strong>
A: Scharf acknowledged that the flow of new active ingredients has slowed and the market has become heavily generic. While all major manufacturers maintain product pipelines, bringing a new active ingredient to market costs hundreds of millions to billions of dollars, and the economics must justify the investment. He noted that the urban pest management market represents a smaller slice of the overall pie compared to agriculture, which affects manufacturer incentives. Scharf encouraged the industry to advocate vocally to manufacturers about the need for new tools, particularly given growing resistance pressures.</p>
<hr />
<h2 id="additional-resources">Additional Resources<a class="headerlink" href="#additional-resources" title="Permanent link">&para;</a></h2>
<p><em>The following resources were referenced by the speaker during the presentation:</em></p>
<ul>
<li>Scharf, M.E. and D.L. Suiter. "Insecticide Primer and Insecticide Mode of Action." <em>PCT Magazine</em>, 2011.</li>
<li>Scharf, M.E. and D.L. Suiter. <em>Insecticide Basics for the Pest Management Professional.</em> University of Georgia publication (available free of charge; URL referenced in presentation slides).</li>
<li>IRAC (Insecticide Resistance Action Committee) — Mode of action classification chart, updated annually. Visit <a href="https://irac-online.org">irac-online.org</a>.</li>
</ul>
<hr />
<p><em>This archive is part of the Getting the Best of Pests Webinar Series, hosted by the University of Georgia Center for Urban Agriculture. For more information about the GTBOP program, visit gabugs.uga.edu.</em></p>
<p><em>Processed for UGA Center for Urban Agriculture / GTBOP Archives</em></p> <p><em>Processed for UGA Center for Urban Agriculture / GTBOP Archives</em></p>
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<h1 id="youtube-description-scharf-insecticide-moa">YouTube Description — Scharf, Insecticide MOA<a class="headerlink" href="#youtube-description-scharf-insecticide-moa" title="Permanent link">&para;</a></h1> <p>Principles of Insecticide Mode of Action | Dr. Michael Scharf | GTBOP Structural Pest Control Webinar Series</p>
<blockquote> <p>Dr. Michael Scharf of Purdue University presents a comprehensive overview of insecticide classification and mode of action for pest management professionals. Scharf covers insect physiology fundamentals, the key-and-lock relationship between insecticides and target sites, and nine insecticide classifications — five neurotoxic and four non-neurotoxic. The presentation concludes with practical factors affecting performance including formulations, pest behavior, sanitation, and resistance management. Q&amp;A moderated by Dr. Dan Suiter.</p>
<p><strong>Placeholder</strong> — Paste your Stage 3 pipeline output here.</p> <p>Presented: October 18, 2017
</blockquote> Series: Getting the Best of Pests — Structural Pest Control Webinar Series
<hr /> Host: UGA Center for Urban Agriculture
<p><em>Processed for UGA Center for Urban Agriculture / GTBOP Archives</em></p> CEU Credits: GA — 2 HPC (Cat 35)</p>
<p>TIMESTAMPS
0:00 Introduction and Speaker Credentials
1:45 Why Understanding Mode of Action Matters
6:03 Presentation Outline
7:13 Additional Resources — PCT Article and UGA Publication
8:26 Insect Physiology Overview — Nervous System, Cuticle, Gut, Trachea, Muscles
14:02 Insecticide Classification Basics — Chemical Structure
16:01 Target Site and Mode of Action — Key and Lock Analogy
17:51 Four Basic Modes of Action — Stimulation, Blockage, Modulation, Inhibition
19:41 The LD50 Concept and Mammalian Safety
22:46 Overview of Neurotoxic and Non-Neurotoxic Classifications
23:36 The Insect Nervous System — Neurons, Synapses, Neurotransmitters
26:45 Neurophysiology Demonstration — Fipronil and Nerve Excitation
28:40 Nervous System Target Sites — Roadmap of Ion Channels and Receptors
32:24 Sodium Channel Insecticides — Pyrethroids, Indoxacarb, Metaflumizone
34:12 Chloride Channel Insecticides — Fipronil, Isoxazolines, Abamectin
36:20 Acetylcholine Receptor Insecticides — Nicotinoids, Sulfoximines, Spinosyns
37:28 Acetylcholinesterase Inhibitors — Organophosphates and Carbamates
38:04 Combination Products — Nicotinoid-Pyrethroid Potentiation
39:07 Non-Neurotoxic Insecticides Overview
40:02 Muscular Calcium Channel Agents — Diamides
41:42 Insect Growth Regulators — JH Analogs and Chitin Synthesis Inhibitors
45:18 Inhibitors of Energy Production — Hydramethylnon, Chlorfenapyr, Fumigants
46:56 Cuticle Dehydrating Dusts — Silica Gel and Diatomaceous Earth
48:15 Factors Affecting Insecticide Efficacy
48:46 Stability, Persistence, and Formulations
51:02 Pest Behavior — Secondary and Tertiary Kill, Trophallaxis
53:04 Sanitation and IPM
54:19 Resistance Management — Rotation Strategies
56:30 Summary Points
57:44 Additional Resources
57:53 Q&amp;A — Combination Product Resistance
59:53 Q&amp;A — Flow of New Active Ingredients to Market
1:01:08 Q&amp;A — Chlorantraniliprole and Non-Target Invertebrates
1:01:40 Q&amp;A — IRAC Classification System
1:02:38 Q&amp;A — Nicotinoids vs. Neonicotinoids
1:03:43 Q&amp;A — Oral vs. Dermal Toxicity Routes
1:04:43 Q&amp;A — Repellent vs. Non-Repellent Insecticides
1:05:32 Q&amp;A — Essential Oils and 25B Exempt Products</p>
<p>FREQUENTLY ASKED QUESTIONS</p>
<p>Q: What are the four basic insecticide modes of action?
A: All insecticides disrupt target sites through stimulation, blockage, modulation, or inhibition. Understanding these four mechanisms provides a framework for classifying any product a professional might encounter.</p>
<p>Q: Why are diamide insecticides considered especially safe for mammals?
A: Diamides target insect-specific muscular calcium channels. Their mammalian toxicity is so low that the EPA initially required no signal word, though manufacturers voluntarily adopted a "caution" label.</p>
<p>Q: Why is resistance a major concern in cockroach management?
A: Research has documented cockroaches surviving on bait as their sole food source for a month. Even combination products face dual resistance. Rotate active ingredients every three months or monthly.</p>
<p>Q: How does the IRAC help pest management professionals?
A: The Insecticide Resistance Action Committee classifies active ingredients by mode of action, helping professionals plan rotations between different target site groups rather than simply switching trade names.</p>
<p>Q: What is the difference between repellent and non-repellent insecticides?
A: The distinction largely comes down to pyrethroids versus everything else. Pyrethroids are highly detectable to insects — like "pepper spray" — while most other actives are not nearly as detectable.</p>
<p>RESOURCES
• Scharf &amp; Suiter, "Insecticide Primer and Insecticide Mode of Action," PCT Magazine, 2011
• Scharf &amp; Suiter, "Insecticide Basics for the Pest Management Professional," UGA publication
• IRAC Mode of Action Classification Chart: https://irac-online.org</p>
<h1 id="pestmanagement-insecticides-modeofaction-ceu-structuralpestcontrol-ipm-uga-gtbop">PestManagement #Insecticides #ModeOfAction #CEU #StructuralPestControl #IPM #UGA #GTBOP<a class="headerlink" href="#pestmanagement-insecticides-modeofaction-ceu-structuralpestcontrol-ipm-uga-gtbop" title="Permanent link">&para;</a></h1>
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