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
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.
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.
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.
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.
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 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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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)