Servall Q & A from Ask Mr. Pest Control

Question:

I have done research regarding the mode of action that pyrethroids have on labeled target pests. Generally, I understand that a pyrethroid opens neural passages and leaves them on. I understand it paralyzes them and leaves their chances of recovering almost zero. But, most sites I tried then say the insect just eventually dies. What is it that kills them (heart/lung failure?), and how long does that likely take before they are more than just poisoned/locked 'on'?

Answer:

This really is a fascinating topic, to me at least. First comment is that the internal workings of a bug - any arthropod - are strongly similar to the internal workings of humans and other mammals. Both bugs and mammals have hearts, digestive systems, blood, and an exchange of oxygen for carbon dioxide. Bugs, as do humans, have a nervous system made up of individual nerve cells that pass a nerve impulse along from one point (the antenna of a bug or the finger of a human) to the brain, and illicit a response that travels back to that sensory point. This impulse is carried from nerve cell (neuron) to nerve cell by essentially the same chemicals and processes in both bugs and people. There are some differences though, such as the presence of a neurotransmitter called Octopamine, found only in arthropods and not mammals, that many of the plant oil insecticides work on.


So, with that preamble behind us, what do Synthetic Pyrethroids do? Their specific mode of action is Axonic Poisons that affect the GABA Gated Sodium Channel. GABA means "gamma amino-butyric acid", and it is an inhibitory neurotransmitter that acts to stop a nerve impulse and allow the neuron to calm back down again. Another "channel" along nerves is the Chloride Channel, and these channels exist as pathways for proteins that help regulate the nerve impulse. When an active ingredient "blocks" that channel it prevents the proper function of the nerve, and generally this causes the nerve to continue to fire the impulses along, resulting is over-excitation and eventual collapse of important organs in the insect. Sort of like running a motor at too high a speed until it finally overheats and dies.


GABA-gated Sodium Channel blockers include our pyrethroids, natural pyrethrum, and DDT, all of which open that channel and leave it open to cause over-excitation of the nerves and organs. Other active ingredients may block that channel to actually stop the nerve impulse and shut down the important organs, and these include Indoxacarb (Advion). You can see the relation between old DDT and our current pyrethroids, and understand why bed bugs, resistant to DDT, also became so resistant to pyrethroids in a short time.


It takes only miniscule levels of a pyrethroid active ingredient to cause this effect on arthropods, and once exposed the a.i. attacks the neurons very quickly, generally causing loss of function within minutes and death a short time later. They die because their organs and their nervous system shut down. Natural pyrethrum has the same general mode of action, but some insects have the ability to rapidly metabolize the pyrethrum molecule, excreting it before it has the chance to kill them. This is the case with the German Cockroach, which may fall over comatose from the exposure but lie there still alive and still working to rid its system of the pyrethrum molecules. Then, it recovers and goes on about its business. The addition of the synergists, such as PBO, to most pyrethrum formulations helps to block the insect's ability to metabolize the pyrethrum.

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