Pro-Insecticide, The other face of metabolic resistance.

Insect pests like German cockroaches, Bed bugs, and House flies have been bothering humanity for millenniums. We, humans, have tried different paths to avoid their annoyance, some taking the extreme of covering themselves in mud to avoid bugs biting and landing. We have tried a variety of mechanisms to control infestations, including mechanical, biological, and chemical approaches. Since the implementation of synthetic pesticides in the global market, several studies have found that insects adapt and survive to our approaches through a mechanism called natural selection.

In the case of most concentrated pesticides, we deliver a molecule that controls by killing or repelling a specific target, in this case, we will talk about Insecticides.

How do most insecticides work?

In the case of The United States, the most popular classes of insecticides are Synthetic pyrethroids (Type l or ll), Carbamates, Neonicotinoids, phenyl-pyrazole, etc. These insecticides work by delivering an active molecule that binds to a site in order to excite, open-block, inhibit or promote. Thus, causing a disturbance that in most cases could be lethal if the proper dose is applied.

Something curious happens when insecticide applications are the sole approach to addressing a pest situation. Natural mutations happen constantly in animal populations in the world, us included. Since not every individual is the same, we have sets of alleles that contain unique information. Insecticide applications create what is called a ''Bottleneck effect'' that reduces a population dramatically in a given space, allowing only those who have the ability to survive due to a random mutation get to live and reproduce. Thus, passing their genes to the next generation.

With the continuous use of insecticides that work in the same target area (organochlorine class to pyrethroid), and the sole reliance on chemical approaches, Pest control operators and homeowners have been reinforcing specific mutations over the years, killing the susceptible ones and sparing those with the mutations that enable them to survive, thrive and reproduce. Eventually, with enough reduction of the Gene pool, quick reproduction, and isolation, resistance to insecticides occurs.

How do insects resist chemical applications?

There are 4 types of resistance

• Behavioral resistance
• Metabolic resistance
• Physiological resistance (Target insensibility)
• Physical resistance (Thickening of the exoskeleton)

In this post, we will focus on Metabolic resistance. Insects (for example cockroaches) that were able to express significantly higher detoxifying enzymes, were able to survive and reproduce. These enzymes break down conventional insecticides (like Deltamethrin) into molecules called ''Metabolites'', which do not cause significant damage to the insect. If enough molecules get metabolized and the dose is not lethal, the insect can get back on its legs.

In modern days, we have three ways of managing this: 1st, we provide a contact application that delivers several times the lethal dose, overloading the insect with the active ingredient. 2nd, we use more active ingredients per sq ft to ''increase the dose'' or by using a synergist that will ''weaken'' the insect.

What is a synergist?

If you have ever used natural pyrethrins or a pyrethroids type one, you would notice they often come along with ''Piperonil butoxide'' or ''Mgk 264''. These two compounds work as synergists by inhibiting the formation of the enzymes that break down the active ingredient, causing more molecules to interact with the active site, and having a permanent knockdown. The following insecticide has both of them:

another example, a synthetic pyrethroid type l (quick knockdown, quick breakdown by enzymes, non-residual effects) not so lethal by itself.

By this point, I hope we have a clear understanding of what Regular metabolic resistance is and how it is usually managed. Let's get real now on what we came for:

What in the world is a ''Pro-insecticide''?

Pro-insecticides are active ingredients that require metabolic activation (enzymes breaking down a molecule) to become harmful to the target insect. In the day-to-day operations, we have 2 active ingredients that are pro-insecticides:

• Indoxacarb =Advion brand (syngenta), Doxem brand (Control solutions, Inc)
• Chlorfenapyr = Phantom (Basf), Spectre 2 (Control solutions, Inc)

Let's talk about Indoxacarb: This molecule has been on the market since late 90's, and has worked like a charm for German cockroaches. But, why is it so powerful?

Well, turns out that it takes the bad side of regular metabolic resistance to its favor. How come?: Indoxacarb (chemically a carbamate) is NOT the actual molecule that causes the damage, it is like a trojan horse. Once Indoxacarb enters the cockroach system, a metabolic process begin, where the enzymes start to break down the molecule into Metabolites, in most molecules the metabolites are unharmful, but in this case, it is the metabolite (DCJW) the one that causes the actual damage to the cockroach. The more prone the cockroach is to quickly break down the active ingredient (which will make it survive if you were using a conventional insecticide) the more DCJW is in the cockroach system. The ''tougher'' the cockroach, the weaker it becomes to a pro-insecticide like Phantom or Advion.

Due to the pro-insecticide needing to be activated to cause mortality, non-target organisms with a slower metabolism will not be likely to be killed by this pro-insecticide. That doesn't mean we should only buy pro-insecticides as the ''silver bullet'' for resistant organisms, rather we should change the drive from pesticide applications to integrated pest management.

Hope this article helped you understand how pro-insecticides work, thanks for reading!

-- Jorge Bedoya, ACE

New York Exterminating, Inc