There are a number of ways insects can become resistant to insecticidal crop protection and public health products:

Metabolic resistance

Resistant insects may detoxify or destroy the toxin faster than susceptible insects, or quickly rid their bodies of the toxic molecules. Metabolic resistance is the most common mechanism and often presents the greatest challenge. Insects use their internal enzyme systems to break down insecticides. Resistant strains may possess higher levels or more efficient forms of these enzymes. In addition to being more efficient, these enzyme systems also may have a broad spectrum of activity (i.e., they can degrade many different insecticides).

Target-site resistance

The target site where the insecticide acts in the insect may be genetically modified to prevent the insecticide binding or interacting at its site of action thereby reducing or eliminating the pesticidal effect of the insecticide.

Penetration resistance

Resistant insects may absorb the toxin more slowly than susceptible insects. Penetration resistance occurs when the insect’s outer cuticle develops barriers which can slow absorption of the chemicals into their bodies. This can protect insects from a wide range of insecticides. Penetration resistance is frequently present along with other forms of resistance, and reduced penetration intensifies the effects of those other mechanisms.

Behavioural resistance

Resistant insects may detect or recognize a danger and avoid the toxin. This mechanism of resistance has been reported for several classes of insecticides, including organochlorines, organophosphates, carbamates and pyrethroids. Insects may simply stop feeding if they come across certain insecticides, or leave the area where spraying occurred (for instance, they may move to the underside of a sprayed leaf, move deeper in the crop canopy or fly away from the target area).

There are two common mechanisms by which insects and mites overcome the toxic action of pesticides, increased metabolic detoxication and decreased target site sensitivity. Resistant pests with enhanced metabolic detoxication are able to disarm toxic pesticide molecules more rapidly than susceptible individuals. As a result, less of the active pesticide sprayed on the field reaches the target site in the pest.

With the second common mechanism, decreased target site sensitivity, the physiological target for the pesticide in the resistant insect is less sensitive to poisoning than in susceptible individuals. For example, organophosphate insecticides kill pests by inhibiting acetylcholinesterase, an enzyme that is important in nerve function. Some insects, mites, and ticks resistant to organophosphates have a form of the target enzyme that is less sensitive to poisoning.

Resistance also can