The mechanisms of insecticide resistance in crop pests

Learn about the four insecticide resistance mechanism groups associated with UK crop pests and the mode of action (MoA) groups affected.

Insect populations can evolve to resist the insecticides designed to control them.

AHDB invests in strategic monitoring of resistance to identify trends and adapt pest management guidance. 

Scientists use laboratory bioassays to screen live pest samples to establish if the level of mortality deviates from known insecticide-susceptible baselines.

They also develop DNA-based tools to identify the genetic resistance mechanism(s) present in any sample.

There are four main groups of insecticide resistance mechanism:

1. Target-site resistance
2. Metabolic resistance
3. Penetration resistance
4. Behavioural resistance

Target-site resistance involves a mutation(s) in a target protein(s) that insecticides normally bind to, block or inactivate. This makes the pest less sensitive to the insecticidal effect.

There are several known target-site mechanisms, which may occur in the same species and result in resistance to multiple plant protection products.

Knockdown resistance (kdr and super-kdr)

Active ingredients in mode of action group 3, which include pyrethroids, are sodium channel modulators.

Sodium channels are essential for the movement of signals in the nervous system of insects.

Pyrethroids act on a protein that causes these channels to remain ‘open’.

This overexcites the nervous system and kills the pest.

Aphids with knockdown resistance (kdr) contain a modified sodium channel protein that limits or prevents this response.

Kdr confers moderate levels of resistance.

Super-kdr confers high levels of resistance.

Bioassays show strong resistance to pyrethroids in UK peach-potato aphid populations.

DNA-based tests determine the frequency of the mechanisms present:

• Most peach-potato aphids carry super-kdr (71% of the samples in 2021)
• Some peach-potato aphids carry kdr (24% of the samples in 2021)
• No peach-potato aphids (0% of the samples in 2020) carry both mutations

Modified acetylcholinesterase (MACE)

Active ingredients in mode of action group 1, which include carbamates (1A) and organophosphates (1B), are acetylcholinesterase inhibitors.

These insecticides inhibit an enzyme (acetylcholinesterase) that regulates the flow of a chemical messenger across the gap (synapse) between a pest’s nerve cells. The disruption kills the pest.

Modified acetylcholinesterase (MACE) aphids have a modified enzyme that does not allow the disruption process to occur effectively.

Peach-potato aphids with this type of resistance are highly resistant to pirimicarb (a carbamate).

In the UK, pirimicarb is the only approved insecticide affected by MACE resistance. Pirimicarb is only authorised for use in a limited number of UK crops.

The continued detection of MACE may be due to the resistance mutation ‘hitch hiking’ alongside super-kdr in the UK’s ‘super-resistant’ aphid clones.

Neonicotinoid resistance

Active ingredients in mode of action group 4, which include neonicotinoids (4A), are nicotinic acetylcholine receptor competitive modulators.

The first neonicotinoid, imidacloprid, was introduced in the early 1990s.

Soon after, low levels of resistance in peach-potato aphid populations were observed. However, aphids were still controlled effectively at recommended rates.

Initial resistance was due to a combination of enhanced expression of a gene responsible for the detoxification of neonicotinoids and/or reduced penetration of neonicotinoids through the aphid cuticle.

However, in 2009, a clone of peach-potato aphid (collected from a peach in southern France) showed strong (Nic-R++) resistance to neonicotinoids.

This was closely followed by highly resistant aphids on other hosts in southern Europe, North Africa and, most recently, Belgium.

This resistance is conferred by a simple point mutation that renders the insecticide target immune to neonicotinoids.

To date, no neonicotinoid control failures or resistant forms have been reported in the UK. However, a subtle, susceptibility shift to neonicotinoids was detected in an aphid sample collected from oilseed rape (November 2021).

Equivalent to metabolic-based resistance (Nic-R+), it is the first time this phenotype (moderate resistance) has been observed in the UK.

The maximum number of applications of any neonicotinoid-containing product is a statutory restriction introduced by CRD, in collaboration with IRAG, as a pro-active resistance management measure. Such restrictions take account of exposure of peach-potato aphids to neonicotinoid sprays when they are not the intended target of the spray.

Insects with this type of resistance make greater amounts of enzymes that break down or wrap up (sequester) insecticide molecules before they reach their target sites (primarily in the insect nervous system).

In pollen beetles, overproduction of a P450 enzyme confers resistance to pyrethroids.

In peach-potato aphids, overproduction of two esterase enzymes confers resistance – primarily to organophosphates, although carbamates and pyrethroids are also affected to a lesser extent.

Based on the quantity of esterases produced, aphids are categorised as either:

• S (susceptible)
• R1 (moderately resistant)
• R2 (highly resistant)
• R3 (extremely resistant).

This species also overproduces P450 enzymes. which confers low resistance to neonicotinoids.

In 2021, for the first time during the current monitoring project, R2 and R3 esterase-based resistance was not detected in peach-potato aphids collected from open-field crops.

The result suggests that the esterase-based resistance mechanism is being selected against now that organophosphate compounds are no longer used in the UK. This is referred to as a ‘fitness cost’.

This resistance helps delay the rate at which insecticides penetrate the body cavity, through modifications to the outer cuticle of insects. It is often present with other forms of resistance and may intensify the effects of those mechanisms.

Pests may also evolve behavioural adaptations that reduce exposure to insecticides.

Adaptions include the cessation of feeding when pesticides are encountered, and movement away from treated areas, such as to leaf undersides, or deeper within or away from the crop canopy.

Although relatively rare in crop pests, compared to pests of medical or veterinary importance, adaptations have been reported for several classes of insecticides, including organochlorines, organophosphates, carbamates and pyrethroids.