The first in a two-part Active Insight series from Steve Broadbent, regional director for Ensystex, on the science of resistance.

Often when a pest manager faces a situation where a treatment program fails to control the target pests, the failure is attributed to ‘insecticide resistance’. Yet the reality is, particularly when considering the urban environment, resistance at levels that will result in control failure are very rare indeed. In other words, application and control technique are more critical factors.

The Entomological Society of America defines resistance as:

‘The development of an insect strain that is capable of surviving a dosage or dose that is lethal to the majority of individuals of the same species by means of a genetic, inheritable change, that has increased in frequency in response to selection, and may impair control in the field’.

This is a classic evolutionary process, one of natural selection – survival of the fittest organisms in the prevailing conditions, such that their characteristics get passed into future generations. This is different to tolerance, which is the natural ability for an insect to withstand insecticide exposure. This may differ between species, or life forms, e.g. in German cockroaches (Blattella germanica) it is well documented that the nymphal stage is more tolerant than the adult stage, and that adult males are more susceptible than females.

Understanding resistance

When it comes to insects, four key types of resistance have been identified.

Metabolic resistance occurs when resistant insects may detoxify or destroy the toxin faster than susceptible insects, or quickly excrete the toxins. Sometimes referred to as physiological resistance, it is the most common resistance mechanism and usually presents the greatest challenge to pest managers. Essentially, insects use their internal enzyme systems to break down the insecticide at a rate that prevents a lethal dose of the insecticide developing inside the insect. These enzyme systems can also have a broad spectrum of activity i.e. they can degrade different insecticides.

Target-site resistance occurs where the insect may be genetically modified to prevent the insecticide binding or interacting at its site of action. Knockdown resistance (known as ‘KDR’) is a classic example of target-site resistance, where amino acid substitution in the voltage- sensitive sodium channels results in reduced sensitivity to DDT and pyrethroids. First identified in the housefly in intensive animal housing situations in Europe, it is the most well understood mechanism conferring resistance against pyrethroids, particularly in mosquitoes.

Penetration resistance occurs when resistant insects absorb the toxin in the insecticide more slowly than susceptible insects. The insect’s outer cuticle develops barriers that slow the rate of absorption of the chemical into their bodies – one example being bed bugs (Cimex lectularius). This mechanism can protect insects from a wide range of insecticides.

Behavioural resistance is the result of a change in animal behaviour that increases the likelihood of its survival when faced with a certain treatment or situation. 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). However, for these behaviours to be classed as behavioural resistance, rather than a simple response to the presence of the insecticide, the behaviour has to be shown to be an inherited, genetic trait. The aversion of German cockroaches to the glucose in cheaper cockroach gel baits would be a well known example of behavioural resistance.

Resistance may develop to only a single insecticide, however it is more common for insects that exhibit resistance to one insecticide to be resistant (or develop resistance more rapidly) to other insecticides with the same mode of action. The housefly, as referenced above, provides a classic example where populations that became resistant to DDT in the 1950s also exhibited resistance – with no previous exposure – to pyrethroid insecticides used decades later. DDT and pyrethroids have the same mode of action. This is known as cross- resistance. Multiple resistance occurs in insect populations that resist two or more insecticide classes with unlike modes of action.

How has resistance come about?

An interesting question is, ‘Which came first, resistance or insecticides?’ The answer is probably that the resistant genotypes were always there. This was best demonstrated from historical pinned specimens of the Australian sheep blowfly (Lucilia cuprina) where it was shown that the mutations conferring resistance to malathion but not to diazinon, were already present in 21 pinned specimens collected before the introduction of organophosphorus insecticides.

This finding is of interest because it suggests that resistance-associated mutations likely had some other function prior to their role in resistance.

Insecticide resistance can quickly develop and spread within a species under certain environmental circumstances. The potential for resistance to spread is heightened when:

  1. Insecticides are used in enclosed environments, e.g. greenhouses, intensive animal housing, where there is little or no immigration of susceptible insects to dilute a population of resistant insects;
  2. The insects produce multiple generations every year and many o spring per generation (an e ect compounded with insects that reproduce asexually, such as aphids);
  3. The insect population is highly susceptible to the insecticide. If a species is highly susceptible, only resistant insects survive the treatment and reproduce. There is no dilution of the resistant population;
  4. The insect population has many genes conferring resistance.

These situations are less commonly encountered in the urban pest situations, but we will explore the levels of resistance in the various urban pests in future articles in this series.

Achieving control is possible

It is a common misconception that if an insect, or rodent for that matter, is resistant to an active, that it cannot be killed by that active. This is untrue, as toxicity is always dose and time dependent; resistant strains of insects simply require higher than normal doses of insecticide and longer exposure periods before they die. Eventually they may suffer no ill effects at all from a given insecticide, but this is rare.

We can measure insecticide resistance by comparing the amount of insecticide required to kill the resistant insect compared to the susceptible insect within the same species. If we say a species has ‘two-fold‘ resistance, this means it takes two times as much insecticide to kill the resistant strain (this would be considered a low level of resistance).

Resistance levels of up to several thousand-fold have been recorded. For example, the adults of the dengue mosquito (Aedes aegypti) strain SP developed 1650-fold resistance to permethrin, with the SP larvae showing 8790-fold resistance. The SP strain of mosquito can still be killed, but a much higher dosage is required.

In the next article in this series, we will look more closely at resistance with respect to fleas and cockroaches.