**1. Introduction**

#### **1.1. What is insecticide resistance?**

Resistance has been defined as 'the development of an ability in a strain of insects to tolerate doses of toxicants which would prove lethal to the majority of individuals in a normal population of the same species' [1] and also recently as a 'genetic change in response to selection by toxicants that may impair control in the field.' [2]. The resistance status also describes the decreased susceptibility of a pest population to a pesticide that was previously effective at controlling the pest, through natural selection with the genetic traits for resistance being passed on to subsequent offspring.

The development of insecticide resistance is dependent on the genetic composition of a species population. It is preadaptive, in the sense that in most cases the insecticide does not induce

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any heritable changes but selects favourable mutations that allow the insect to survive the treatment [3]. The resistant strains thus develop through the survival and reproduction of individuals possessing one or more of many possible mechanisms that allow survival after exposure to an insecticide, each controlled by one or more resistance (R) genes. Strains tend to revert to susceptibility in the absence of insecticide exposure unless they have become homozygous for the R genes [1, 4, 5]. This makes insecticide resistance to be a natural phe‐ nomenon controlled by genes that bring about the biochemical, physiological, or behavioural changes on which resistance is based.

Resistance can shorten the long-term effectiveness of a particular insecticide against a species population prompting the use of an alternative insecticide to which there is no resistance; but unfortunately, this often becomes a temporary solution. The development of cross-resistance may occur to compounds within a group with a similar mode of action, especially if their metabolism and their target site attachment are very similar [6].

Cross-resistance can also occur between groups of insecticides with different modes of action and can be mediated by a single gene, i.e., be monogenic due to a single defense mechanism operating against two or more toxicants. It can also be polygenic where multiple mechanisms are available, which may not act equally against different toxicants. Since multiple resistances involve multiple genes, it can be a most serious development, should it occur in the field [6].
