The Insecticide Resistance Action Committee (IRAC) defines cross-resistance as “occurring when resistance to one insecticide confers resistance to another insecticide, even where the insect has not been exposed to the latter product”. Metcalf (1989) regarded it as a phenomenon that occurred within a class of insecticides, thus essentially reducing it to the results of target-site mutations.
The classic example of this was found in the house fly, where populations that had become resistant to DDT, subsequently exhibited resistance to pyrethroids, even where no previous exposure to pyrethroids had occurred (Busvine, 1951). This was later found to be due to mutations in the voltage gated sodium channel (VGSC) where both pyrethroids and DDT exert their influence.
Further examples of this same cross-resistance pattern were found in several pests including cockroach and mosquito (Scott and Matsumura, 1981; Atencia et al, 2016).
Other target-site based cross resistance examples were also found within organophosphates and carbamates e.g. Green Rice Leafhopper (Hama and Iwata, 1978), olive fruit fly (Vontas et al, 2001) and the neonicotinoids (Mota-Sanchez et al, 2005).
More recently, definitions of cross-resistance have broadened to include inter-class as well as intra-class resistance. Bras et al (2022) considered “cross-resistance as resulting from prior exposure to a different, possibly not chemically related, toxin in a species’ evolutionary history”. This implies that the occurrence of cross-resistance in generalist phytophagous feeders would be more prevalent due to pre-exposure to a wide range of plant toxins (Dermauw et al, 2018). Certainly, cross-resistance between different classes of insecticides is likely to occur due to metabolic resistance mechanisms.
Enhanced P450 activity has been reported as the mechanism behind cross-resistance in phytophagous pests such as Plutella xylostella, brown planthopper and the small brown planthopper (Qian et al, 2008; Liu et al, 2003; Yu 2024).
It is also responsible for cross-resistance in mosquito sp., cockroach and house flies (Ibrahim et al, 2016; Wen and Scott, 1997).
Enhanced esterase activity is also responsible for numerous examples of cross-resistance, due to their wide range of substrates. In mosquito, esterases have been reported to confer cross- resistance between an OP and a pyrethroid (Gordon and Ottea, 2012), in aphids to OPS, carbamates and pyrethroids (Devonshire and Moores, 1982) and strikingly in diamondback moth to pyrethroids and Bacillus thuringiensis (Bt) toxin (Sayyed et al, 2008).
Actions:
Target-site resistance: Mitigation of the effects is undertaken by the “rotation of actives” programme suggested by IRAC. The IRAC MoA (Mode of Action) classification groups classes of insecticides that have a shared MoA. IPM strategies advise that successive generations of a pest should not be sprayed by insecticidal agents from the same MoA group.
Metabolic resistance: There seems no dedicated program to help reduce cross-resistance due to metabolic factors!
Metabolic resistance and consequently also cross-resistance due to metabolic enzymes could be reduced by the use of synergists: In the diamondback moth, for example, the use of a piperonyl butoxide analogue inhibited esterase activity and increased sensitivity to deltamethrin by 210-fold, and to Bt toxin 32-fold (Sayyed et al, 2008).
The P450 gene CYP6a13 has been identified as conferring cross-resistance to chlorpyrifos, deltamethrin and Chlorantraniliprole in the fall armyworm; this was effectively synergised by PBO (Chen YM, 2024). Similarly, metabolic resistance in tomato leafminer to tetraniliprole and found to confer cross-resistance to chloraniliprole and flubendiamide was reduced by the use of PBO (Qu C, 2024). A field population of mosquitoes from Tunisia exhibited resistance to deltamethrin and very high resistance to permethrin. The lack of cross-resistance to DDT indicated that the resistance was metabolic-based. This was completely suppressed by the addition of PBO 4 hrs prior to insecticide (Tabbabi et al, 2018).
REFERENCES
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