Origins And Breadth Of Resistance

Insecticides are not considered to be mutagenic at their field application rates and are, therefore, not the causative agents of insecticide resistance. Rather they act to select favorable mutations inherent in the population to which they are applied. Some attempts to estimate the rates at which resistant mutations occur have been made. The treatment of blow flies (Lucilia cuprina) with a chemical mutagen resulted in the production of dieldrin-resistant target-site mutations in less than one per million individuals. Other studies, however, have found the incidence of resistant mutations to be worryingly high. A recessive allele conferring resistance to Bt toxins in unselected populations of the tobacco budworm, Heliothis virescens, was estimated to be present in about one in every thousand individuals in some areas of North America. Sixteen in every hundred insects were found to carry a Bt-resistant allele in unselected populations of the pink bollworm, Pectinophora gossypiella, in Arizonan cotton fields. Despite this, Bt cotton remains effective in the control of these species, suggesting that such estimates need to be interpreted carefully. Less empirical measures of mutation rates are extremely variable (10-3 to 10-16), but they will undoubtedly be dependent on the resistance mechanism involved.

Resistant mutations seldom confer protection to just a single toxin. Most commonly, they exhibit differing levels of resistance to a range of related and unrelated insecticides. In its strictest sense, the term cross-resistance refers to the ability of a single mechanism to confer resistance to several insecticides simultaneously. A more complex situation is that of multiple resistance, reflecting the coexistence of two or more resistance mechanisms, each with its own specific cross-resistance characteristics. Disentangling cross-resistance from multiple resistance, even at the phenotypic level, is one of the most challenging aspects of resistance research.

Cross-resistance patterns are inherently difficult to predict in advance, because mechanisms based on both increased detoxification and altered target sites can differ substantially in their specificity. The most commonly encountered patterns of cross-resistance tend to be limited to compounds in the same chemical class (equivalent to the term "side-resistance" as used by parasitologists). However, even these patterns can be very idiosyncratic. For example, organophosphate resistance based on increased detoxification or target-site alteration can be broad ranging across this group or highly specific to a few chemicals with particular structural similarities. The breadth of target-site resistance to pyrethroids in houseflies is also dependent on the resistance allele present. The kdr allele itself affects almost all compounds in this class to a similar extent (~ 10-fold resistance), whereas resistance due to the more potent super-kdr allele is highly dependent on the alcohol moiety of pyrethroid molecules, ranging from about 10-fold to virtual immunity. Cross-resistance between insecticide classes is even harder to anticipate, especially for broad-spectrum detoxification systems whose specificity depends not on insecticides having the same mode of action, but on the occurrence of common structural features that bind with detoxifying enzymes.

Empirical approaches for distinguishing between cross-resistance and multiple resistance include repeated back-crossing of resistant populations to fully susceptible ones, to establish whether resistance to two chemicals cosegregates consistently, and reciprocal selection experiments, whereby populations selected for resistance to one chemical are examined for a correlated change in response to another. If available, biochemical or molecular diagnostics for specific resistance genes can assist considerably with tracking the outcome of genetic crosses or with assigning cross-resistance patterns to particular mechanisms.

0 0

Post a comment