By Raymond A. Cloyd (rcloyd@ksu.edu), Department of Entomology, Kansas State University
Pesticide resistance is always a concern because once an arthropod (insect and/or mite) pest population can no longer be adequately suppressed with existing pesticides (in this case, insecticides and miticides) then management options become limited. Resistance is the genetic ability of some individuals in an arthropod pest population to survive an application or multiple applications of a pesticide. In other words, the pesticide(s) no longer effectively kills a sufficient number of individuals in the arthropod pest population. Resistance develops at the population level and is an inherited trait. As such, surviving arthropod pests can pass traits (genetically) onto their offspring (young) or next generation thus enriching the gene pool with resistant genes (alleles). The amount of “selection pressure” or the frequency of applying pesticides is the main factor that influences the ability of an arthropod pest population to develop resistance to pesticides. This then increases the proportion or frequency of resistant individuals. However, there are oftentimes inquires or issues regarding why pesticide resistance is rare or occurs less often in natural enemies (e.g., parasitoids and predators) in comparison to arthropod pests.
There are two hypotheses that may possibly explain this phenomenon: the pre-adaptation hypothesis and food limitation hypothesis. The food limitation hypothesis proposes that natural enemies tend to not readily develop or evolve resistance because pesticide applications, depending on frequency, reduces their food supply by killing susceptible prey (hosts). After applying pesticides, natural enemy populations tend to rebound at a slower rate in response to the lack of food whereas insect and/or mite pests recover quickly in the absence of natural enemies. This is associated with a “low” density of prey, which results in natural enemies being negatively impacted in terms of consumption rates, fecundity, and survival.
The pre-adaptation hypothesis advances the notion that herbivores or plant-feeding insects and mites are already pre-adapted to detoxify pesticides (insecticides and miticides) because they have evolved the ability to detoxify plant defensive compounds (e.g., secondary plant metabolites) such as plant alkaloids. Because plant-feeding insects and mites are typically exposed to a broad diversity of plants and thus plant allelochemicals (non-nutritional chemicals synthesized by an organism that affect growth, survival, and behavior of certain member species) they are able to metabolize a broad range of chemical defenses by producing inducible enzymes in response to particular enzymes associated with specific compounds. The mechanisms by which insect and mite pests can overcome these plant defenses include detoxification of chemicals, altering target site or sites, reduced penetration, and behavioral avoidance. As such, insect and/or mite pests are more likely to be pre-adapted to detoxify pesticides than natural enemies.
For example, the western flower thrips (Frankliniella occidentalis) has various metabolic detoxification enzyme systems designed to overcome secondary plant defenses including esterases, cytochrome P-450 mono-oxygenases, and glutathione S-transferases. These same enzyme systems can be used to detoxify insecticides, which may explain why western flower thrips has developed resistance to numerous insecticides with different modes of action.
Well, how may this influence natural enemy populations? Any remaining resistant arthropod pests that survive, following exposure of a spray application, may have an abundant food supply (e.g. plants). However, those natural enemies that survive an application of an insecticide may find their food supply of prey substantially reduced. Therefore, resistance evolves more slowly in natural enemy populations than arthropod pest populations because natural enemies either starve or immigrate to a new location after spray applications have substantially reduced or eliminated their food source.
Excessive pesticide use may initially result in the suppression of arthropod pest populations; however, natural enemies such as parasitoids and/or predators may starve or emigrate in response to the “low” prey densities present thus resulting in local extinction of natural enemies under intensive pesticide use. As a consequence of natural enemy extinction, frequent applications of pesticides will be required, which may promote rapid resistance development in the prey population due to “selection pressure.” This results in an increase in the proportion or frequency of resistant individuals in the population.
Less pesticide use may still reduce natural enemy numbers; however, prey populations are likely to remain at sufficient levels to sustain natural enemy populations. Furthermore, reducing pesticide usage may decrease resistance developing in prey populations. Applying pesticides at “high” rates may effectively suppress prey populations such that a natural enemy’s food supply is substantially reduced. Additionally, in the absence of immigration, natural enemy populations tend to decline due to the frequency of applying pesticides. As such, natural enemies will starve. This can be avoided by allowing more susceptible individuals to survive, which may be fed upon by natural enemies. This also may slow the evolution of resistance by reducing “selection pressure” or the number of pesticide applications required; and thus resistance developing in arthropod pest populations. Moreover, an increase in the survival of prey results in an abundant food supply for natural enemies—thus decreasing starvation and emigration. Finally, reduced pesticide usage allows natural enemies to maintain or regulate arthropod pest populations over an extended time period.
Author:
Dr. Raymond A. Cloyd
Professor and Extension Specialist in Ornamental Entomology/Integrated Pest
Management
Department of Entomology
KansasStateUniversity
123 Waters Hall
Manhattan, KS66506-4004
Phone: (785) 532-4750
Email: rcloyd@ksu.edu
