Catch 22 - American Chemical Society

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Chapter 5

Catch 22: All Doses Select for Resistance. When Will This Happen and How To Slow Evolution? Jonathan Gressel* Department of Plant and Environmental Sciences, Weizmann Institute of Science, Rehovot, Israel *E-mail: [email protected].

High dose rates of pesticides rapidly select for monogenic target site resistance, especially when the chemical persists in the field or the farmer persists in continuous application, but preclude the evolution of minor gene quantitative resistance. Near sub-lethal low rates select for incrementally creeping quantitative resistance, and is exacerbated by having large pest populations in the field where economic threshold treatment strategies were used. Pest evolution can be delayed by practices that keep populations very low, such as crop and pesticide rotations using mixtures and rotating dose regimes, sanitation, crop breeding and genetic engineering for resistance as well as non-chemical cultivation.

Catch 22: (definition) “a difficult circumstance from which there is no escape because of mutually conflicting, exclusive or dependent conditions”, as originated by Heller (1). A botanical example with such a dual catch is the Australian Calamus muelleri, called lawyer vine because it has spines as well as snagging sharp-hooked tendrils pointed in all directions and‘gets you whether you are coming or going’. When ancestral humans domesticated cultivated agriculture, they created new ecological niches that pests (weeds, arthropods, pathogens) rapidly filled. As different cultural practices were developed to deal with the pests, evolution countered by evolving resistance to the practice, or by filling the new niche

© 2017 American Chemical Society Duke et al.; Pesticide Dose: Effects on the Environment and Target and Non-Target Organisms ACS Symposium Series; American Chemical Society: Washington, DC, 2017.

with naturally resistant pests. Pests did not readily evolve resistance to the earliest pesticides, such as sulfuric acid to kill weeds, arsenicals to kill insects and mercurials against pathogens. Their multi-target toxicity, targeting multiple cellular sites in both pests and humans resulted in a quest for more selective pesticides: herbicides selective between weeds, crops and humans; insecticides and fungicides selective between pest arthropods and pathogens and beneficial insects, fungi and bacteria, and less toxic to humans.


Target Site Resistance to Residual Pesticides Most of the modern (past half century) pesticides commercialized inhibited a single enzyme in a key metabolic pathway. Initially the preferred ones were effective for long durations, providing season long control. The early philosophy of growers was ‘the only good pest is a dead pest’, so the highest registered rates for each pesticide were used. If a pesticide did not have the desired residual effect, it was applied repeatedly during a growing season, with the highest possible selection pressure. Such practices were abetted by advice from industry and extension, each for their own interests. The lack of persistence of some pesticides to provide season long control was overcome by the persistence of farmers to repeatedly apply the same pesticide throughout the season. An inaccurate version of Occum’s razor was invoked: “The simplest solution to a problem is most likely the correct one”, or more cynically “KISS=keep it simple, stupid”. While this extremely strong selection pressure was being exerted, some began constructing models based on simple population genetics and dynamics that indicated that the evolution of resistant arthropods (2), pathogens (3), and weeds (4), was an inevitable consequence. The models were published at about the same time as the first resistances appeared. The models could not be realistically tested in the laboratory with organisms larger than microorganisms, and there was a good possibility laboratory data might not predict field results. For example, the chromosome-inherited target site resistance to penicillin that is easily selected for on petri-plates has yet to be reported to appear in a hospital patient. Plasmid inherited antibiotic inactivation commonly appeared in hospital wards many decades ago, but was not reported to evolve in any petri-plate selections. Pesticide resistance field experiments would require huge areas and immensely large populations as the initial mutation frequencies are very low, and many generations of evolution, well beyond typical budgets as well as time spans for student dissertations. Because of this inability to perform laboratory or field experiments, epidemiology should be used to validate model predictions and elucidate best practices, by analyzing the practices where resistance has evolved, and where it has not. Many competent scientists initially denied the possibility of widespread resistance ‘because we have yet to see it’ or ‘it has only occurred in limited areas’. All the models showed that under constant selection pressure resistance individuals are enriched in an exponential manner from a very low initial mutation frequency. As this number is typically (but not always) less than one in a million, it is generations before resistant individuals become a noticeable fraction of the 62 Duke et al.; Pesticide Dose: Effects on the Environment and Target and Non-Target Organisms ACS Symposium Series; American Chemical Society: Washington, DC, 2017.


population. Resistance was slowly becoming enriched in pest populations while the deniers denied. This is depicted in Figure 1, both as actual measured field data (Figure 1A) as well as how that would appear as population distributions (Figure 1B).

Figure 1. Seemingly sudden appearance of major monogenic target site resistance (A,B) vs. incremental creep of quantitative resistance (C,D). A. Field data from a monoculture maize field treated annually with a high dose of highly persistent atrazine. As the frequency of resistance in the field was exponentially enriched from a very low number, the area covered by Amaranthus was exceedingly low until the area covered suddenly jumped from

Catch 22 - American Chemical Society

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