Ecological and Evolutionary Aspects of Insecticide Resistance. - book reviews

Ecology, April, 1997 by Michael A. Caprio

The evolution of resistance to pesticides in insects has become a major problem worldwide. Over 600 species of insects have become resistant to one or more insecticides. Loss of critical insecticides has resulted in drastic changes in agricultural communities, and has often had an impact in health related issues, as when resistance contributed to the demise of the W.H.O. effort to eradicate malaria. Despite the opportunity insecticide resistance would seem to offer population geneticists for testing genetic hypotheses, the evolution of resistance has generally not received much attention from the broader area of ecological genetics. McKenzie has attempted to bridge the gap between basic ecological genetics and recent studies in the evolution of resistance, and to provide an introduction for students of evolution to the findings of insecticide resistance. This book is essentially a continuation of the excellent review by Roush and McKenzie (1987) (Roush, R. T. & J. A. McKenzie. 1987. Ecological genetics of insecticide and acaricide resistance. Annual Review of Entomology 32:361-380), and I expect it to be of similar value to those interested in insecticide resistance. McKenzie's work is refreshing because he provides a broader introduction to the genetics of insecticide resistance and its interaction with toxicology and ecology rather than emphasizing toxicological aspects. While the genetic components of resistance models have been sound, the experimental utilization of colonies of resistant and susceptible insects (often by non-geneticists) has often been suspect. For example, the ability of backcross experiments to detect if more than one gene is involved in resistance is compromised by the lack of a common genetic background in both colonies, and yet most comparisons fail to address this problem. McKenzie includes examples on the impact of genetic background on the expression of resistance as well as appropriate methods to eliminate this problem.

McKenzie has taken care to make the book readable for those not familiar with the idiosyncrasies of resistance studies. It will be most useful for those involved with the study of resistance, but the examples of population responses to insecticide stress should be valuable to students in other areas. At the very least, these examples provide underutilized testing beds for ecological genetics models. McKenzie uses the first chapter of the book to establish the basic ecological genetics framework upon which the remainder of the book rests. This chapter outlines those areas of population genetics theory most relevant to the evolution of resistance. While McKenzie notes that selection coefficients in resistance are large, he argues that such coefficients may not be unusual in natural ecosystems, and many classic examples of selection are from ecosystems with large selection coefficients. McKenzie proposes three topics from the study of insecticide resistance that should be addressed in an evolutionary or ecological context. These include the genetic basis of traits such as resistance (are they controlled by one or multiple loci), how selection acts to bring about genetic changes (fitness and dominance and how these interact with ecological parameters), and finally how this information can be used to manipulate systems to delay the onset of resistance.

The second chapter of the book is devoted to the genetic basis of insecticide resistance. McKenzie begins with the basic models of the relationship between insecticide dose and mortality of different genotypes (assuming monogenic resistance). This is convenient for individuals who have not encountered the literature on resistance previously. The relationship between the phenotypic expression of dominance and insecticide dose is also covered. McKenzie then discusses the evolution of monogenic and polygenic traits. He argues that selection in laboratory populations occurs within the phenotypic distribution and therefore leads to polygenic resistance. This is a contentious issue among those who select for resistance in laboratory populations. While I agree with McKenzie's position that selection of susceptible populations in the lab may increase the tendency for development of polygenic resistance, I disagree with his interpretation of the work by Lande (1983. The response to selection on major and minor mutations affecting a metrical trait. Heredity 50:47-65) upon which he builds his case. The fitness costs associated with most resistance alleles are small compared to the selection coefficients for resistance, and under these conditions monogenic and polygenic resistance should evolve at approximately the same rates. Most discussion of this topic errs in the application of models assuming infinite population size to small finite populations in which rare alleles or allele combinations may not even exist. McKenzie also covers localization of genes with visible genetic markers, though some coverage of more recent techniques such as QTL mapping and other molecular techniques is missing.