Insecticides cross-resistance

As described in the section on Cross-resistance in this chapter, it was found that some insect species showed extremely low cross-resistance to three ingredients, pyrethrins as well as d-allethrin and prallethrin, although they developed resistance to photostable synthetic pyrethroids. The latter two compounds of d-allethrin and prallethrin have quite similar chemical structures and the same configuration as cinerin I (an ingredient of pyrethrins). It is considered preferable to develop pyrethroids retaining the characteristics of natural pyrethrins and household insecticides containing them in the perspectives of safety and low cross-resistance. 

In 1958, Barthel et al. [25] reported dimethrin (15), which was the first substituted benzyl alcohol ester of chrysanthemic acid. This compound was not put into practical use due to its low insecticidal activities. Phenothrin (16), one of the m-phenoxybenzyl alcohol esters developed by Fujimoto et al. [26], was found to have superior chemical stability as well as safety, and has been the sole pyrethroid used as a lice control agent for humans. Further improvement was made by Matsuo et al. [27] who introduced a cyano function at the a position of the benzyl part of phenothrin, leading to a-cyano-m-phenoxybenzyl alcohol esters (17). Thereafter, this alcohol moiety has been used as a component for a number of photostable pyrethroids for agricultural purposes however, the development of cross-resistance can be seen in some pests. 

A. aegypti colonies were found to have developed cross-resistance to even polyfluoro benzylalcohol ester pyrethroids with potent insecticidal activity. Mosquito coils of these compounds were effective against allethrin-susceptible A. aegypti colonies at ultra-low concentration, but needed several times higher concentrations for A. aegypti colonies in Group III in Table 8 (unpublished). 

Cross-resistance to pyrethroids for outdoor use has developed markedly in M. domestica, mosquitoes, cockroaches, and so on however, it has also been found that natural pyrethrins as well as d-allethrin and prallethrin (ETOC ), which have very similar chemical structures and the same configuration as natural pyrethrins, show an extremely low degree of cross-resistance development by these highly-resis-tant sanitary pests compared to photostable pyrethroids. Many novel synthetic pyrethroids recently developed as household insecticides have tended to pursue efficacy improvements in terms of rapid knock-down effects, residual efficacy or volatility. 

Insects treated with such analogs, could rapidly become tolerant not only to the analog, but also to the natural allelochemlc. There are examples of cross-resistance in which an insect treated with one chemical was found to have resistance to a chemical with which it had never been treated. A strain of house-fly which had developed resistance to the synthetic Insecticide, DDT, was found to be resistant to the natural pyrethrln insecticides (286). 

These two insecticides are chemically very different, and yet they may react at the same site Inducing cross-resistance. 

Resistance to insecticides can be due to enhanced oxidative metabolism caused by cytochrome P450 monooxygenases. This type of resistance usually results in producing less toxic metabolites. Even when the metabolites are more toxic, often resistance prevails, perhaps because the toxic metabolites are less stable, cannot reach the site of action due to change in polarity, or are neutralized by other factors. As we have already seen (Chapter 8), the cytochrome P450 enzyme system is rather nonspecific in its attack on organic compounds. Hence, this resistance factor is nonspecific, explaining much of the cross-resistance observed. 

Cross-resistance refers to a situation in which a strain that becomes resistant to one insecticide automatically develops resistance to other insecticides to which it has not been exposed. For example, selection of a strain of Spodoptera littoralis with fenvalerate resulted in a 33-fold increase in tolerance to fenvalerate. The resistant strain also showed resistance to other pyrethroids (11- to 36-fold) and DDT (lower than for the pyrethroids). Exposure of Cidex qninquefasciatus to fenitrothion resulted in the development of resistance to the carbamate insecticide propoxur. Similarly, selection of a housefly strain with permethrin resulted in a 600-fold increase in resistance to permethrin. The resistant strain also showed resistance to methomyl, DDT, dichlorvos, and naled (Hassall, 1990). 

Yu and Nguyen (1996) showed that selection of a strain of diamondback moth (Plu-tella xylostella) with permethrin for 21 generations resulted in over 600-fold resistance to permethrin in this strain. The resistant strain was also cross-resistant to all pyrethroids tested, including bifenthrin, fenvalerate, esfenvalerate, A.-cyhalothrin, fluvalinate, and tral-omethrin. However, it remained susceptible to organophosphate, carbamate, cyclodiene, neonicotinoid, avermectin, and microbial insecticides tested. Biochemical studies indicated that pyrethroid resistance observed in this strain was most likely due to decreased target site sensitivity. 

It is noteworthy that negative cross-resistance has been reported in some cases. Negative cross-resistance refers to a situation in which increasing resistance to one insecticide in an insect population confers an increasing susceptibility to another. The best example of... 

Cross-resistance is not the same as multiple resistance. Multiple resistance may occur when a population of insects comes into contact with two or more different insecticides. Thus, cross-resistance refers to those cases in which a single defense mechanism confers resistance against various insecticides, whereas multiple resistance refers to cases of resistance to various insecticides conferred by different mechanisms. In general, multiple resistance is due to the sequential selection of populations with replacement insecticides. Each new insecticide selects one or more mechanisms of resistance, and each mechanism usually confers cross-resistance to several other insecticides (Georghiou and Taylor, 1976). Table 10.8 shows the multiple resistance to organophosphate, carbamate, and organochlo-rine insecticides in two strains of Culex pipiens quinquefasciatus. 

The use of selected insecticide mixtures should retard resistance development because it should be more difficult for an insect to develop several adaptations simultaneously. The concept of joint use of insecticides assumes that the mechanisms of resistance to each member chemical exist in such low frequencies that they do not occur together in any single individual in the population. Thus, insects that may survive one of the chemicals are killed by the other. This approach delays resistance in laboratory experiments and has been, at least temporarily, successful in a few field cases, particularly with certain organo-phosphate combinations (Hopkins and Moore, 1980). The use of insecticide mixtures is not without problems. Resistance to both compounds used in mixtures has sometimes developed rapidly. Cross-resistance also occurs among some of the pesticides. 

Villatte, F., Auge, D., Touton, P, Delorme, R., and Fournier, D., Negative cross-resistance in insecticide-resistant cotton aphid Aphis gossypii Glover, Pestic. Biochem. Physiol., 65,55,1999. 

Yu, S. and McCord, E., Jr., Lack of cross-resistance to indoxacarb in insecticide-resistant Spodoptera frugiperda (Lepidoptera Noctuidae) and Plutella xylostella (Lepidoptera Yponomeutidae), Pest Manag. Sci., 63, 63, 2007. 

Tphe search for insecticides with modes of action different from the A well-known acetylcholinesterase inhibition led us to uncouplers of oxidative phosphorylation (1, 2). An inherent advantage of such pesticides would be the absence of cross-resistance with organophosphorus compounds and chlorinated hydrocarbons. The number of commercial pesticides which are likely to act by uncoupling of oxidative phosphorylation is small. All of them can be regarded as derivatives of the... 

Boyd, C.E. and Ferguson, D.E. (1964) Spectrum of cross-resistance to insecticides in the mosquito fish, Gambusia affinis. Mosquito News, 24, 19-21. 

Koiitv, A.C. and Sales, N, (1994), Cross resistance spectra and eHeels ol synergists in insecticide resistant strains of Lucilia cuprinct (Diplera Calliphoridae). Bull Enio-moi. Res. 4, 355-360. 

In the presence of a continued selection pressure, metabolic resistance may facilitate the evolution of other defenses such as target site resistance, reported for the OPs and carbamates 6 and 10 years after metabolic resistance. Target site resistance to OPs and carbamates resides in modified forms of acetyl-cholinesterases (AChEs) with reduced affinity for the insecticides. AChE-based target site resistance does not necessarily confer cross resistance to all other OPs and carbamates and may be unstable in the absence of a selection pressure. 

As in vitro methods for studying cytochrome P-450 in insects became available (11-131, it soon became clear that insects with high cytochrome P-450 activities were resistant to carbamates and most other insecticides. This phenomenon is termed metabolic cross resistance and derives from the characteristic of cytochrome P-450 of accepting a very wide range of molecular structures as substrates the cytochrome binds the substrate very loosely by a lipophilic interaction and rapidly oxidizes it by an oxygen free radical-mediated reaction, a very powerful combination. Moreover, the cytochrome occurs in several or many different isoenzymic forms with broadly overlapping substrate preferences. A normally infrequent form may be selectively induced by allelochemicals in the crop plants (14), and if the induced form has survival value in the presence of an insecticide, it could be selected to dominate in the exposed population (15). 

The existence of multiple AChE isoenzymes has several consequences. First, it increases the chances of an insect having one that is, or by a minor genetic change can be rendered, insensitive. The molecular redundancy combined with a selection pressure in the form of persistent insecticide applications would facilitate target site resistance development. Second, it could be a factor in the frequent lack of target site cross resistance between OPs and carbamates, and even between different OPs. Third, it would facilitate the disappearance of the insensitive form(s) in the absence of a selection pressure. This would especially easily explain observed instability of resistance if the form(s) with decreased affinity for the inhibitors also have decreased affinity for the neurotransmitter. Insensitivity to the inhibitor may be accompanied by a reduced rate of neurotransmitter hydrolysis (56. 28), but this is not always the case. It seems that the reduced rate of neurotransmitter hydrolysis does not impair survival, at least in laboratory cultures of insects. It is unclear what impact such reduced rates have in field populations. 

---