Research on the resistance to abamectin
It is an indisputable fact that the natural population including pests and mites has become resistant to abamectin.
In 1995, diamondback moth (Pluttella xylostell (L)) in Malaysia had caused 17-195 times of high resistance on abamectin insecticide. Brazil and Argentina reported that potato tuberworms (Tuta absoluta) also became resistant to abamectin. Campos and Dybas reported that the twospotted spider mites (Tetranychus urticae Koch) that were gathered from 10 nursery gardens in California in 1995 had big sensitivity difference to abamectin. In addition, in 1996 in Florida, America and Netherlands as well as in 1997 in Washington State, America, scientists successively found that twospotted spider mites (Tetranychus urticae Koch) had become resistant to abamectin. In the two biggest vegetable production bases in Taiwan province, China, diamondback moth resistance to abamectin has reached up to 2500-5000 times; in Tonghai County, Yunnan province, diamondback moth population resistance to abamectin has increased to 46.1 times. In Sichuang area, China, tetranychus cinnabarinus (Boiduval) resistance to abamectin has reached to the middle resistance level.
Resistance inheritance research shows that housefly strain (Musca domestica LPR) resistance to abamectin is controlled by polygenes which are respectively located in chromosome 2 and 3, besides, it belongs to high recessive heredity instead of sex linkage or cytoplasmic inheritance. The diamondback moth resistance inheritance to abamectin is autosomal and incomplete recessive. Besides, it may be controlled by polygenes. Tetranychus cinnabarinus resistance inheritance to abamectin is subject to polygenic and non-complete recessiveness or semirecessive inheritance, besides, it does not have maternal effect or extranuclear effect.
Research on four twospotted spider mites population which derived from different regions shows that the resistance of three strains has nothing to do with the decrease of cuticula penetrability, while the other strain is closely related with it. By studying the two of the strains resistance to abamectin miticide, it can be seen that the resistance is mainly caused by the increasing discharge capacity of polypide. Meanwhile, the polypide may conjugate with the residual of abamectin in vivo and enhance its metabolic capacity.
In 1986, Scott and Georghiou firstly discovered that the indoor selected housefly strain (LPR) which is resistant to permethrin has 76 times of cross resistance to abamectin. Although the housefly that is resistant to permethrin is easy to become cross resistant to abamectin, the strain which is highly resistant to abamectin will not have cross resistance to other types of drugs, such as organophosphorus, synthetic pyrethroids, lindane, cyclopentadiene pesticides and so on. Research shows that the housefly cross resistance to abamectin which is caused by its resistance to pyrethroid is likely to be caused by the enhancement of multifunctional function oxidase (MFO) metabolism and the decrease of cuticula penetrability. The resistance can be partially inhibited by the multi-function oxidase inhibitors (Pbo).
In 1990, Argentine and Clark measured that potato beetle strain (Leptinnotarsa decemlineata) which is highly resistant to organophosphorus and synthetic pyrethroids in the field has no cross resistance to abamectin. Resistance inheritance research shows that potato beetle resistance to abamectin is not belonged to sex-linkage and cytoplasmic inheritance, its resistance factor is polygenic and is located in the autosome, which belongs to incomplete recessive. Multifunctional oxidase inhibitor (Pbo) has obvious synergism both on the indoor and field selected resistant strains (the synergic ratio-SR is respectively as 15 times and 19 times), which shows that the multifunctional oxidase is related with resistance. Further study has shown that P-450 contents of these two resistant strains are both significantly improved. Besides, the abamectin oxide metabolites content in vitro and vivo metabolites are also obviously increased, which proves that as the multifunctional oxidase increase its oxidative metabolism to abamectin, it may cause the resistance. Carboxylic acid inhibitor-DEP (isopropyl fluorophosphates) will have significant synergism with the resistant population, which shows that enhancement activity of carboxylesterase is one of the factors that cause the resistance. Another research shows that potato beetle resistance to abamectin has nothing to do with the decrease of cuticula penetrability. However, the rapid discharge is one of the factors that cause resistance.
Researchers discovered that diamondback moth resistance to abamectin may be caused by the multifunctional oxidase and carboxylesterase. In addition, many resistance monitoring show that liriomyza trifolii, blattella germanica, citrus thrips and frankliniella occidentalis all have certain resistance to abamectin pesticide, but little researches have been carried out on their resistance mechanism. Due to the biological characteristics of termite, its resistance is hard to inherit. Currently we have not seen any reports about termite resistance to chemical drugs including abamectin and its similar drugs.