Abstract
Populations of European red mite, Panonychus ulmi (Koch), selected in the laboratory showed ca. 9-fold resistance to cyhexatin. Initial crosses between cyhexatin-R (resistant) and -S (susceptible) mites produced a strain showing ca. 3-fold resistance in the F1 generation. Tests with back crosses indicated that cyhexatin resistance was complex; i.e., due to more than one gene. Measurements of fecundity, life span, sex ratio, and rate of development of cyhexatin-resistant and -susceptible strains did not show any large reproductive disadvantage associated with cyhexatin resistance. In simulated population cage tests beginning with F1 mites, cyhexatin resistance was lost after four to six generations, thus providing further evidence that resistance was due to the interaction of multiple genes. Dicofol resistance in another population was ca. 15-fold. Initial test crosses between resistant and susceptible populations produced a strain similar in response to the susceptible strain. Results of back crosses indicated that resistance was probably due to a single recessive gene. Fitness tests similar to those with cyhexatin-resistant populations indicated that dicofol-resistant populations were not very different from the susceptible strain. Population cage tests with an initial population of F1 (R × S) mites showed no reversion of dicofol resistance over eight generations, suggesting that dicofol resistance was stable within a population for long periods. Crosses between cyhexatin- and dicofol-resistant strains, followed by selection with mixtures of both acaricides, produced strains showing resistance to both acaricides. Long term rotations of acaricides are suggested as a way to manage cyhexatin and dicofol resistance.