The Effects of Temperature on the Efficiency of Insecticides Applied Topically to Boll Weevils Differing in Susceptibility to Chlorinated Hydrocarbon Insecticides

Abstract

Greater mortality of the boll weevil ( Anthonomus grandis Boh.) resulted at the higher rather than at the lower extreme of the post-treatment range of temperatures with one exception–the response of the resistant strain to the endrin-malathion combination wherein greater mortality resulted at the lower extreme of the temperature range. The two strains (resistant and susceptible or reference) differed greatly in their susceptibility to the chlorinated hydrocarbons. Toxaphene and endrin were ineffective against the resistant strain. Endrin and malathion, when combined, were antagonistic at 90° F., hut showed a synergistic effect at 60° and 80° F. On the other, hand, toxaphene and malathion combined were antagonistic at 60° F., but showed a synergistic effect at 80° and 90° F. The resistant and reference strains responded similarly to temperature changes for each insecticide used in respect to antagonistic or synergistic effects. These findings indicated that the mechanism which causes synergistic effect and antagonistic effect had differing temperature coefficients of action for the two combinations (endrin-malathion and toxaphene-malathion). The fact that the same strain (either resistant or susceptible) responded differently to each of the three insecticides (endrin, toxaphenp, and malathion) when held at different post-treatment temperatures, indicated that each insecticide had a different mode of action. The difference in the amount of insecticide required to control the reference strain as compared with the amount required to control the resistant strain, when held at varying post-treatment temperature levels, is further supporting evidence for such a conclusion. This is the logical expectation in the case of malathion (an organic phosphate) and the chlorinated hydrocarbons as a group. However, it is noteworthy that endrin and toxaphene, both being chlorinated hydrocarbons, appeared to have different modes of action. In addition to susceptibility to chlorinated hydrocarbons, there was an indication that the two strains differ in other physiological functions. The fact that more malathion was required to control the chlorinated-hydrocarbon-susceptible strain than was required to control the resistant strain prevents the assumption that the susceptibility to malathion and the susceptibility to endrin or toxaphene was controlled by the same mechanism. It is also significant that although endrin was relatively non-toxic to the resistant strain, it still influenced the toxicity of malathion to this strain.