Imidacloprid [BSA]

Multiple pesticides originating from plant protection treatments and the treatment of pests infecting honey bees are frequently detected in beehive matrices. Therefore, winter honey bees, which have a long life span, could be exposed to these pesticides for longer periods than summer honey bees. In this study, winter honey bees were exposed through food to the insecticide imidacloprid, the fungicide difenoconazole and the herbicide glyphosate, alone or in binary and ternary mixtures, at environmental concentrations (0 (controls), 0.1, 1 and 10 mu g/L) for 20 days. The survival of the honey bees was significantly reduced after exposure to these 3 pesticides individually and in combination. Overall, the combinations had a higher impact than the pesticides alone with a maximum mortality of 52.9% after 20 days of exposure to the insecticide-fungicide binary mixture at 1 mu g/L. The analyses of the surviving bees showed that these different pesticide combinations had a systemic global impact on the physiological state of the honey bees, as revealed by the modulation of head, midgut and abdomen glutathione-S-transferase, head acetylcholinesterase, abdomen glucose-6-phosphate dehydrogenase and midgut alkaline phosphatase, which are involved in the detoxification of xenobiotics, the nervous system, defenses against oxidative stress, metabolism and immunity, respectively. These results demonstrate the importance of studying the effects of chemical cocktails based on low realistic exposure levels and developing long-term tests to reveal possible lethal and adverse sublethal interactions in honey bees and other insect pollinators.

Imidacloprid is an insecticide that is used globally and is suspected to be at least partly responsible for the decrease in the number of pollinator insects. The effects of an LC20 of imidacloprid on the parasitic behavior of the parasitoid wasp Leptopilina boulardi were investigated. Two genetically identical L. boulardi strains were used for the experiments. The strains differed in that one was infected by LbFvirus and the other was not. LbFvirus is a virus that induces an increase in the superparasitism behavior of the wasp. Results of two previous works have shown that the organophosphorus insecticide chlorpyrifos induces an increase in the superparasitism rate of L. boulardi through its specific action on cholinergic nervous pathways. Imidacloprid targets receptors implicated in cholinergic nervous pathways and thus it was expected that imidacloprid would also increase the superparasitism rate of L. boulardi. However, the results of the present experiment demonstrate that imidacloprid does not interfere with the parasitic behavior of L. boulardi and does not increase the rate of superparasitization. It can then be concluded that the major target of imidacloprid, namely type 1 alpha-bungarotoxin resistant nicotinic acetylcholine receptors (nAChR1), which imidacloprid is an agonist of, and the minor target, type D alpha-bungarotoxin sensitive nicotinic acetylcholine receptors (nAChRD), which imidacloprid is an antagonist of, are not involved in the superparasitism behavior by L. boulardi. Therefore, the superparasitism behavior of the parasitoid wasp is controlled by cholinergic pathways that do not involve nAChR1 or nAChRD subtype receptors. These findings may enable a better understanding of the mechanisms by which the LbFvirus acts, and contribute to a better evaluation of the potential environmental impact of imidacloprid use.